低温联合七氟醚对兔心肌单相动作电位及跨室壁复极离散度的影响

Effects of hypothermia combined with sevoflurane on myocardial monophasic action potential and transmural dispersion of repolarization of ventricles in rabbits

目的评价低温联合七氟醚对兔心室肌单相动作电位和跨室壁复极离散度的影响。方法成年家兔，体重1．5～2．0kg，雌雄不拘，成功制备Langendorff离体心脏灌注模型的48个心脏，随机分为6组（n=8），用K—H液平衡灌注后，正常对照组（c组）继续灌注37℃K—H液30min；低浓度七氟醚组（s，组）、高浓度七氟醚组（s2组）分别灌注2．4％及4．8％七氟醚饱和的37℃K—H液30min；低温组（H组）灌注30℃K—H液30min；低温联合低浓度七氟醚组（HS，组）和低温联合高浓度七氟醚组（HS2组）分别灌注2．4％及4．8％七氟醚饱和的30℃K—H液30min。灌注期间记录左心室前壁外膜层、中层和内膜层心肌单相动作电位。计算单相动作电位复极90％的时程（MAPD。）和跨室壁复极离散度（TDR）。记录早期后除极、延迟后除极及心律失常的发生情况。结果与C组比较，H组三层心肌MAPD90均明显延长，心律失常的发生率升高（P〈0．05）；各组间TDR比较差异无统计学意义（P〉0．05）。HS1组和HS2组心律失常的发生率低于H组（P〈0．05）。七氟醚与低温无交互作用（P〉0．05），仅表现为低温可延长MAPD90（P〈0．05）。结论低温联合七氟醚对兔心肌单相动作电位及跨室壁复极离散度无明显影响，七氟醚可抑制低温诱发心肌复极时间延长，从而降低了低温诱发心律失常的发生机率。

Objective To investigate the effects of hypothermia combined with sevoflurane on myocardial monophasic action potential （MAP） and transmural dispersion of repolarization （ TDR ） of the left ventricle in rabbits in vitro. Methods Adult rabbits weighing 1.5-2.0 kg were sacrificed after heparinized and anesthetized. The hearts were immediately removed and perfused with K-H soluation saturated with 95 % O2-5 % CO2 at 37 ℃ in a Langendorff apparatus. Forty-eight isolated hearts were randomly divided into 6 groups （ n = 8 each） ： I control group （group C）, II low concentration sevoflurane group （group S1 ）, III high concentration sevoflurane group （group S2 ）, IV hypothermia group （group H）, V hypothermia ＋ low concentration sevoflurane （group HS1 ） and V/ hypothermia ＋ high concentraion sevoflurane （group HS2 ）. Group C received continous perfusion. Group S1 and S2 received perfusion with K-H solution saturated with 2.4% and 4.8% sevoflurane at 37℃ for 30 min respectively. Group H received perfusion with K-H solution at 30 ℃ for 30 rain. Group HSI and HS2 received perfusion with K-H solution saturated with 2.4% and 4.8% sevoflurane at 30 ℃ respectively. MAPs of epicardimn, mid-myocardium and endocardimn of the left ventricle were recorded. MAP duration at 90% repolarlzation （ MAPDgo ） and TDR were calculated. Early after-depolarization, delayed after-depolarization and arrhythmia were also recorded. Results Compared with group C, MAPD90 of the 3 layers of ventricle was significantly prolonged, the incidence of arrhythmia increased in group H （P 〈 0.05 ）. There was no significant difference in TDR among all groups （ P 〉 0.05）. There was no interaction between sevoflurane and hypothennia （P 〉 0.05 ）, and it only showed that MAPD90 was prolonged by hypothermia （P 〈 0.05 ）. Conclusion Hypothermia combined with sevoflurane exerts no significant effects on myocardial MAP and TDR of ventricles in rabbits, and sevoflurane decreases the incidence of hypothermia-induced arrhythmia through inhibiting the prolongation of MAPD90.