Qin Su-lan, Liu Shan-ling, Wang Ru-rong
Department of Anesthesiologyology, West China Hospital, Sichuan University, Chengdu, 610041, China.
Sichuan Da Xue Xue Bao Yi Xue Ban. 2008 Jul;39(4):550-4.
To explore whether the capsaicin offers protective effect and possible mechanism on against myocardial ischemia-reperfusion injury of rat in vivo.
Ligating the left anterior descending coronary artery for 45 min and loosing it for 120 min were performed to establish the rat model of local myocardial ischemia-reperfusion injury in vivo. Forty healthy male rats were randomly divided into control group, capsaicin group, capsazepine group, and S-3144 group. In 10 min and 5 min before ischemia, all drugs for this study were delivered into rat left ventricle (LV) via right carotid artery. Variations of left ventricular function were successively monitored with ECG (electrocardiogram). Levels of creatine kinase MB (CKMB) in serum were determined. Evans-blue and TTC were utilized to identify the area at risk and the infarct size of LV.
In all groups, the variables of left ventricular developed pressure (LVDP) significantly decreased after ischemia and reperfusion (P < 0.05). Except capsaicin group, heart rates (HR) of three other groups markedly reduced with reperfusion for 120 min as compared to pre-reperfusion (P < 0.05). In capsaicin group, there were significant increases in HR and LVDP with reperfusion for 120 min when compared with the other three groups (P < 0.05). At the end of experiment, the levels of CKMB and infract size were lower in capsaicin group than in the other three groups (P < 0.05), and there was no statistical significance among the other three groups (P > 0.05).
Pretreatment with capsaicin can attenuate myocardial ischemia-reperfusion injury, of which the likely mechanism is by stimulating capsaicin receptor or TRPV1 and further activating substance P receptor in the rat in vivo.
探讨辣椒素对大鼠体内心肌缺血再灌注损伤是否具有保护作用及其可能机制。
通过结扎左冠状动脉前降支45分钟后再松开120分钟,建立大鼠局部心肌缺血再灌注损伤模型。将40只健康雄性大鼠随机分为对照组、辣椒素组、辣椒素拮抗剂组和S-3144组。在缺血前10分钟和5分钟,将本研究中的所有药物通过右颈动脉注入大鼠左心室。连续监测心电图以观察左心室功能变化。测定血清肌酸激酶同工酶MB(CKMB)水平。利用伊文思蓝和TTC鉴定左心室的危险区域和梗死面积。
所有组在缺血再灌注后左心室舒张末压(LVDP)均显著降低(P<0.05)。除辣椒素组外,其他三组在再灌注120分钟时心率(HR)较再灌注前明显降低(P<0.05)。与其他三组相比,辣椒素组在再灌注120分钟时HR和LVDP显著升高(P<0.05)。实验结束时,辣椒素组的CKMB水平和梗死面积低于其他三组(P<0.05),其他三组之间无统计学意义(P>0.05)。
辣椒素预处理可减轻心肌缺血再灌注损伤,其可能机制是通过刺激辣椒素受体或TRPV1,并进一步激活大鼠体内的P物质受体。