Acute Compartment Syndrome and Intra-Abdominal Hypertension, Decompression, Current Pharmacotherapy, and Stable Gastric Pentadecapeptide BPC 157 Solution
Abstract
:1. Introduction
2. Clinical Evidence
3. Basic Evidence
3.1. IAH’s Effectiveness Depending on the Organ(s) Investigated
3.2. Agents’ Effectiveness Depending on the IAH’s Level(s) Investigated
3.3. Agents’ Effectiveness Depending on the Organ(s) Investigated
3.4. Agents’ Effectiveness Considering Application Time
3.5. Agents’ Effectiveness Considering the Animal Model
4. BPC 157 Evidence
4.1. BPC 157 Primary Abdominal Compartment Syndrome
4.2. BPC 157 and Reperfusion After Decompression
4.3. Final Remarks for BPC 157 and Other Agents Used in ACS/IAH Studies
5. Conclusions
Author Contributions
Funding
Data Availability Statement
Conflicts of Interest
References
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Ref. | Agent | IAH Procedure | Target | Outcome |
---|---|---|---|---|
[8] | Stable gastric pentadecapeptide BPC 157 (10 µg/kg, 10 ng/kg sc) given at 3 min reperfusion times | Reperfusion following maintained intra-abdominal hypertension (i) grade III: 25 mmHg/60 min or (ii), (iii) grade IV: (ii) 30 mmHg/30 min; (iii) 40 mmHg/30 min. Reperfusion for 60 min (i) or for 30 min (ii/iii) | Decompression/reperfusion-induced occlusion/occlusion-like syndrome: lesions and malondialdehyde (MDA) in the brain, heart, lung, liver, kidney, and gastrointestinal tract, thrombosis, hemorrhage, intracranial, portal, caval hypertension, aortal hypotension | Counteracted decompression/reperfusion-induced occlusion/occlusion-like syndrome as a whole. Counteracted: lesions and malondialdehyde (MDA) in the brain, heart, lung, liver, kidney, and gastrointestinal tract, thrombosis, hemorrhage, intracranial, portal, caval hypertension, aortal hypotension |
[30] | L92, containing the single species L. acidophilus, 2.1 × 109 CFU/kg/day, calculated as 200 × 108 CFU for 7 days. Amino acid (AA) mixture treatment (trade name Elental) 25 g/kg/day for 7 days | 90-min nitrogen pneumoperitoneum: IAP was 12 mm Hg | Colon histology, colonic reduced glutathione (GSH) and malondialdehyde (MDA) were used to evaluate the changes in oxidative responses. Colonic interleukin-1β (IL-1β) was measured to assess the inflammatory responses, 5-HT and 5-HIAA in plasma. | Orally gavaged Lactobacillus acidophilus L-92 (L92) and a mixture of AA in rats with induced IAH. The results showed that both L92 and AA pretreatments effectively mitigated IAH-induced intestinal damage. Interestingly, L92 but not AA prevented metagenomic changes induced by IAH. |
[7] | Rats with intra-abdominal hypertension (grade III, grade IV) received BPC 157 (10 µg or 10 ng/kg sc) or saline (5 mL) after 10 min. | Intra-abdominal pressure in thiopental-anesthetized rats at 25 mmHg (60 min), 30 mmHg (30 min), 40 mmHg (30 min), 50 mmHg (15 min), and in esketamine-anesthetized rats at 25 mmHg for 120 min | Lesions in the brain, heart, lung, liver, kidney, and gastrointestinal tract, thrombosis, hemorrhage, intracranial, portal, caval hypertension, aortal hypotension | Counteracted occlusion/occlusion-like syndrome as a whole. Counteracted: lesions and malondialdehyde (MDA) in the brain, heart, lung, liver, kidney, and gastrointestinal tract, thrombosis, hemorrhage, intracranial, portal, caval hypertension, aortal hypotension |
[31] | C. butyricum 1 × 109 colony-forming units (CFUs) of C. butyricum, Butyrate 100 mg/kg body weight of sodium butyrate in 1.0 mL of normal saline; for 10 days | Severe acute pancreatitis retrograde infusion, 4.5% sodium taurocholate (0.1 mL/100 g) 24 h after the operation, the IAP of each rat was determined | The plasma levels of several markers (amylase, diamine oxidase (DAO), fluorescein isothiocyanate (FITC)-dextran, tumor necrosis factor alpha (TNF-α), interleukin (IL)-6, IL-1β, IL-12, lipopolysaccharide (LPS)) and fecal butyric acid level were determined. The pancreas and intestine were examined using histology, and RT-PCR and Western blotting of intestinal tissues were used to measure the expression of six markers (tight junction proteins (zonula occludens protein-1 (ZO-1), claudin-1, claudin-2, occluding) matrix metalloproteinase 9 (MMP9), and TNF-α). The gut flora of the rats was examined by 16S rRNA sequencing | Rats that received oral C. butyricum or butyrate had reduced intestinal injury and plasma levels of DAO, LPS, and inflammatory cytokines. |
[32] | Before blood was drawn, rats in the combined + bFGF group were treated with bFGF (10 μg/kg; intraperitoneal (IP) injection). FGFR1 antagonist, PD173074 (10 mg/kg; IP injection) 2 min before the administration of bFGF. PD98059 (ERK antagonist; 20 mg/kg; IP injection) 2 min before bFGF administration. | For moderate TBI, the impact depth was set as 2.0 mm, the dwell time was set as 100 ms, and the velocity was set as 3.5 m/s. Blood samples were taken (0.5 mL/min) within 10 min after the surgery, blood pressure was maintained at 30–40 mmHg for 1.5 h, then the reperfusion was induced by Ringer’s solution (30 mL/h, using an infusion pump). After 5 min, nitrogen was peritoneally injected until the IAP reached 12 mmHg. | Intracranial pressure (ICP) monitoring, brain water content, Evans blue permeability detection, immunofluorescence staining, real-time PCR, and Western blot analysis | The effects of bFGF on alleviating the rat BBB injuries were determined, indicating that bFGF regulated the expression levels of the tight junction (TJ), adhesion junction (AJ), matrix metalloproteinase (MMP), and IL-1β, as well as reduced BBB permeability, brain edema, and intracranial pressure. Moreover, the FGFR1 antagonist PD 173074 and the ERK antagonist PD 98059 decreased the protective effects of bFGF. |
[33] | Hypodermic injection of hydrogen gas (0.2 mL/kg), and after 10 min they received an abdominal insufflation of CO2 for 90 min at an intra-abdominal pressure of 15 mmHg. | Abdominal insufflation of CO2 for 90 min at an intra-abdominal pressure of 15 mmHg. | Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were measured to evaluate liver function. Malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione (GSH) content were measured to evaluate oxidative stress. Nuclear factor E2-related factor 2 (Nrf2) and Nrf2 downstream target genes, apoptosis-related genes and inflammatory cytokine mRNA and protein expression were detected. Liver injury was detected under the microscope. | Liver function, antioxidants content, inflammation and liver injury were improved after hydrogen preconditioning |
[34] | i.v. glycine (1.5 mL, 300 mM) 10 min before pneumoperitoneum. | CO2 pneumoperitoneum (12 mmHg) for 90 min. Assessment at 1, 2, and 8 h after pneumoperitoneum | Transaminases, hepatic microcirculation, and phagocytosis of latex beads indexing both liver injury and KC activation were examined following pneumoperitoneum. | Glycine significantly decreased lactate dehydrogenase at 1 h and both aspartate aminotransferase and alanine aminotransferase at 2 h after pneumoperitoneum. In parallel, glycine significantly decreased both the rate of permanent adherence of leukocytes to the endothelium by up to 35% and the rate of phagocytosis by >50% compared to the control group. |
[35] | CORM-3, CO donor, and GYY4137, H2S donor, were administered at the dose of 10 mg/kg and 50 mg/kg, respectively, via the carotid artery, just before decompression of the abdomen. Decompression 20–30 min. | 2 h, an abdominal plaster cast and intraperitoneal CO2 insufflation at 20 mmHg. Decompression 20–30 min | Sinusoidal perfusion, inflammatory response and cell death were quantified in exteriorized livers. Respiratory, liver, and renal dysfunction was assessed biochemically. | Improved hepatic microvasculature, counteracted hepatic cell death, and inflammatory, metabolic, and renal dysfunction in a rat model of ACS |
[36] | In the melatonin group (MT, n = 8), after blood reinfusion, rats were infused with melatonin (50 mg/kg), then resuscitated with Ringer solution (LR) (30 mL/h × 6 h). In the hypertonic saline group (HS, n = 8), after blood reinfusion, rats were infused with 7.5% hypertonic saline (HS) (6 ml/kg), then resuscitated with LR (30 mL/h × 6 h). In the hydroxyethyl starch group (HES, n = 8), after blood reinfusion, rats were infused with hydroxyethyl starch 130/0.4 (HES) (30 mL/kg), then resuscitated with LR (30 mL/h × 6 h). | Portal hypertension 1 h, abdominal restraint device, and hemorrhaging to mean arterial pressure (MAP) of 40 mmHg for 2 h. After blood reinfusion, the rats were treated with lactated Ringer solution (LR) (30 mL/h), for 6 h. The secondary IAH was determined by an elevation of 12.5 mmHg (170 mmH2O) of IVCP from the starting point. | The intestinal permeability, immunofluorescence of tight junction proteins, transmission electron microscopy, level of inflammatory mediators (TNF-a, IL-1β, IL-6) and of biochemical markers of oxidative stress (malondialdehyde, myeloperoxidase activity, and glutathione peroxidase) were assessed. Expressions of the protein kinase B (Akt) and of tight junction proteins were detected by Western blot. | Compared with LR, HS, and HES, melatonin was associated with less inflammatory and oxidative injury, less intestinal permeability and injury, and lower incidence of secondary IAH in this model. The salutary effect of melatonin in this model was associated with the upregulation of intestinal Akt phosphorylation. |
[37] | Melatonin (50 mg/kg), and SB-203580 (10 μmol/kg) immediately after blood reinfusion | Portal hypertension 1 h, abdominal restraint device, and hemorrhaging to mean arterial pressure (MAP) of 40 mmHg for 2 h. After blood reinfusion, the rats were treated with lactated Ringer solution (LR) (30 mL/h), for 6 h. The secondary IAH was determined by an elevation of 12.5 mmHg (170 mmH2O) of IVCP from the starting point. | MAP, the inferior vena cava pressure and urine output were monitored. Intestine histopathological examination, immunofluorescence of tight junction proteins, and transmission electron microscopy were administered. Intestinal permeability, myeloperoxidase activity, malondialdehyde, glutathione peroxidase, and levels of TNF-a, IL-2, and IL-6. The expression of extracellular signal-regulated kinase, p38, c-Jun NH2-terminal kinase, translocation of nuclear factor kappa B subunit, signal transducers and activators of transcription and tight junction proteins were detected by Western blot. | Melatonin inhibited the inflammatory responses, decreased expression of p38 MAPK, attenuated intestinal injury, and prevented secondary IAH. Moreover, administration of SB203580 abolished the increase in p38 MAPK and also attenuated intestinal injury. |
[38] | An arginase inhibitor 2(S)-amino-6-boronohexanoic acid (ABH) subcutaneous injection (5 mg/kg) 1 h before induction of pneumoperitoneum (insufflation to intraperitoneal pressure of 15 mmHg for 60 min) | Pneumoperitoneum (insufflation to intraperitoneal pressure of 15 mmHg for 60 min) | After desufflation, blood was collected to determine levels of plasma nitrite, NOS, inflammatory cytokines, and malondialdehyde, a marker of oxidative stress. Lung tissue was obtained for histological evaluation. | Pretreatment with an arginase inhibitor may protect against lung injury caused by pneumoperitoneum. |
[39] | 5 mg/kg of theophylline intraperitoneally before setting pneumoperitoneum model. | The pneumoperitoneum was generated by insufflating inside the abdomen by CO2 at 14 mmHg fixed pressure for 1 h, and desufflation was waited for 30 min | Urea, creatinine, cystatin-C, tissue and serum total antioxidant capacity, total oxidant capacity and oxidative stress index in two groups were measured and compared with each other. Apoptosis and histopathological conditions in the renal tissues were examined. | Lower cystatin-C levels in the group, where Theophylline was given, are suggestive of lower renal injury in this group. However, this opinion is interrogated as there is no difference in terms of tissue and serum TAS, TOS, OSI and urea values between the groups. |
[40] | Selective melanocortin 4 receptor agonist RO27-3225 (180 μg/kg ip) 2 min before blood was drawn. The selective melanocortin 4 receptor antagonist HS024 (130 μg/kg) 2 min before the RO27 3225 administration. The nicotinic acetylcholine receptor antagonist chlorisondamine (250 μg/kg) 2 min before the RO27 3225 administration | IAH rat models were induced by hemorrhagic shock/resuscitation with the mean arterial pressure (MAP) maintained at 30 mm Hg for 90 min followed by the reinfusion of the withdrawn blood with lactated Ringer’s solution. Then, air was injected into the peritoneal cavity of the rats to maintain an intra-abdominal pressure of 20 mm Hg for 4 h. | Mean arterial pressure, reduced tumor necrosis factor-a, and interleukin-1b messenger RNA expression increased by IAH, histologic damage, and superoxide dismutase activity in the intestine, the levels of intestinal fatty acid-binding protein, intestinal edema and intestinal permeability, the expression of Rho-associated coiledecoil-containing protein kinase 1 and phosphorylated myosin light chain. | RO27-3225 restored mean arterial pressure, reduced tumor necrosis factor-a, and interleukin-1b messenger RNA expression increased by IAH, alleviated histologic damage, and improved superoxide dismutase activity in the intestine. Compared with the IAH group, the levels of intestinal fatty acid-binding protein, intestinal edema and intestinal permeability were lower in the RO group. Furthermore, the RO27-3225 treatment increased the expression of Rho-associated coiledecoil-containing protein kinase 1 and phosphorylated myosin light chain. Chl and HS024 abrogated the protective effects of RO27-3225. |
[41] | Selective melanocortin 4 receptor agonist RO27-3225 (180 μg/kg ip) 2 min before blood was drawn. Selective melanocortin 4 receptor antagonist HS024 (130 μg/kg) 2 min before the RO27 3225 administration. The nicotinic acetylcholine receptor antagonist chlorisondamine (250 μg/kg) 2 min before the RO27 3225 administration | IAH rat models were induced by hemorrhagic shock/resuscitation (with the mean arterial pressure (MAP) maintained at 30 mm Hg for 90 min followed by the reinfusion of the withdrawn blood with lactated Ringer’s solution). Then, air was injected into the peritoneal cavity of the rats to maintain an intra-abdominal pressure of 20 mmHg for 4 h. | The permeability of the BBB, brain water content. The left brain hippocampus AQP4, MMP9, IL-1β and TNF-α concentrations were detected using an ELISA kit | The effects of the melanocortin 4 receptor agonist RO27-3225 in alleviating the rats’ IAH brain injuries were observed, which indicated that RO27-3225 could reduce brain edema, the expressions of the IL-1β and TNF-α inflammatory cytokines, the blood–brain barrier’s permeability and the aquaporin4 (AQP4) and matrix metalloproteinase 9 (MMP9) levels. Moreover, the nicotinic acetylcholine receptor antagonist chlorisondamine and the selective melanocortin 4 receptor antagonist HS024 can negate the protective effects of the RO27-3225. |
[42] | Caffeic acid phenethyl ester (CAPE) at 10 μmol/kg was administered as a single intraperitoneal injection 1 h before the desufflation period | CO2 pneumoperitoneum 15 mmHg for 60 min. | The bronchoalveolar lavage was obtained twice with 3 mL of saline to investigate biochemical parameters, including paraoxonase (PON1) activity, total antioxidant status (TAS), total oxidative status (TOS) levels, and cytokine concentration. | CAPE to prevent CO2 pneumoperitoneum-induced oxidative stress and inflammatory reactions in lung tissue |
[43] | Loading aprotinin dose of 28,000 KIU/kg ip straight after the onset of pneumoperitoneum, followed by lower maintenance doses (7500 KIU/kg), which were administered per hour until the termination of insufflation | Constant 12 mmHg pneumoperitoneum was maintained for 4 h. The duration of the reperfusion period was 60 or 180 min. | Several cytokines and markers of oxidative stress were measured in liver, small intestine, and lungs to compare the aprotinin group with the control group. Tissue inflammation was also evaluated and compared between groups using a five-scaled histopathologic score. | In the aprotinin group values of biochemical markers (tumor necrosis factor-a, interleukin 6, endothelin 1, C-reactive protein, pro-oxidant-antioxidant balance, and carbonyl proteins) were lower in all tissues studied. Statistical significance was greater in liver and lungs. Histopathologic examination revealed a significant difference between the control and aprotinin groups in all tissues examined. Aprotinin groups showed mild to moderate lesions, while in control groups, severe to very severe inflammation was present. The aprotinin subgroup with prolonged reperfusion period (180 min) showed milder lesions in all tissues than the rest of the groups. |
[44] | Low-dose ketamine (KP1, 5 mg/kg; KP2, 10 mg/kg) | CO2 pneumoperitoneum of 15 mmHg. | Three hours after pneumoperitoneum, serum concentrations of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), malondialdehyde (MDA), superoxide dismutase (SOD) and intestinal fatty acid binding protein (iFABP) were measured and liver, kidney, lung, and intestine were evaluated for tissue damage. | Pretreatment with low-dose ketamine before general anesthesia protects against potential oxidative damage and inflammatory response caused by CO2 pneumoperitoneum. |
[45] | Intraperitoneal injection of caffeic acid phenethyl ester (CAPE) 10 μmol/kg one hour before the desufflation period | 60 min of pneumoperitoneum with 15 mmHg IAP. | Kidneys, testicles, and prostate: Histology and the levels of the total oxidant status (TOS) and total antioxidant status (TAS) | In rat model, increased IAP had an oxidative effect on kidney and testis but not on prostate. Moreover, it could affect the testicular Johnsen score. According to kidney and testis tissues’ histologic evaluation, no significant alteration was obtained in 15 mmHg pressure groups for 1-h insufflation period. All these adverse effects of IAP on both kidney and testis could be prevented by CAPE administration. Further studies are needed to show oxidative effect of IAP against the tissues with more detailed morphological and biochemical analysis. |
[46] | 100 µg intraperitoneal dexmedetomidine 30 min before establishment of pneumoperitoneum. | 60 min pneumoperitoneum was established under 12 mmHg pressure; intraperitoneal dexmedetomidine (100 µg) was administered 30 min before abdominal insufflation to establish 60 min pneumoperitoneum under 12 mmHg pressure. | Plasma total oxidant status (TOS), total antioxidant status (TAS), and oxidative stress index (OSI) activity were measured 30 min after the conclusion of pneumoperitoneum. | Dexmedetomidine decreases oxidative stress caused by pneumoperitoneum and strengthens the antioxidant defense system. |
[47] | Dopamine infusion (3 μg/kg/min) before increasing IAP, a 60-min infusion of dopamine was performed; following this, IAP was raised, and the dopamine infusion (3 μg/kg/min) was continued for another 60 min. | IAP of 20 mmHg was maintained for 60 min by air insufflation | Renal artery perfusion was measured continuously for 30 min with a Doppler probe. Mean arterial pressure, myeloperoxidase (MPO) activity, lipid peroxidation and glutathione (GSH) levels were measured in tissue samples, and histopathological scoring was carried out. | Dopamine infusion before and during ACS, increases renal perfusion and decreases free oxygen radicals. Degenerations in the kidney tissues of the rats were clearly improved when the animals were treated by dopamine during and before ACS |
[48] | Minocycline (20 mg/kg) was intravenously administered immediately after resuscitation. | Hemorrhagic shock/resuscitation was induced by blood drawing (mean arterial pressure: 40–45 mm Hg for 60 min) followed by shed blood/saline mixture reinfusion. Subsequently, intra-abdominal pressure (IAP) was increased to 25 mm Hg by injecting air into the preplaced intraperitoneal latex balloon to induce ACS. IAP was maintained at 25 mmHg for 6 h. | The levels of polymorphonuclear leukocyte infiltration, the wet/dry weight ratio, and the concentrations of inflammatory molecules (e.g., chemokine, cytokine, and prostaglandin E2) in lung and liver tissues | Minocycline ameliorates inflammatory response and organ dysfunction in the lungs and liver induced by hemorrhagic shock/resuscitation plus abdominal compartment syndrome, and ameliorated lung and liver injuries. |
[49] | Dexmedetomidine administration (intraperitoneal injection of 100 mg/kg) 30 min before pneumoperitoneum. | Intra-abdominal pressure of 12 mmHg for 60 min. The rats were rested for 30 min after abdominal deflation. | Blood samples were obtained for plasma malondialdehyde and ischemia-modified albumin (IMA) analyses. Lung tissue samples were taken for histopathologic examination and malondialdehyde analysis. | Dexmedetomidine prophylaxis resulted in significantly less IMA production and significantly less neutrophil infiltration, thereby helping to protect the lungs from injury after pneumoperitoneum. |
[50] | Tadalafil (10 mg/kg/day) for 4 days before the experiment | Rats with compensated and decompensated chronic heart failure (CHF) induced by the placement of an aorto-caval fistula (ACF), Rats with myocardial infarction induced by the left anterior descending (LAD) artery ligation and sham controls subjected to IAPs: 7, 10, 14 mmHg. | Urine flow rate (V), Na+ excretion (UNaV), glomerular filtration rate (GFR), renal plasma flow (RPF) | Amelioration of the adverse effects of high IAP |
[51] | Two hours after operation, 10 mL/kg dachengqi tang (DCQT) was administered orally | Acute necrotic pancreatitis was induced by retrograde infusion of 5% taurocholic acid into the pancreatic duct. | Aterial blood, pancreas and lung tissues were collected for biomarkers and histopathology 24 h after operations. Intra-abdominal pressure and intestinal propulsion rate were also measured. | DCQT treatment reduced intra-abdominal pressure and improved intestinal propulsion rate compared with those treated with saline. The ANP rats treated with DCQT had a lower wet to dry weight ratio, and milder myeloperoxidase activity and histopathology changes in the pancreas and lung than those treated with saline. Higher pressure of oxygen (PO2) was found in the rats treated with DCQT. |
[52] | Dopamine infusion (3 μg/kg/min) before increasing IAP, a 60-min infusion of dopamine was performed; following this, IAP was raised, and the dopamine infusion (3 μg/kg/min) was continued for another 60 min. | IAP of 20 mm Hg was maintained for 60 min by air insufflation. | Superior mesenteric artery (SMA) perfusion was measured continuously for 30 min with a Doppler probe. Mean arterial pressure, myeloperoxidase (MPO) activity, lipid peroxidation, and glutathione (GSH) levels were measured in tissue samples, and histopathological scoring was carried out. | Improved intestinal epithelium, improved glandular structure, SMA perfusion, counteracted hypotension, increased MPO activity, and decreased GSH. |
[53] | Doxycycline (10 mg/kg i.p.) during the induction of ACS. Doxycycline (10 mg/kg i.p.) at 1 h after decompression | Intra-abdominal pressure at 20 mmHg by insufflating CO2 gas for 60 min. Decompression 1 h and 24 h. | Creatinine, kidney MDA, IL-1b, IL-6, TNF-a, MMP-2, and TIMP-1 were studied, and the apoptotic cells were enumerated histopathologically, and apoptosis and bcl-2 expression were immunohistochemically assessed. | Doxycycline had protective effects on I/R injury by decreasing apoptosis via reducing the level of pro-inflammatory cytokines, increasing the level of TIMP-1, and inhibiting the activity of MMP-2. |
[54] | Glutamine through gastric gavage for 10 days at a dose of 1 mL per day (1 g/kg/day) | 20 mmHg pressure was applied for 2 h using CO2. | Intestine, lung, and liver samples were removed for determination of tissue malondialdehyde (MDA) and glutathione (GSH) levels as oxidative injury parameters and of myeloperoxidase (MPO) activity as an inflammatory parameter. the alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels. | Glutamine decreased MDA levels and MPO activities and increased GSH levels. |
[55] | Doxycycline (10 mg/kg IP) was injected during induction of ACS, and, similarly, intestinal samples were removed at 1 and 24 h after decompression. | IAP of 20 mmHg was maintained by insufflating with carbon dioxide gas for 60 min. Decompression 1 h and 24 h. | Intestine malondialdehyde (MDA), interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, matrix metalloproteinase-2 (MMP-2), and tissue inhibitor of metalloproteinase-1 were studied and the apoptotic cells were enumerated histopathologically. Apoptosis and β-cell lymphoma 2 (βcl-2) expression were assessed immunohistochemically. | Doxycycline was associated with protective effects against I/R injury through decreasing apoptosis via attenuating the response of proinflammatory cytokines and inhibiting the activity of MMP-2 in this rat model. |
[56] | Pentoxifylline (50 mg/kg ip) immediately before pneumoperitoneum. | CO2 pneumoperitoneum of 13 mmHg was established. At the first hour of insufflation, blood samples were taken to study the same parameters as in the control group. One hour following desufflation of CO2, blood samples were drawn again to study the same parameters. | The arterial pH, partial arterial oxygen pressure (PaO(2)), venous PO(2), arterial and venous PO(2) difference (P((a-v))O(2)), serum aspartate aminotransferase (AST), serum alanine aminotransferase (ALT), and thiobarbituric acid-reactive substances (TBARS) were studied at the end of the first and second hours | Pentoxifylline may reduce the oxidative injury following laparoscopic procedures. |
[57] | Nitroglycerine (NTG) (i.v., prime 1.5 mg/kg and sustained infusion of 15 mg/kg/h) beginning 60 min before the application of 14 mmHg insufflation pressure for 1 h, followed by desufflation to 0 mmHg (recovery). L-arginine methylester (L-NAME) 100 mg/l added to drinking water for 4 days before the experiment. | IAP of 14 mmHg, over 1 h, followed by a deflation period of 1 h (recovery). | Urine flow rate (V), Na+ excretion (UNaV), glomerular filtration rate (GFR), renal plasma flow (RPF), and blood pressure | Counteraction of pneumoperitoneum-induced renal hypoperfusion and dysfunction (nitroglycerine). Aggravation of pneumoperitoneum-induced renal hypoperfusion and dysfunction (L-NAME) |
[58] | Octreotide (50 µg/kg intraperitoneally) immediately before the decompression. | IAH 20 mmHg for 1 h, decompression 1 h. | ALT and AST levels, liver and intestinal tissues, malondialdehyde (an index of lipid peroxidation) and glutathione (a key to antioxidant) levels and myeloperoxidase (an index of tissue neutrophil infiltration) activity | Octreotide treatment reversed these oxidant responses, and reduced the elevations in both ALT and AST levels. |
[59] | Melatonin (10 mg/kg, i.p.) immediately before the decompression of IAP. | IAH 20 mmHg for 1 h, decompression 1 h. | ALT and AST levels, liver and intestinal tissue, malondialdehyde (an index of lipid peroxidation) and glutathione (a key to antioxidant) levels and myeloperoxidase (an index of tissue neutrophil infiltration) activity, urea nitrogen (BUN), creatinine | Octreotide treatment reversed these oxidant responses, and reduced the elevations in ALT and AST, BUN and creatinine levels. |
[60] | Octreotide (50 µg/kg intraperitoneally) immediately before the decompression | IAH 20 mmHg for 1 h, decompression 1 h. | Lung and kidney tissue, malondialdehyde (an index of lipid peroxidation) and glutathione (a key to antioxidant) levels and myeloperoxidase (an index of tissue neutrophil infiltration) activity urea nitrogen (BUN), creatinine | Octreotide treatment reversed these oxidant responses, and reduced the elevations In ALT and AST, BUN and creatinine levels. |
[61] | Dopamine was dissolved in saline and applied as a continuous intravenous infusion at a rate of 3 µg/kg/min using a microperfusion pump with a volume of 2 mL/h. The selective endothelin-1 (ET-I) antagonist, JKC-30 l, was dissolved in saline and administered at 200 µg/kg intravenously as a single-shot injection. | Intraabdominal insufflation pressures were elevated in a stepwise manner from 2 to 12 mmHg (2, 4, 6, 8, 10, and 12 mmHg) every 10 min. At the end of the experimental procedure, the abdomen was desufltated and the portal venous blood flow recovery was measured for another 30 mm. | Portal blood flow was measured during intraabdominal pressures 2 to 12 mmHg. | Dopamine and ET-1 antagonism restore portal blood flow during laparoscopic surgery independently of the insufflation gas. |
[62] | AVP V2 receptor antagonist, OPC-31260 (5 mg/kg) before pneumoperitoneum | 1 h to carbon dioxide pneumoperitoneum (PP) with an intra-abdominal pressure of 8 mmHg. | Glomerular filtration rate (GFR). Urine output, excretion of water, and urea nitrogen, serum osmolality and serum sodium levels, blood urea nitrogen levels | OPC-31260 pretreatment did not affect GFR. Results suggest that plasma AVP contributes to the oliguria due to PP. OPC-31260 may be useful in treating the water retention associated with PP. |
Ref. | Agent/Species | IAH Procedure | Target | Outcome |
---|---|---|---|---|
[121] | Pigs. After 2 h of IAH, infusion of NO-donor PDNO (in a dose of 30 nmol kg−1 min−1) and the placebo drug was initiated and continued for 4 h until the experiment was ended. | IAH was induced by CO2 insufflation to 30 mmHg, after 2 h, decompression 4 h until the experiment was ended | Blood gases, invasive venous and arterial blood pressure, intestinal microcirculation and superior mesenteric blood flow were measured | NO-donor PDNO decreased systemic and pulmonary vascular resistances, elevated the cardiac index score, and, most importantly, counteracted decreased microcirculatory blood flow in the intestinal mucosa during IAH in a porcine model. |
[122] | Mice. 120 μg (10 μL) hydromorphone 15 min before the establishment of pneumoperitoneum | Abdominal pressure to 15 mmHg for insufflation (for 1 h) and deflation with CO2 (for 3 h). | Lung injury myeloperoxidase (MPO), total oxidant status (TOS), and oxidative stress index (OSI), total antioxidant status (TAS). HO-1-regulated mitochondrial dynamics. | Hydromorphone alleviated lung injury in mice that underwent CO2 insufflation, decreased the levels of myeloperoxidase (MPO), total oxidant status (TOS), and oxidative stress index (OSI), and increased total antioxidant status (TAS). Hydromorphone protects against CO2 pneumoperitoneum-induced lung injury via HO-1-regulated mitochondrial dynamics. |
[123] | Rabbits. Mydocalm (tolperison, 5 mg/kg single dose) at initiation of 3 h of IAH. | IAH level was modeled at 200 mmH2O with the subsequent stopping of further receipt of liquid during 3 h in an elastic container in the abdominal cavity. | Tone of muscles of the frontal abdominal wall, local blood flow, dilatation, constriction oxygen tension | Mydocalm reduces the tone of muscles of the frontal abdominal wall, which leads to a decrease in IAH (maximum effect after 1.5 h) and prevents decrease in the local blood flow, suppression of dilation and constriction, reactivity of vessels, and reduction in oxygen tension at the end of experiment. |
[124] | Pigs. Ethyl nitrite (ENO) at a rate of 1.0 L/min in pigs using a high-flow clinical insufflator | The peritoneal cavity was next insufflated to a final intraperitoneal pressure of 15 mmHg with CO2 in the presence or absence of ENO at a rate of 1.0 L/min using a high-flow clinical insufflator. Pneumoperitoneum was maintained for 4 h during which gas was constantly vented from the peritoneal cavity to ensure continual CO2 and ENO exposure. After 4 h, insufflation was discontinued and the abdomen manually deflated. Monitoring was continued under anesthesia for an additional 2 h. | Regional tissue blood flow brain, heart, liver, kidney, stomach, small intestine, colon, spleen, pancreas, venous red blood cell SNO-Hb concentration | The data indicate ethyl nitrite can effectively attenuate insufflation-induced decreases in organ blood flow and nitric oxide bioactivity leading to reductions in markers of acute tissue injury. |
[125] | Mice. Pentoxifyllin before IAH induction. | IAH was induced in mice by intraperitoneal infusion of mineral oil to a pressure of 20 mm Hg. 4 h of IAH followed by 1 h of decompression. | Brain blood barrier (BBB) integrity was determined by extravasation of 2% Evans blue (EB) | Pentoxifyllin improved BBB integrity |
[126] | Mice. 50%, 80%, or 100% oxygen inhalation after establishing acute IAH | 15, 20, 30, or 40 cmH2O IAP. The 40 cmH2O group seemed to be appropriate for follow-up experiments. | Liver and blood samples were used to compare the rates of apoptosis using the TUNEL assay as well as alanine aminotransferase (ALT), aspartate aminotransferase (AST); Caspase-3, 9, MDA, and SOD concentrations. | As the oxygen concentration increased, the survival time was prolonged among the 40 cmH2O IAP group, and the number of apoptotic hepatic cells decreased (P 0.01), with a concomittent decrease in caspase 3 and 9 as well as malondialdehyde, although superoxide dismutase showed the opposite results. |
[127] | Dogs. Following preparation, fentanyl (1 μg kg(−1)) was injected over 30 s IV. | The abdomen was insufflated with CO(2) (11–16 cmH(2) O). Data were recorded 5 min before, during and 5 min after treatment. The following time points were selected for analysis: −160, −140, −120, −100, −80, −60, −40, −20, 0, 30, 50, 70, 90, 110, 130 and 150 s after the start of fentanyl injection. | Peak inspiratory and end-expiratory intra-abdominal pressures continuously decreased over time during the whole experiment and fentanyl exaggerated the decrease in inspiratory pressures but did not affect the rate of decrease in expiratory pressures. | Fentanyl did not increase intra-abdominal pressures in dogs. |
[128] | Pigs. CO2 enriched with 100 ppm ethyl nitrite (ENO) in pigs. | Final intraperitoneal pressure of 15 mmHg. After 35 min, ENO was introduced into the peritoneal space by passing the CO2 gas insufflated for 60 min and then monitored for an additional 60 min after termination of insufflation | Liver and kidney blood flows. | Inclusion of ethyl nitrite (a nitric oxide-containing compound) within the insufflating gas significantly attenuated the decreases in liver blood flow produced during and after a 60-min period of carbon dioxide pneumoperitoneum. |
[129] | Dogs. Enalaprilat (5 mg) 15 min before | Abdominal pressure was maintained automatically at 15 mmHg over a 60-min period. 15 and 30 min utes after deflation of the abdominal cavity | Body weight, hematologic values, hemodynamic parameters, and renal function (plasma renin activity, urinary debt, creatinine clearance, and sodium-excretory fraction) | The decline in urinary debt and in creatinine clearance observed during pneumoperitoneum was less accentuated with the administration of enalaprilat. |
[130] | Pigs. CO2 was insufflated into the peritoneal cavity to reach an intraabdominal pressure of 15 mmHg. After 60 min, animals received dopamine (5 microg × kg(−1) × min(−1); n = 8), dobutamine (5 microg × kg(−1) × min(−1)). | CO2 was insufflated into the peritoneal cavity to reach an intraabdominal pressure of 15 mmHg. | Heart rate, mean arterial pressure, and systemic vascular resistance, with decreases in cardiac output and hepatic artery and portal vein blood flows | Dobutamine infusion, in contrast to dopamine, corrected, at least in part, cardiac output, systemic vascular resistance, and hepatic artery blood flow alterations, but neither drug restored total hepatic blood flow. |
[131] | Pigs. CO2 was insufflated into the peritoneal cavity to reach an intra-abdominal pressure of 15 mmHg, and 60 min later, animals received dopamine (5 microg/kg/min; n = 10), dobutamine (5 microg/kg/min; n = 10), or saline (n = 5) for 30 min. | CO2 was insufflated into the peritoneal cavity to reach an intra-abdominal pressure of 15 mmHg, and 60 min. | A laser Doppler probe was positioned in the lumen of the ileum to measure arterial and intestinal mucosal blood flows. | Dobutamine infusion reversed the decrease in cardiac output, it failed to restore superior mesenteric artery blood flow; however, intestinal mucosal blood flow returned to baseline levels. Dopamine also attenuated the decrease in cardiac output, but it had no beneficial effect on splanchnic hemodynamic variables. |
[132] | Pigs. The pneumoperitoneum was carefully evacuated, and after a l0-min rest, similar airway and abdominal pressure measurements were repeated after the pigs received a 4 mg/kg intravenous injection of atracurium. | Insufflation was discontinued when IAP was more than 15 mmHg. | Elastic properties of the abdomen (elastance). | High peak inspiratory airway pressures and intraabdominal pressures during laparoscopy are not affected by neuromuscular block. |
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Sikiric, P.; Seiwerth, S.; Skrtic, A.; Staresinic, M.; Strbe, S.; Vuksic, A.; Sikiric, S.; Bekic, D.; Penovic, T.; Drazenovic, D.; et al. Acute Compartment Syndrome and Intra-Abdominal Hypertension, Decompression, Current Pharmacotherapy, and Stable Gastric Pentadecapeptide BPC 157 Solution. Pharmaceuticals 2025, 18, 866. https://doi.org/10.3390/ph18060866
Sikiric P, Seiwerth S, Skrtic A, Staresinic M, Strbe S, Vuksic A, Sikiric S, Bekic D, Penovic T, Drazenovic D, et al. Acute Compartment Syndrome and Intra-Abdominal Hypertension, Decompression, Current Pharmacotherapy, and Stable Gastric Pentadecapeptide BPC 157 Solution. Pharmaceuticals. 2025; 18(6):866. https://doi.org/10.3390/ph18060866
Chicago/Turabian StyleSikiric, Predrag, Sven Seiwerth, Anita Skrtic, Mario Staresinic, Sanja Strbe, Antonia Vuksic, Suncana Sikiric, Dinko Bekic, Toni Penovic, Dominik Drazenovic, and et al. 2025. "Acute Compartment Syndrome and Intra-Abdominal Hypertension, Decompression, Current Pharmacotherapy, and Stable Gastric Pentadecapeptide BPC 157 Solution" Pharmaceuticals 18, no. 6: 866. https://doi.org/10.3390/ph18060866
APA StyleSikiric, P., Seiwerth, S., Skrtic, A., Staresinic, M., Strbe, S., Vuksic, A., Sikiric, S., Bekic, D., Penovic, T., Drazenovic, D., Becejac, T., Tepes, M., Madzar, Z., Novosel, L., Beketic Oreskovic, L., Oreskovic, I., Stupnisek, M., Boban Blagaic, A., & Dobric, I. (2025). Acute Compartment Syndrome and Intra-Abdominal Hypertension, Decompression, Current Pharmacotherapy, and Stable Gastric Pentadecapeptide BPC 157 Solution. Pharmaceuticals, 18(6), 866. https://doi.org/10.3390/ph18060866