Takeshima S, Vaage J, Valen G
Department of Thoracic Surgery, Karolinska Hospital, Stockholm, Sweden.
Scand J Clin Lab Invest. 1997 Nov;57(7):637-46. doi: 10.3109/00365519709055288.
In studies of preconditioning, a variety of models have been used. The aim of the present study was to find the optimal preconditioning model for preservation of cardiac function during reperfusion of globally ischaemic, Langendorff-perfused rat hearts. Cardiac function was assessed by the occurrence of severe reperfusion arrhythmias (ventricular fibrillation or asystolia), heart rate (HR), left ventricular systolic (LVSP), end diastolic (LVEDP), and developed pressures (LVDP = LVSP - LVEDP), as well as coronary flow (CF). Series 1 (n = 17) in each group: control perfusion for 20 min without preconditioning or 2 episodes of 2, 3, 4, or 5 min of ischaemia, each followed by 5 min reperfusion, before 25 min ischaemia and 60 min reperfusion. Preconditioning reduced the incidence of reperfusion arrhythmias, attenuated the reperfusion-induced increase of LVEDP, and increased CF, but did not influence LVSP, LVDP, or rate x pressure-product (RPP = LVSP x HR) during reperfusion. The greatest effect was found by 2 min ischaemia and 5 min reperfusion. In series 2 (n = 17 in each group) control perfusion for 7 or 28 min, or preconditioning with 1-4 episodes of 2 min ischaemia and 5 min reperfusion before 35 min ischaemia and 60 min reperfusion were compared. Reduction of severe reperfusion arrhythmias and LVEDP elevation, as well as improvement of CF, LVDP, and HR in preconditioned hearts were observed in series 2. Optimal cardioprotection was achieved by only one episode of preconditioning. In conclusion, preconditioning before global ischaemia improved cardiac function during reperfusion of isolated rat hearts. The most marked effects were reduction of severe reperfusion arrhythmias and attenuation of diastolic dysfunction. Although all preconditioning models employed were cardioprotective, 1 episode of 2 min ischaemia provided optimal protection.
在预处理研究中,已使用了多种模型。本研究的目的是找到在全心缺血、Langendorff灌注的大鼠心脏再灌注期间保存心脏功能的最佳预处理模型。通过严重再灌注心律失常(室颤或心搏停止)的发生情况、心率(HR)、左心室收缩压(LVSP)、舒张末期压力(LVEDP)、发展压力(LVDP = LVSP - LVEDP)以及冠状动脉血流量(CF)来评估心脏功能。每组系列1(n = 17):在25分钟缺血和60分钟再灌注之前,进行20分钟无预处理的对照灌注,或进行2次、3次、4次或5次2分钟、3分钟、4分钟或5分钟的缺血,每次缺血后再灌注5分钟。预处理降低了再灌注心律失常的发生率,减轻了再灌注诱导的LVEDP升高,并增加了CF,但在再灌注期间不影响LVSP、LVDP或心率×压力乘积(RPP = LVSP×HR)。发现2分钟缺血和5分钟再灌注产生的效果最大。在系列2(每组n = 17)中,比较了7分钟或28分钟的对照灌注,或在35分钟缺血和60分钟再灌注之前进行1 - 4次2分钟缺血和5分钟再灌注的预处理。在系列2中观察到预处理心脏中严重再灌注心律失常的减少和LVEDP升高的减轻,以及CF、LVDP和HR的改善。仅一次预处理即可实现最佳心脏保护。总之,全心缺血前的预处理改善了离体大鼠心脏再灌注期间的心脏功能。最显著的作用是减少严重再灌注心律失常和减轻舒张功能障碍。尽管所采用的所有预处理模型均具有心脏保护作用,但2分钟缺血一次可提供最佳保护。