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首页> 外文期刊>Japanese Journal of Pharmacology >CORONARY VASODILATATION AND ADRENERGIC RECEPTORS IN THE DOG HEART AND CORONARY
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CORONARY VASODILATATION AND ADRENERGIC RECEPTORS IN THE DOG HEART AND CORONARY

机译:狗心和冠状动脉中的冠状动脉血管舒张和肾上腺素受体

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References(23) Cited-By(12) The question of whether the coronary blood vessels contain an intrinsic adrenergic mechanism for vasodilatation of physiological significance has been examined in the canine heart-lung preparation with a donor by studying the response of the coronary vessels to epinephrine, norepinephrine, isoproterenol and salbutamol in combination with practolol. To differentiate the vasodilatation mediated through adrenoceptors in the coronary vessels from that resulting from an increase in the myocardial O2 consumption, a special method of analysis was developed based on the linear relation between the coronary flow and the myocardial O2 consumption. It was found that all four compounds produced an increase in the coronary flow attributable to an increased myocardial O2 consumption. Epinephrine and norepinephrine produced a decrease in the coronary flow after practolol which completely abolished the increase in the myocardial O2 consumption as well as the positive inotropic and chronotropic effects produced by these compounds, while isoproterenol and salbutamol produced an increase. These results indicate that adrenergic β-receptor exists in the coronary subserving a vasodilatation. However, the vasodilatation through this mechanism is of minor importance under physiological conditions and becomes completely masked in the presence of an overwhelmingly strong vasodilatation consequent to an increase in the myocardial O2 consumption.
机译:参考文献(23)By-By(12)通过研究冠心病患者对冠状动脉的反应,在供体的犬心肺制剂中检查了冠状血管是否包含具有生理意义的血管舒张的内在性肾上腺素能机制的问题。肾上腺素,去甲肾上腺素,异丙肾上腺素和沙丁胺醇联合倍他洛尔。为了区分由冠状动脉中肾上腺素受体介导的血管舒张与心肌氧消耗量增加所引起的血管舒张之间的差异,基于冠状动脉血流和心肌氧消耗之间的线性关系,开发了一种特殊的分析方法。已经发现,由于心肌氧消耗的增加,所有四种化合物均产生了冠状动脉血流增加。肾上腺素和去甲肾上腺素引起了倍他洛尔使用后冠状动脉血流的减少,这完全消除了心肌O2消耗量的增加以及这些化合物产生的正性变力和变时性作用,而异丙肾上腺素和沙丁胺醇却增加了。这些结果表明肾上腺素β受体存在于冠状动脉中,维持血管舒张。然而,在生理条件下,通过这种机制进行的血管舒张作用次要,在由于心肌氧消耗增加而导致的血管舒张压强的情况下,血管舒张作用被完全掩盖。

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