| Summary: | 碩士 === 國防醫學院 === 航太醫學研究所 === 88 === Ischemic preconditioning ( IPC ) is a protective phenomenon during acute myocardial ischemia / reperfusion injury. The lower body negative pressure ( LBNP ) can decrease the venous return and change the cardiac size. However, if the LBNP activates myocardial mechanical receptors and simulates the protective effect of IPC is still unknown. Therefore, we hypothesized that LBNP could activate myocardial mechanical receptors, translocate protein kinase C, open KATP channels and then generate the effect of IPC. SD rats were anesthetized by pentobarbital. Artificial ventilation, right common carotid artery and jugular vein cannulation, ECG electrodes placement, midline sternotomy, and left coronary artery loop snare were performed. The rats were divided into eight groups. First ( control, n = 9 ) : The coronary artery was occluded for 45 min and reperfused for 60 min. The mean arterial pressure, central venous pressure, heart rate, venous pH, PCO2, lactate, arrhythmia, survival rate, and myocardial infarct size were measured. Second ( IPC, n = 7 ) : The coronary artery was occluded for 3 min and reperfused for 5 min twice to precondition the myocardium. The following procedures were the same as the first group. Third ( Gd3+ + IPC, n = 6 ) : Gadolinium ( Gd3+, 3 mg / kg ) was injected intravenously and the following procedures were the same as the second group. Fourth ( LBNP, n = 8 ) : The LBNP was performed for 25 min to precondition the myocardium. The following procedures were the same as the first group. The fifth, sixth, seventh and eighth groups were intravenous injection of Gd3+ ( 3 mg / kg, n = 6 ), Chelerythrine ( 0.025 mg / kg, n = 6 ), Glibenclamide ( 0.25 mg / kg, n = 6 ) and Vehicle ( DMSO, n = 6 ), respectively, and the following procedures were all the same as the fourth group. The results showed that the mean arterial pressure, central venous pressure, heart rate, venous pH, PCO2, lactate,
arrhythmia and survival rate did not have any significant change before and after coronary artery occlusion. The infarct size of IPC and LBNP groups were 30.6 ± 4.4 % and 46.7 ± 1.7 %, respectively, and all significantly differed from control ( 63.1 ± 2.1 %, P < 0.05 ). Gd3+ infusion completely abolished the LBNP-induced but only partially blocked the IPC-induced decreases of myocardial infarct size. The infusion of chelerythrine and glibenclamide but not vehicle also eliminated the LBNP-induced decrease of myocardial infarct size. We conclude that the LBNP can activate myocardial mechanical receptors, translocate protein kinase C, open KATP channels and decrease infarct size following coronary artery occlusion and reperfusion. The IPC can evoke both chemo- and mechanical receptors then generate the more profound cardioprotective effect than LBNP.
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