Banitt P F, Dai H B, Wang S Y, Friedman M, Sellke F W
Division of Cardiothoracic Surgery, Beth Israel Hospital, Boston, MA 02215, USA.
Cardiovasc Res. 1995 Jun;29(6):827-33.
The aim was to examine agonist induced and myogenic venular responses after crystalloid cardioplegia in conditions simulating cardiopulmonary bypass.
Hearts of pigs were arrested with cold hyperkalaemic ([K+] = 25 mM) crystalloid cardioplegic solution for 1 h under conditions of cardiopulmonary bypass. In another group, hearts were arrested and then reperfused with warm blood for 1 h while being separated from cardiopulmonary bypass. In a third group, animals were supported on cardiopulmonary bypass for 75 min without diversion of coronary blood flow. Hearts from non-instrumented animals served as controls. Coronary venules (91-197 microns in internal diameter) were studied in vitro in a pressurised no flow state using video microscopy. Agonist induced responses were assessed in vessels precontracted with the thromboxane A2 analogue U46619.
Endothelium dependent relaxations to adenosine diphosphate (ADP, P = 0.11 v control), or serotonin (P = 0.67), and endothelium independent relaxations to the beta adrenergic cyclic AMP mediated agonist isoprenaline (P = 0.20), adenosine (P = 0.98), or the KATP channel opener pinacidil (P = 0.40) were not significantly altered after cold cardioplegia alone. After cardioplegia followed by 1 h of warm blood reperfusion, venular responses to ADP (P = 0.003 v control), isoprenaline (P = 0.013), adenosine (P = < 0.001), and pinacidil (P = 0.005) were reduced compared to the respective control responses, while the response to serotonin (P = 0.97) remained unchanged. Endothelium independent cyclic GMP mediated relaxation to sodium nitroprusside was similar in all groups (P > 0.90). Myogenic reactivity was assessed after incremental increases in the intraluminal pressure from 2-40 mm Hg. As intraluminal pressure was increased, the diameter of control venules increased and reached a plateau. Following cardioplegia, the pressure-diameter relationship of venules was shifted upward (P = 0.04 v control) suggesting impaired myogenic tone. After reperfusion, myogenic tone partially recovered. Extracorporeal circulation without diversion of coronary perfusion did not significantly affect venular responses.
Ischaemic cardioplegia using a cold hyperkalaemic solution under conditions of cardiopulmonary bypass does not significantly alter agonist induced venular responses, whereas myogenic contraction is slightly reduced. After 1 h of reperfusion, agonist induced relaxations of coronary venules are significantly impaired, whereas myogenic contraction recovers. These findings may have implications for the control of myocardial perfusion and diastolic properties of the heart after ischaemic cardioplegia under conditions of extracorporeal circulation.
本研究旨在探讨在模拟体外循环的条件下，晶体停搏液灌注后激动剂诱导的和肌源性微静脉反应。
在体外循环条件下，用冷高钾（[K⁺]=25 mM）晶体停搏液使猪心脏停搏1小时。另一组中，心脏停搏后，在脱离体外循环的情况下用温血再灌注1小时。第三组中，动物在体外循环支持下75分钟，不进行冠状动脉血流分流。未插管动物的心脏作为对照。使用视频显微镜在体外加压无血流状态下研究内径为91 - 197微米的冠状微静脉。在用血栓素A2类似物U46619预收缩的血管中评估激动剂诱导的反应。
单独冷停搏后，对二磷酸腺苷（ADP，P = 0.11，与对照组相比）或5 - 羟色胺（P = 0.67）的内皮依赖性舒张，以及对β肾上腺素能环磷酸腺苷介导的激动剂异丙肾上腺素（P = 0.20）、腺苷（P = 0.98）或钾通道开放剂吡那地尔（P = 0.40）的非内皮依赖性舒张均无显著改变。停搏后再进行1小时温血再灌注，与各自的对照反应相比，微静脉对ADP（P = 0.003，与对照组相比）、异丙肾上腺素（P = 0.013）、腺苷（P = < 0.001）和吡那地尔（P = 0.005）的反应降低，而对5 - 羟色胺的反应（P = 0.97）保持不变。对硝普钠的非内皮依赖性环鸟苷酸介导的舒张在所有组中相似（P > 0.90）。在管腔内压力从2 - 40 mmHg逐渐增加后评估肌源性反应性。随着管腔内压力增加，对照微静脉直径增加并达到平台期。停搏后，微静脉的压力 - 直径关系向上移位（P = 0.04，与对照组相比），提示肌源性张力受损。再灌注后，肌源性张力部分恢复。未进行冠状动脉灌注分流的体外循环对微静脉反应无显著影响。
在体外循环条件下使用冷高钾溶液进行缺血性停搏不会显著改变激动剂诱导的微静脉反应，而肌源性收缩略有降低。再灌注1小时后，激动剂诱导的冠状微静脉舒张显著受损，而肌源性收缩恢复。这些发现可能对体外循环条件下缺血性停搏后心肌灌注的控制和心脏舒张特性有影响。
