Tofukuji M, Stamler A, Li J, Hariawala M D, Franklin A, Sellke F W
Department of Surgery, Beth Israel-Deaconess Medical Center, Boston, MA 02215, USA.
Ann Thorac Surg. 1997 Nov;64(5):1360-7. doi: 10.1016/S0003-4975(97)00990-9.
Cardioplegia is known to affect coronary vascular reactivity. We examined the effects of intermittent cold and continuous warm blood cardioplegia on beta-adrenoceptor-mediated, adenosine triphosphate-sensitive K+ (K+ATP)-channel-mediated, and endothelium-dependent relaxation and on the myogenic tone of coronary arterioles.
Pigs were placed on cardiopulmonary bypass. Hearts were arrested for 1 hour with a cold blood cardioplegic solution administered intermittently (n = 12; iCB-CP) or with a warm blood cardioplegic solution delivered continuously (n = 12; cWB-CP). Selected hearts (n = 6 in each group) were then reperfused for 1 hour. In vitro relaxation responses of precontracted microvessels (50 to 160 microns) were studied in a pressurized no-flow state.
Relaxation in response to isoproterenol (beta-adrenergic agonist) was similar after iCB-CP and cWB-CP, whereas forskolin (adenylate cyclase activator)-induced relaxation was impaired more after iCB-CP than after cWB-CP. After reperfusion the respective responses were similar. Both iCB-CP and cWB-CP preserved receptor-mediated, endothelium-dependent relaxation in response to adenosine, 5'-diphosphate; non-receptor-mediated endothelium-dependent relaxation in response to A23187; endothelium-independent cyclic guanosine monophosphate-mediated relaxation in response to sodium nitroprusside, and K+ATP-channel-mediated relaxation. Relaxations in response to 8-bromo-cyclic guanosine monophosphate (a cyclic guanosine monophosphate-dependent protein kinase activator) and to 8-bromo-cyclic adenosine monophosphate (a cyclic adenosine monophosphate-dependent protein kinase activator) were impaired after iCB-CP alone and after reperfusion, whereas the respective responses were not affected after cWB-CP. Myogenic tone was decreased similarly after iCB-CP and cWB-CP but was not further altered after reperfusion. Cardiac function was similar after iCB-CP and cWB-CP.
These results suggest that cWB-CP is similar to iCB-CP in its ability to preserve endothelium-dependent relaxation and K+ATP-channel function. The superior preservation of beta-adrenergic-cyclic adenosine monophosphate-mediated coronary responses after cWB-CP is brief and associated with minimal improvement of myocardial function and myogenic tone.
已知心脏停搏液会影响冠状动脉血管反应性。我们研究了间歇性冷血和持续性温血心脏停搏液对β-肾上腺素能受体介导的、三磷酸腺苷敏感性钾离子（K⁺ATP）通道介导的以及内皮依赖性舒张的影响，以及对冠状动脉小动脉肌源性张力的影响。
将猪置于体外循环。心脏分别用间歇性给予的冷血心脏停搏液（n = 12；iCB-CP）或持续性给予的温血心脏停搏液（n = 12；cWB-CP）停搏1小时。然后每组选取6颗心脏再灌注1小时。在加压无血流状态下研究预收缩微血管（50至160微米）的体外舒张反应。
iCB-CP和cWB-CP后，对异丙肾上腺素（β-肾上腺素能激动剂）的舒张反应相似，而毛喉素（腺苷酸环化酶激活剂）诱导的舒张在iCB-CP后比在cWB-CP后受损更严重。再灌注后各自的反应相似。iCB-CP和cWB-CP均保留了对腺苷、5'-二磷酸的受体介导的内皮依赖性舒张；对A23187的非受体介导的内皮依赖性舒张；对硝普钠的内皮非依赖性环鸟苷单磷酸介导的舒张以及K⁺ATP通道介导的舒张。单独iCB-CP后以及再灌注后，对8-溴环鸟苷单磷酸（一种环鸟苷单磷酸依赖性蛋白激酶激活剂）和对8-溴环腺苷单磷酸（一种环腺苷单磷酸依赖性蛋白激酶激活剂）的舒张反应受损，但这些反应在cWB-CP后未受影响。iCB-CP和cWB-CP后肌源性张力同样降低，但再灌注后未进一步改变。iCB-CP和cWB-CP后的心脏功能相似。
这些结果表明，cWB-CP在保留内皮依赖性舒张和K⁺ATP通道功能方面与iCB-CP相似。cWB-CP后β-肾上腺素能-环腺苷单磷酸介导的冠状动脉反应的更好保留是短暂的，且与心肌功能和肌源性张力的最小改善相关。
