内源性阿片肽介导大鼠后肢缺血预适应的保护作用

研究了内源性阿片肽介导大鼠后肢缺血预适应的保护作用. 后肢缺血2 h，乙酰胆碱（ACh）诱导的血管内皮依赖性舒张性反应明显下降. 缺血预适应（缺血5 min，再灌5 min，重复3 次）能显著减弱长时间缺血对ACh舒血管效应的抑制作用，这种保护作用可被纳洛酮（3 mg·kg^-1）取消. 预先给予吗啡（300 μg·kg^-1）也能产生与缺血预适应相同的血管内皮保护作用. 然而，预先用辣椒素（50 mg·kg^-1）耗竭降钙素基因相关肽后，吗啡的保护作用被取消. 结果提示，内源性阿片肽介导大鼠后肢缺血预适应的血管保护作用，其机理可能涉及内源性降钙素基因相关肽.

Protection of ischemic preconditioning mediated by endogenous opioid peptides in rat hindquarters

The mediation of endogenous opioid peptides in the protection of ischemic preconditioning in the rat hindquarters was investigated. Rat hindquarters were subjected to 2 h of ischemia, and endothelium-dependent vasorelaxation to acetylcholine (ACh) was examined. Preconditioning induced by three cycles of 5 min aortic occlusion and 5 min blood reperfusion markedly reduced the impairment of vasodilator responses to ACh by long-term ischemia. This protective effect of preconditioning was abolished by naloxone（3 mg·kg^-1）. Similarly, pretreatment with morphine (300 μg·kg^-1) also attenuated the impairment of vasodilator responses to ACh, and the vasoprotection of morphine was abolished by pretreatment with capsaicin （50 mg·kg^-1） to deplete calcitonin gene related peptide(CGRP). These results suggest that endogenous opioid peptides participate in the mediation of the vasoprotection of ischemic preconditioning, which may involve endogenous CGRP in the rat hindquarters.