%0 Journal Article
%T Exogenous nitric oxide requires an endothelial glycocalyx to prevent postischemic coronary vascular leak in guinea pig hearts
%A Dirk Bruegger
%A Markus Rehm
%A Matthias Jacob
%A Daniel Chappell
%A Mechthild Stoeckelhuber
%A Ulrich Welsch
%A Peter Conzen
%A Bernhard F Becker
%J Critical Care
%D 2008
%I BioMed Central
%R 10.1186/cc6913
%X Isolated guinea pig hearts were subjected to 15 minutes of warm global ischemia followed by 20 minutes of reperfusion in the absence (Control group) and presence (NO group) of 4 ¦ÌM NO. In further experiments, the endothelial glycocalyx was enzymatically degraded by means of heparinase followed by reperfusion without (HEP group) and with NO (HEP+NO group).Ischemia and reperfusion severely damaged the endothelial glycocalyx. Shedding of heparan sulfate and damage assessed by electron microscopy were less in the presence of NO. Compared with baseline, coronary fluid extravasation increased after ischemia in the Control, HEP, and HEP+NO groups but remained almost unchanged in the NO group. Tissue edema was significantly attenuated in this group. Coronary vascular resistance rose by 25% to 30% during reperfusion, but not when NO was applied, irrespective of the state of the glycocalyx. Acute postischemic myocardial release of lactate was comparable in the four groups, whereas release of adenine nucleotide catabolites was reduced 42% by NO. The coronary venous level of uric acid, a potent antioxidant and scavenger of peroxynitrite, paradoxically decreased during postischemic infusion of NO.The cardioprotective effect of NO in postischemic reperfusion includes prevention of coronary vascular leak and interstitial edema and a tendency to forestall both no-reflow and degradation of the endothelial glycocalyx.Myocardial damage and coronary microvascular dysfunction, including the no-reflow phenomenon and edema formation, evolve from coronary occlusion and consecutive reperfusion. These are relatively common clinical occurrences, for example, in conjunction with percutaneous coronary angioplasty (PTCA), coronary artery bypass grafting (CABG), and heart transplant reperfusion [1]. Over the past 20 years, major advances have been made toward understanding the role of nitric oxide (NO) in the ischemic biology of the heart and it has become clear that NO, either endogenous or exog
%U http://ccforum.com/content/12/3/R73