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New Molecular Insights into Ischemia/Reperfusion: 2nd Edition

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Guest Editor
Department of Emergency Medicine, Kangwon National University Hospital, School of Medicine, Kangwon National University, Chuncheon 24289, Republic of Korea
Interests: ischemia/reperfusion; neurodegeneration; neurogenesis; cerebral ischemia; aging in CNS
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Special Issue Information

Dear Colleagues,

Ischemia/reperfusion (IR) causes a complex pathophysiological process, called IR injury, defined as the paradoxical exacerbation of cellular dysfunction and death following the restoration of blood flow to previously ischemic tissues. IR injury happens in a wide range of organs, including the heart, brain, spinal cord, gut, kidney, and skeletal muscle. IR injury not only involves the ischemic organ itself but also induces systemic damage to distant organs. Huge efforts have been made to develop potential treatments for IR injury, but the molecular and cellular mechanisms of IR injury are not fully understood regarding organs. Therefore, many researchers have been investigating the mechanisms of IR injury in diverse organs using various experimental animal models of IR injury (i.e., different methods of the occlusion of blood vessels and different periods of occlusion time). Principally, the mechanisms of IR injury include excitotoxicity, oxidative stress, and inflammation. Nevertheless, the mechanisms are significantly different depending on the organs. For instance, blood–brain (spinal cord) barrier damage is one of the mechanisms of IR injury in the central nervous system. Therefore, investigation into the molecular mechanisms of IR injury in various organs is warranted so that we can treat or protect against IR injury. Thus, this Special Issue will focus ischemia/reperfusion in various organs, including the heart, brain, spinal cord, liver, and kidneys.

Prof. Dr. Moo-Ho Won
Guest Editor

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Keywords

  • vital organs
  • ischemic injury
  • cell and organ dysfunction
  • oxidative stress
  • inflammation
  • excitotoxicity

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Published Papers (1 paper)

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Research

11 pages, 2454 KiB  
Article
Glibenclamide Serves as a Potent Vasopressor to Treat Vasoplegia After Cardiopulmonary Bypass and Reperfusion in a Porcine Model
by Andreas Winter, Pascal Nepper, Marcus Hermann, Franziska Bayer, Stephanie Riess, Razan Salem, Jan Hlavicka, Anatol Prinzing, Florian Hecker, Tomas Holubec, Kai Zacharowski, Thomas Walther and Fabian Emrich
Int. J. Mol. Sci. 2025, 26(9), 4040; https://doi.org/10.3390/ijms26094040 - 24 Apr 2025
Viewed by 128
Abstract
The hemodynamic stabilization of patients after complex cardiac surgery is a daily challenge. The use of high doses of catecholamines is common but has potential adverse effects. Glibenclamide, a KATP blocker, seems to attenuate vasoplegia in different animal models of septic shock. [...] Read more.
The hemodynamic stabilization of patients after complex cardiac surgery is a daily challenge. The use of high doses of catecholamines is common but has potential adverse effects. Glibenclamide, a KATP blocker, seems to attenuate vasoplegia in different animal models of septic shock. Therefore, the aim of this study was to investigate the impact of Glibenclamide on the vasoplegic syndrome after cardiopulmonary bypass in a porcine model. In this experimental study, 20 landrace pigs were randomized into two groups and examined: In the control group, standard medical therapy, including norepinephrine, was used, and in the study group standard medical therapy plus additional Glibenclamide was administered. Following general anesthesia, prolonged cardiopulmonary bypass and aortic cross-clamping was performed. In the study group, Glibenclamide was administered 45 min after weaning from cardiopulmonary bypass. The dosage used was 10 mg/kg as a bolus, followed by a continuous infusion of 10 mg/kg/h. Hemodynamic and laboratory measurements were performed. Glibenclamide had a relevant effect on circulatory parameters. With increasing vascular resistance and blood pressure, norepinephrine was able to be reduced. While the heart rate dropped to physiological levels, the cardiac index decreased as well. The results lead to the conclusion that Glibenclamide was able to break through vasoplegic syndrome and could therefore serve as a potent drug to stabilize patients after cardiac surgery. Full article
(This article belongs to the Special Issue New Molecular Insights into Ischemia/Reperfusion: 2nd Edition)
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