Previous experiments showed evidence of impaired receptor-mediated production of EDRF/NO following reperfusion injury could be due to G-protein dysfunction which links endothelial cell receptors to the pathway of EDRF/NO synthesis. This experimental research suggested that criocrystalloid cardioplegia, associated to topic hypotermia, could prevent or reverse the endothelium disfunction under same experimental conditions. More experiments will be necessary to get definitive conclusions, because fine statystical analysis suggested increasing the number of experiments. Otherwise, the present study proved for the first time that hypothermia alone can cause the release of PGI2 and EDRF/NO from the endothelium. This suggests that the endothelium could be an important temperature sensor and has important implications for the understanding of cardiopulmonary bypass physiology and local vascular autoregulation.
Heart arrest, induced; Myocardial ischemia; Myocardial reperfusion; Cardioplegic solutions; Hypothermia; Acetylcholine; Adenosine diphosphate; Sodium, fluoride; Phospholipase C; Ionophoros; Isoproterenol; Nitroprusside; Coronary vessels; Reperfusion injury; Endothelium; Extracorporeal circulation
