Kollár A, Kékesi V, Juhász-Nagy A
Department of Cardiovascular Surgery, Semmelweis University Medical School, Budapest, Hungary.
Jpn Heart J. 1989 Sep;30(5):709-21. doi: 10.1536/ihj.30.709.
The ineffectiveness of beta-adrenergic blockade in abolishing adenosine-induced coronary vasodilation was utilized to demonstrate that dopamine (DA) is capable of eliciting very strong coronary vasoconstrictor actions in vivo. In 2 separate groups of dogs anesthetized with pentobarbital, responses to DA were assessed either by flowmeter recordings or by computer-aided infrared thermography, which senses coronary blood flow-dependent heat emission from the epicardium. In untreated controls, submaximal DA infusions (16 micrograms.kg-1.min-1 iv) elicited a coronary vasodilator response. The thermographic equivalent of this hemodynamic action was an increased epicardial temperature. Pretreatment with oxprenolol (0.5 mg.kg-1 iv) preserved both basic heart activity and cardiac heat emission at levels which were comparable to the control state, but prevented DA mediated excitation of cardiac and coronary beta-adrenoceptors. In this state, DA infusion constricted the coronary arteries and tended to decrease heart emission. However, both types of effects were moderate, and only the hemodynamic effect was statistically significant. If DA was given after the coronary bed had been dilated submaximally by adenosine (30 micrograms.kg-1.min-1 infused into the left heart), the flow-reducing effect of DA became a dramatic phenomenon, and the DA-induced epicardial cooling was significantly potentiated. The results show that after eliminating conventional beta-effects, DA affects the coronary arteries through vasoconstrictor mechanisms. This finding suggests that the DA-induced constriction is limited in undilated coronary arteries by the metabolic autoregulatory capacity of the vessels.
利用β-肾上腺素能阻滞剂不能消除腺苷诱导的冠状动脉舒张这一现象，来证明多巴胺（DA）在体内能够引发非常强烈的冠状动脉收缩作用。在两组分别用戊巴比妥麻醉的犬中，通过流量计记录或计算机辅助红外热成像来评估对DA的反应，红外热成像可检测来自心外膜的与冠状动脉血流相关的热发射。在未处理的对照组中，次最大剂量的DA输注（16微克·千克⁻¹·分钟⁻¹静脉注射）引发冠状动脉舒张反应。这种血流动力学作用在热成像上的表现是心外膜温度升高。用氧烯洛尔（0.5毫克·千克⁻¹静脉注射）预处理可使基础心脏活动和心脏热发射维持在与对照状态相当的水平，但可防止DA介导的心脏和冠状动脉β-肾上腺素能受体兴奋。在这种状态下，DA输注使冠状动脉收缩，并倾向于减少心脏热发射。然而，这两种效应都很轻微，只有血流动力学效应具有统计学意义。如果在冠状动脉床被腺苷（30微克·千克⁻¹·分钟⁻¹注入左心）次最大程度扩张后给予DA，DA的血流减少效应就会变得很显著，并且DA诱导的心外膜冷却会明显增强。结果表明，在消除传统的β效应后，DA通过血管收缩机制影响冠状动脉。这一发现表明，在未扩张的冠状动脉中，DA诱导的收缩受到血管代谢自动调节能力的限制。
