Su-lan Qin1, Shan-ling Liu, Ru-rong Wang. 1. Department of Anesthesiologyology, West China Hospital, Sichuan University, Chengdu, 610041, China.
Abstract
OBJECTIVE: To explore whether the capsaicin offers protective effect and possible mechanism on against myocardial ischemia-reperfusion injury of rat in vivo. METHODS: 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. RESULTS: 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). CONCLUSION: 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.
OBJECTIVE: To explore whether the capsaicin offers protective effect and possible mechanism on against myocardial ischemia-reperfusion injury of rat in vivo. METHODS: 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. RESULTS: 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). CONCLUSION: 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.