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目的:研究硝酸甘油增强心停搏液的保护作用与促进降钙素基因相关肽释放的关系。方法:在StThomas Hospital心停搏液条件下,离体心脏低温缺血4h后再灌40min,记录心率、冠脉流量及心功能,并测定灌注液中降钙素基因相关肽(CGRP)的浓度及肌酸激酶(CK)的释放量。结果:硝酸甘油(0.1或1μmol/L)改善心功能,降低CK释放,同时促进CGRP的释放。CGRP(5或10nmol/L)也改善心功能及降低CK释放。预先用辣椒素耗竭感觉神经递质后。硝酸甘油的心肌保护和升高灌注液中CGRP浓度作用消失。选择性CGRP受体拮抗剂CGRP_(8-37)也能取消硝酸甘油的心肌保护作用。格列苯脲对硝酸甘油和CGRP的心保护作用均无影响。结论:硝酸甘油增强心停搏液的保护作用是通过内源性CGRP所介导,其保护作用与ATP敏感的钾通道无关。
Objective: To investigate the protective effect of nitroglycerin on cardiac cardioplegia and its relationship with the release of calcitonin gene-related peptide. Methods: Heart rate, coronary flow and heart function were recorded after reperfusion for 4 hours after hypothermic ischemia in vitro in St Thomas Center Cardioplegia. The concentrations of CGRP And creatine kinase (CK) release. Results: Nitroglycerin (0.1 or 1 μmol / L) improved cardiac function, decreased CK release, and promoted CGRP release. CGRP (5 or 10 nmol / L) also improves heart function and reduces CK release. After pre-sensory neurotransmitter depletion with capsaicin. Myocardial protection of nitroglycerin and increase in perfusion fluid CGRP concentration disappeared. Selective CGRP receptor antagonist CGRP_ (8-37) also abolished myocardial protection of nitroglycerin. Glibenclamide had no effect on the cardioprotective effect of nitroglycerin and CGRP. CONCLUSION: The protective effect of nitroglycerin on cardiac cardioplegic solution is mediated by endogenous CGRP, and its protective effect is independent of ATP-sensitive potassium channel.