Galiñanes M, Hearse D J
Cardiovascular Research, Rayne Institute, St Thomas' Hospital, London, U.K.
Cardioscience. 1990 Jun;1(2):127-43.
Isolated hearts from rabbits, hamsters, ferrets, gerbils, rats, mice and guinea pigs were used to investigate species differences in (i) stability during aerobic perfusion, (ii) susceptibility to ischemic injury and (iii) responsiveness to cardioplegic protection. During 120 minutes of continuous aerobic perfusion, the rate of functional deterioration differed between species. The rabbit was the most stable and the guinea pig the least: the mean +/- SEM of the left ventricular developed pressure falling, after 120 minutes of perfusion, to 82 +/- 4% and 60 +/- 6%, respectively. In studies with 30 minutes of ischemia and 60 minutes of reperfusion, the developed pressure recovered to 72 +/- 2, 71 +/- 2, 65 +/- 3, 64 +/- 2, 58 +/- 3, 50 +/- 8 and 50 +/- 2% of its pre-ischemic value in the rabbit, hamster, ferret, gerbil, rat, mouse and guinea pig, respectively. With 60 minutes of ischemia, the recovery of developed pressure in the guinea pig, rabbit, rat, mouse, hamster, ferret and gerbil was 5 +/- 1, 19 +/- 2, 22 +/- 3, 30 +/- 5, 55 +/- 4, 60 +/- 2 and 45 +/- 5%, respectively. Creatine kinase leakage and changes in tissue metabolite content generally reflected the degree of functional injury. In further studies, groups of 6 hearts were infused for 2 minutes with St. Thomas' Hospital Cardioplegic Solution, then subjected to 30 minutes of ischemia. Cardioplegia improved the recovery of developed pressure in the rabbit, hamster, gerbil, rat and mouse (from 72 +/- 2, 71 +/- 2, 64 +/- 2, 58 +/- 3 and 50 +/- 8% to 82 +/- 3, 103 +/- 3, 84 +/- 4, 77 +/- 2 and 78 +/- 5%, respectively; p less than 0.05 for each species). However, no protection was observed in the ferret and guinea pig (65 +/- 3 and 50 +/- 2% versus 66 +/- 3 and 47 +/- 6%, respectively; p = NS). With cardioplegia, tissue high-energy phosphates increased significantly in all species except the gerbil. Rat and guinea pig hearts were taken for time-response studies (ischemia for 15, 20, 30, 45, 50 and 60 minutes in the rat and 15, 30, 45 and 60 minutes in the guinea pig) with or without cardioplegia. In the rat, cardioplegia improved recovery over an ischemic time-window of 20-45 minutes, but in the guinea pig no improvement was detected. Creatine kinase leakage reflected the patterns of functional recovery. In contrast, high-energy phosphates were preserved better in both species after 30 minutes of ischemia.(ABSTRACT TRUNCATED AT 400 WORDS)
采用来自兔、仓鼠、雪貂、沙鼠、大鼠、小鼠和豚鼠的离体心脏,研究以下方面的种属差异:(i)有氧灌注期间的稳定性;(ii)对缺血性损伤的易感性;(iii)对心脏停搏保护的反应性。在120分钟的持续有氧灌注期间,各物种之间功能恶化的速率有所不同。兔最稳定,豚鼠最不稳定:灌注120分钟后,左心室舒张末压的平均值±标准误分别降至82±4%和60±6%。在30分钟缺血和60分钟再灌注的研究中,兔、仓鼠、雪貂、沙鼠、大鼠、小鼠和豚鼠的舒张末压分别恢复至缺血前值的72±2%、71±2%、65±3%、64±2%、58±3%、50±8%和50±2%。缺血60分钟时,豚鼠、兔、大鼠、小鼠、仓鼠、雪貂和沙鼠的舒张末压恢复率分别为5±1%、19±2%、22±3%、30±5%、55±4%、60±2%和45±5%。肌酸激酶泄漏和组织代谢物含量的变化一般反映了功能损伤的程度。在进一步的研究中,将6组心脏用圣托马斯医院心脏停搏液灌注2分钟,然后进行30分钟缺血。心脏停搏改善了兔、仓鼠、沙鼠、大鼠和小鼠舒张末压的恢复(分别从72±2%、71±2%、64±2%、58±3%和50±8%提高到82±3%、103±3%、84±4%、77±2%和78±5%;每种动物p<0.05)。然而,在雪貂和豚鼠中未观察到保护作用(分别为65±3%和50±2%对66±3%和47±6%;p=无显著性差异)。使用心脏停搏液时,除沙鼠外,所有物种的组织高能磷酸盐均显著增加。取大鼠和豚鼠心脏进行时间反应研究(大鼠缺血15、20、30、45、50和60分钟,豚鼠缺血15、30、45和60分钟),有或无心脏停搏液。在大鼠中,心脏停搏在20 - 45分钟的缺血时间窗内改善了恢复情况,但在豚鼠中未检测到改善。肌酸激酶泄漏反映了功能恢复的模式。相比之下,缺血30分钟后,两种动物的高能磷酸盐保存得更好。(摘要截断于400字)