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Inhaled NO and its effects on the endothelial glycocalyx |
In 2003 Dr Markus Rehm of the Ludwig-Maximilians-University in Munich, Germany, was awarded a GEMI Fund grant to research inhaled NO (nitric oxide) and its effects on the endothelial glycocalyx.
The glycocalyx is also known, descriptively, as the slime or algae layer. Doctor Rehm’s research into the effect of NO on this layer of the cells inside the blood vessels set out to examine the mechanisms by which NO may keep them functioning normally - what is known as preserving vascular homeostasis - especially during ischaemia (stopping of the blood flow) and reperfusion (when normal blood flow returns to the cells).
Dr Rehm conducted his studies using isolated perfused guinea pig hearts which were found to provide an ideal model. The hearts were exposed to stopped-flow ischaemia and then reperfused, with the results compared in the absence of NO and in the presence of 4 µM NO.
The major findings of this study were that NO, when applied at the onset of reoxygenation, protected isolated hearts against post-ischaemic reperfusion injury These findings are potentially very valuable since the prevention of post-ischaemic reperfusion damage is a goal in many clinical settings. They also provide first evidence that the endothelial glycocalyx in humans is damaged after intra-operative ischemia/reperfusion interventions.
Dr Rehm considers it is conceivable that prophylactic or even therapeutic approaches could be considered to inhibit damage of the human glycocalyx and the research with guinea pig hearts indicates that one option could be the application of nitric oxide. Dr Rehm believes that human studies investigating the role of NO in this context (major surgery with ischemia and reperfusion, organ transplantation, with and without NO) are urgently needed. |
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