Clinical application of recombinant human SOD for the prevention of ischemia-reperfusion injury during open heart surgery

Myocardial ischemia-reperfusion injury continues to be observed during open heart surgery. Various experimental models have been developed to overcome this injury and to increase postoperative prognosis. This study was conducted to assess the effect that iloprost, a prostacyclin analogue, can have on myocardial ischemia-reperfusion injury. We evaluated tissue damage by measuring the levels of malonyldialdehyde (MDA), glutathione, and nitric oxide (NO) in tissue and perfusates. In this study, 20 guinea pig hearts were prepared by using the modified Langendorff perfusion apparatus to form control (n = 10) and experimental study groups (n = 10). Following a preischemic period of perfusion and an ischemic period of 20 minutes, control hearts were perfused with Krebs–Henseleit solution. In the experimental group, iloprost (0.45 µg/kg per hour) was included in the perfusates for the last 10 minutes of the preischemic phase. Following cardiac stabilization, heart rate (pulse/min), contractility (mm), and aortic pressure (mmHg) values were recorded at the end of preischemia, postischemia, and reperfusion. Perfusate and tissue analyses for glutathione, MDA, and NO levels were made in each group at the end of experiments. Iloprost was found to have protective effects against myocardial ischemia by means of increased myocardial contractility, decreased tissue/perfusate glutathione levels and inhibited rise of tissue/perfusate MDA observed in the iloprost-treated experimental group. Future investigations on myocardial ischemia-reperfusion injury must evaluate iloprost-related mechanisms.

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Endothelial glycocalyx during early reperfusion in patients undergoing cardiac surgery

PLoS ONE ◽

10.1371/journal.pone.0251747 ◽

2021 ◽

Vol 16 (5) ◽

pp. e0251747

Author(s):

Arie Passov ◽

Alexey Schramko ◽

Ulla-Stina Salminen ◽

Juha Aittomäki ◽

Sture Andersson ◽

...

Keyword(s):

Cardiac Surgery ◽

Heparan Sulfate ◽

Coronary Sinus ◽

Heart Surgery ◽

Coronary Circulation ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Open Heart Surgery ◽

Endothelial Glycocalyx ◽

Early Reperfusion

Background Experimental cardiac ischemia-reperfusion injury causes degradation of the glycocalyx and coronary washout of its components syndecan-1 and heparan sulfate. Systemic elevation of syndecan-1 and heparan sulfate is well described in cardiac surgery. Still, the events during immediate reperfusion after aortic declamping are unknown both in the systemic and in the coronary circulation. Methods In thirty patients undergoing aortic valve replacement, arterial concentrations of syndecan-1 and heparan sulfate were measured immediately before and at one, five and ten minutes after aortic declamping (reperfusion). Parallel blood samples were drawn from the coronary sinus to calculate trans-coronary gradients (coronary sinus–artery). Results Compared with immediately before aortic declamping, arterial syndecan-1 increased by 18% [253.8 (151.6–372.0) ng/ml vs. 299.1 (172.0–713.7) ng/ml, p < 0.001] but arterial heparan sulfate decreased by 14% [148.1 (135.7–161.7) ng/ml vs. 128.0 (119.0–138.2) ng/ml, p < 0.001] at one minute after aortic declamping. There was no coronary washout of syndecan-1 or heparan sulfate during reperfusion. On the contrary, trans-coronary sequestration of syndecan-1 occurred at five [-12.96 ng/ml (-36.38–5.15), p = 0.007] and at ten minutes [-12.37 ng/ml (-31.80–6.62), p = 0.049] after reperfusion. Conclusions Aortic declamping resulted in extracardiac syndecan-1 release and extracardiac heparan sulfate sequestration. Syndecan-1 was sequestered in the coronary circulation during early reperfusion. Glycocalyx has been shown to degrade during cardiac surgery. Besides degradation, glycocalyx has propensity for regeneration. The present results of syndecan-1 and heparan sulfate sequestration may reflect endogenous restoration of the damaged glycocalyx in open heart surgery.

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Markers of endothelial dysfunction after cardiac surgery: Soluble forms of vascular-1 and intercellular-1 adhesion molecules

Medicina ◽

10.3390/medicina45060056 ◽

2009 ◽

Vol 45 (6) ◽

pp. 434 ◽

Cited By ~ 12

Author(s):

Mindaugas Balčiūnas ◽

Loreta Bagdonaitė ◽

Robertas Samalavičius ◽

Alis Baublys

Keyword(s):

Cardiac Surgery ◽

Endothelial Dysfunction ◽

Reperfusion Injury ◽

Adhesion Molecules ◽

Heart Surgery ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Transplant Rejection ◽

Vascular Wall ◽

Tissue Ischemia

Endothelium forms an inner layer of vascular wall. It plays an important role in inflammatory process, regulation of vascular tone, and synthesis of thromboregulatory substances. Leukocyte and endothelium interactions during inflammation are regulated by different families of adhesion molecules. Increased levels of soluble forms of adhesion molecules have been detected in the circulating blood in conditions such as autoimmune diseases, transplant rejection, ischemia-reperfusion injury in addition to neutrophil- and endothelial membrane-bound forms reflecting the level of endothelial dysfunction. It is known that endothelial dysfunction is a risk factor for ischemic events such as stroke, myocardial infarction, unstable angina pectoris, ventricle fibrillation, necessity of revascularisation procedures, and death from cardiovascular reasons. Clinical studies showed that cardiac surgery has an impact on vascular endothelial function as well. The amount of endotheliumderived soluble forms of vascular-1 and intercellular-1 adhesion molecules increases after cardiopulmonary bypass suggesting endothelial dysfunction. However, further investigations are needed to be done to support the evidence that endothelial dysfunction proceeding heart surgery is one of the reasons of tissue ischemia-reperfusion injury.

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