Khuri S F, Warner K G, Josa M, Butler M, Hayes A, Hanson R, Siouffi S, Barsamian E M
Department of Surgery, Brockton/West Roxbury Veterans Administration Medical Center, MA 02132.
J Thorac Cardiovasc Surg. 1988 Mar;95(3):442-54.
The effects of sanguineous and asanguineous cardioplegia on the generation of myocardial acid in the hypertrophied human heart during aortic clamping and reflow were elucidated by continuous intraoperative monitoring of myocardial pH in 42 patients undergoing valve replacement, with or without coronary bypass. The patients were divided into three groups: Group I (n = 14) received intermittent crystalloid cardioplegia; group II (n = 14) received intermittent blood cardioplegia; and group III (n = 14) received continuous blood cardioplegia. The groups were matched according to six previously elucidated determinants of myocardial acidosis. Measurements were made of myocardial pH, hydrogen ion concentration ([H+]), and the difference in pH units between myocardial pH and the pH of neutrality of water at the corresponding temperature (delta pHn). Throughout aortic clamping, myocardial pH in groups I and II fell significantly by 0.46 +/- 0.08 and 0.15 +/- 0.07 units, respectively (p less than 0.001) between the groups). In contrast, myocardial pH remained statistically unchanged throughout aortic clamping in group III (p less than 0.001 compared to groups I and II). Similar relationships were observed in [H+] and delta pHn during aortic clamping. During the early reflow, myocardial acidosis was observed in all three groups and delta pHn in group III increased from -0.26 +/- 0.10 at the end of aortic clamping to -0.57 +/- 0.07 during reperfusion (p less than 0.03). Patients in groups II and III required significantly less inotropic and mechanical cardiac support than patients in group I (p = 0.017). Hence, although continuous blood cardioplegia does not completely prevent acid accumulation during reflow, it provides better metabolic protection of the hypertrophied human heart than either intermittent crystalloid or intermittent blood cardioplegia.
通过对42例接受瓣膜置换术（无论是否行冠状动脉搭桥术）患者术中持续监测心肌pH值，阐明了含血和无血心脏停搏液对主动脉阻断及再灌注期间肥厚型人心脏心肌酸生成的影响。患者分为三组：第一组（n = 14）接受间断晶体心脏停搏液；第二组（n = 14）接受间断含血心脏停搏液；第三组（n = 14）接受持续含血心脏停搏液。根据先前阐明的六个心肌酸中毒决定因素对各组进行匹配。测量心肌pH值、氢离子浓度（[H+]）以及心肌pH值与相应温度下水的中性pH值之间的pH单位差值（δpHn）。在整个主动脉阻断期间，第一组和第二组的心肌pH值分别显著下降0.46±0.08和0.15±0.07个单位（两组间p<0.001）。相比之下，第三组在整个主动脉阻断期间心肌pH值在统计学上保持不变（与第一组和第二组相比p<0.001）。在主动脉阻断期间，[H+]和δpHn也观察到类似关系。在早期再灌注期间，三组均观察到心肌酸中毒，第三组的δpHn从主动脉阻断结束时的-0.26±0.10增加到再灌注期间的-0.57±0.07（p<0.03）。第二组和第三组患者所需的正性肌力和机械心脏支持明显少于第一组患者（p = 0.017）。因此，尽管持续含血心脏停搏液不能完全防止再灌注期间的酸积累，但与间断晶体或间断含血心脏停搏液相比，它能为肥厚型人心脏提供更好的代谢保护。
