A Supraceliac Aortic Cross Clamping Model to Explore Remote Lung Injury and the Endothelial Glycocalyx

Palmier, Mickaël; Cornet, Emlyn; Renet, Sylvanie; Dumesnil, Anaïs; Perzo, Nicolas; Cohen, Quentin; Plissonnier, Didier

doi:10.1016/j.avsg.2022.12.075

Cited by 1 publication

(1 citation statement)

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“…Degradation of the glycocalyx can result in myocardial edema and microvascular obstruction in patients following myocardial infarction [213]. Glycocalyx damage is also reported following aortic cross-clamping in rats [214] and in cardiac surgery pa-tients [215,216]. During remote ischemic conditioning, glycocalyx thickness was improved in patients after myocardial infarction [217], and anesthetic conditioning protects the glycocalyx layer.…”

Section: Glycocalyxmentioning

confidence: 99%

Pharmacological Cardioprotection against Ischemia Reperfusion Injury—The Search for a Clinical Effective Therapy

Wang,

Zuurbier,

Huhn

et al. 2023

Cells

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Pharmacological conditioning aims to protect the heart from myocardial ischemia-reperfusion injury (IRI). Despite extensive research in this area, today, a significant gap remains between experimental findings and clinical practice. This review provides an update on recent developments in pharmacological conditioning in the experimental setting and summarizes the clinical evidence of these cardioprotective strategies in the perioperative setting. We start describing the crucial cellular processes during ischemia and reperfusion that drive acute IRI through changes in critical compounds (∆GATP, Na+, Ca2+, pH, glycogen, succinate, glucose-6-phosphate, mitoHKII, acylcarnitines, BH4, and NAD+). These compounds all precipitate common end-effector mechanisms of IRI, such as reactive oxygen species (ROS) generation, Ca2+ overload, and mitochondrial permeability transition pore opening (mPTP). We further discuss novel promising interventions targeting these processes, with emphasis on cardiomyocytes and the endothelium. The limited translatability from basic research to clinical practice is likely due to the lack of comorbidities, comedications, and peri-operative treatments in preclinical animal models, employing only monotherapy/monointervention, and the use of no-flow (always in preclinical models) versus low-flow ischemia (often in humans). Future research should focus on improved matching between preclinical models and clinical reality, and on aligning multitarget therapy with optimized dosing and timing towards the human condition.

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