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目的:研究降钙素基因相关肽与前列腺素在豚鼠心脏缺血预适应中的相互作用。方法:采用Langen-dorff方法灌注豚鼠离体心脏。记录心率、冠脉流量、左室内压以及最大变化速率,并测定冠脉流出液中降钙素基因相关肽(CGRP)与6-酮-PGF_(1α)的释放量。结果:内皮素-1(200 pmoL)引起心功能下降,表现为冠脉流量、心率、左室内压及其最大变化速率降低。缺血预适应可明显减轻内皮素-1引起的心脏损伤,同时预适应期间CGRP与6-酮-PGF_(1α)的释放量明显增加。应用辣椒素耗竭内源性CGRP后,缺血预适应的保护作用被取消。选择性CGRP_1受体拮抗剂CGRP_(8-37)100nmol/L也能取消缺血预适应的保护作用。环氧化酶抑制剂吲哚美辛(10μmol/L)可取消缺血预适应的保护作用,同时缺血预适应促进CGRP与6-酮-PGF_(1α)释放的作用也被取消。结论:前列腺素参与了缺血预适应对豚鼠心脏的保护作用,前列腺素的作用是由CGRP所介导。
Objective: To study the interaction between calcitonin gene-related peptide and prostaglandin in ischemic preconditioning in guinea pig hearts. Methods: Guinea pig isolated heart was infused by Langen-dorff method. The heart rate, coronary flow, left ventricular pressure and maximal rate of change were recorded. The levels of CGRP and 6-keto-PGF_ (1α) in coronary effluent were measured. Results: Endothelin-1 (200 pmoL) caused a decrease in cardiac function with a decrease in coronary flow, heart rate, left ventricular pressure, and its maximum rate of change. Ischemic preconditioning can significantly reduce endothelin-1-induced cardiac injury, while preconditioning CGRP and 6-keto-PGF_ (1α) release increased significantly. The protective effect of ischemic preconditioning was abolished after the depletion of endogenous CGRP by capsaicin. Selective CGRP_1 receptor antagonist CGRP_ (8-37) 100nmol / L can also cancel the protective effect of ischemic preconditioning. Cyclooxygenase inhibitor indomethacin (10μmol / L) can cancel the protective effect of ischemic preconditioning, while the role of ischemic preconditioning to promote CGRP and 6-keto-PGF_ (1α) release was also abolished. CONCLUSION: Prostaglandins are involved in the protective effect of ischemic preconditioning on guinea pig hearts, and prostaglandin is mediated by CGRP.