Sun Hai-Tao, Xue Fu-Shan, Liu Kun-Peng, Sun Li, Xu Ya-Chao, Liao Xu, Yang Quan-Yong, Zhang Yan-Ming
Department of Anesthesiology, Cancer Hospital and Institute, CAMS and PUMC, Beijing 100021, China.
Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 2009 Oct;31(5):612-5.
To investigate the delayed cardioprotection induced by remifentanil in intact rat ischemia-reperfusion (I/R) models.
Totally 42 adult male Wistar rats weighing 200-300 g were randomly divided into 7 groups (n = 6 in each group): In Group I, rats were injected with normal saline via tail vein, performed with the regimen of 3 x 5-min intravenous (i.v.) infusion at a rate of 0.1 ml x kg(-1) min(-1) 24 h before I/R; In Group II, rats were treated according to the same experimental protocols as in Group I except receiving additional naloxone (0.1 mg/kg) 10 minutes before normal saline pretreatment; In Groups III, IV, V, and VI, rats were treated with remifentanil via tail vein, performed with the regime of 3 x 5-min i.v. infusion at a rate of 2 microg x kg(-1) x min(-1) 12 h, 24 h, 48 h, and 72 h before I/R; In Group VII, the rats were treated according to the same experimental protocols as in Group IV except that they received additional naloxone (0.1 mg/kg) 10 minutes before remifentanil pretreatment. Heart rate (HR), mean arterial pressure (MAP), and a lead II electrocardiogram were continuously monitored during IR process. To determine plasma concentration of creatine kinase myocardial isoenzyme-MB (CK-MB), arterial blood samples were obtained immediately before ischemia, and at the end of ischemia and reperfusion. After a 120-min reperfusion, heart was removed for the measurement of myocardial infarct size. Infarct size (IS) was expressed as percentage of the area at risk.
HR, MAP, and rate-pressure product were not significantly different at each time points among all groups (P > 0.05). Compared with Group I, plasma concentrations of CK-MB at the end of ischemia and reperfusion and myocardial infarct size were significantly lower in Groups IV and V (P < 0.05). Compared with Group IV, plasma concentrations of CK-MB at the end of ischemia and reperfusion were significantly higher and myocardial infarct size was significantly larger in Group VII (P < 0.05).
Remifentanil preconditioning induces delayed cardioprotection in intact rat ischemia-reperfusion model, which may be triggered via opioid receptors.
研究瑞芬太尼在完整大鼠缺血再灌注(I/R)模型中诱导的延迟性心脏保护作用。
将42只体重200 - 300 g的成年雄性Wistar大鼠随机分为7组(每组n = 6):I组大鼠经尾静脉注射生理盐水,在I/R前24小时按照0.1 ml·kg⁻¹·min⁻¹的速率进行3次5分钟的静脉输注;II组大鼠按照与I组相同的实验方案处理,但在生理盐水预处理前10分钟额外给予纳洛酮(0.1 mg/kg);III、IV、V和VI组大鼠经尾静脉给予瑞芬太尼,分别在I/R前12小时、24小时、48小时和72小时按照2 μg·kg⁻¹·min⁻¹的速率进行3次5分钟的静脉输注;VII组大鼠按照与IV组相同的实验方案处理,但在瑞芬太尼预处理前10分钟额外给予纳洛酮(0.1 mg/kg)。在缺血再灌注过程中持续监测心率(HR)、平均动脉压(MAP)和II导联心电图。为测定血浆肌酸激酶心肌同工酶-MB(CK-MB)浓度,在缺血前、缺血结束时和再灌注结束时采集动脉血样本。再灌注120分钟后,取出心脏测量心肌梗死面积。梗死面积(IS)以危险区域面积的百分比表示。
所有组在各时间点的HR、MAP和心率-压力乘积无显著差异(P > 0.05)。与I组相比,IV组和V组在缺血结束时和再灌注时的血浆CK-MB浓度及心肌梗死面积显著降低(P < 0.05)。与IV组相比,VII组在缺血结束时和再灌注时的血浆CK-MB浓度显著升高,心肌梗死面积显著增大(P < 0.05)。
瑞芬太尼预处理可在完整大鼠缺血再灌注模型中诱导延迟性心脏保护作用,其可能通过阿片受体触发。