Tofukuji M, Stamler A, Li J, Franklin A, Wang S Y, Hariawala M D, Sellke F W
Department of Surgery of Beth Israel-Deaconess Medical Center, Boston, Massachusetts, USA.
J Surg Res. 1997 May;69(2):233-9. doi: 10.1006/jsre.1997.5003.
We compared the effect of hypermagnesium and hyperkalemic crystalloid cardioplegia on beta-adrenoceptor-mediated and endothelium-dependent relaxation and myogenic responses of coronary arterioles. Pigs were placed on cardiopulmonary bypass. Hearts were arrested with cold hypermagnesium (25 mM Mg2+, hyper-Mg, n = 12) or hyperkalemic (25 mM K+, hyper-K, n = 12) crystalloid cardioplegia for 1 hr. Hearts of selected pigs (n = 6 in each group) were then reperfused for 1 hr. In vitro relaxation responses of acetylcholine-pre-contracted arterioles were studied in a pressurized no-flow state with video-microscopy. Relaxation of pre-contracted coronary microvessels (70-150 microns) to isoproterenol (beta-adrenergic agonist) and forskolin (adenylate cyclase activator) was preserved after cardioplegia using a hyper-Mg solution. In contrast, responses were impaired to isoproterenol [P < 0.01 (two-factor ANOVA) vs. controls, n = 6] and forskolin (P < 0.01) after hyper-K cardioplegia. After 1 hr of reperfusion, relaxation responses to isoproterenol and forskolin were partially recovered. Hyper-Mg cardioplegia and post-cardioplegic reperfusion did not affect receptor-mediated endothelium-dependent relaxation to ADP, non-receptor-mediated endothelium-dependent relaxation to A23187, and endothelium-independent relaxation to nitroprusside. However, responses to ADP (P < 0.01) and A23187 (P < 0.05) were selectively impaired after hyper-K cardioplegia. Myogenic contraction was impaired after either hyper-Mg or hyper-K cardioplegia. Left ventricular systolic pressure, coronary blood flow, and +dP/dt were similar after hyper-Mg or hyper-K cardioplegia. These results suggest that hyper-Mg cardioplegia is superior to hyper-K cardioplegia in terms of preserving beta-adrenoceptor-mediated and endothelium-dependent regulation of the coronary microcirculation, yet it has minimal if any additional beneficial effect on preserving myogenic responses or myocardial contractile function.
我们比较了高镁和高钾晶体停搏液对冠状动脉小动脉β-肾上腺素能受体介导的、内皮依赖性舒张及肌源性反应的影响。将猪置于体外循环。心脏用冷高镁（25 mM Mg2+，高镁组，n = 12）或高钾（25 mM K+，高钾组，n = 12）晶体停搏液停搏1小时。然后对部分猪心脏（每组n = 6）进行1小时再灌注。采用视频显微镜在无血流加压状态下研究乙酰胆碱预收缩小动脉的体外舒张反应。使用高镁溶液停搏后，预收缩冠状动脉微血管（70 - 150微米）对异丙肾上腺素（β-肾上腺素能激动剂）和福斯可林（腺苷酸环化酶激活剂）的舒张反应得以保留。相比之下，高钾停搏后对异丙肾上腺素的反应受损[P < 0.01（双因素方差分析），与对照组相比，n = 6]，对福斯可林的反应也受损（P < 0.01）。再灌注1小时后，对异丙肾上腺素和福斯可林的舒张反应部分恢复。高镁停搏液及停搏后再灌注不影响受体介导的对ADP的内皮依赖性舒张、非受体介导的对A23187的内皮依赖性舒张以及对硝普钠的非内皮依赖性舒张。然而，高钾停搏后对ADP（P < 0.01）和A23187（P < 0.05）的反应选择性受损。高镁或高钾停搏后肌源性收缩均受损。高镁或高钾停搏后左心室收缩压、冠状动脉血流量及 +dP/dt相似。这些结果表明，在保留冠状动脉微循环的β-肾上腺素能受体介导及内皮依赖性调节方面，高镁停搏液优于高钾停搏液，但在保留肌源性反应或心肌收缩功能方面，即便有额外有益作用也极小。
