Gattullo D, Pagliaro P, Linden R J, Merletti A, Losano G
Dipartimento di Scienze Cliniche e Biologiche, Università di Torino, Ospedale San Luigi Gonzaga, Orbassano, Italy.
Pflugers Arch. 1995 May;430(1):96-104. doi: 10.1007/BF00373844.
In the coronary bed vasodilation can be mediated by several mechanisms including endothelium-produced nitric oxide. To examine the contribution of nitric oxide, three different techniques to cause vasodilation in the coronary vessels were used in the anaesthetized dog: intracoronary injection of 1 microgram acetylcholine, sudden reduction of the aortic blood pressure inducing a myogenic response and transient occlusion followed by release of the left circumflex coronary artery causing reactive hyperaemia. Each manoeuvre was performed before and after intracoronary administration of 100 mg N-nitro-L-arginine, an inhibitor of the synthesis of nitric oxide. In contrast to previous investigations, the inhibition of nitric oxide synthesis was prevented from causing an increase in blood pressure by the use of a blood-pressure-compensating device. The results observed during each of the three techniques, suggest that the initial cause of the vasodilatation is not the result of the increase of the production of nitric oxide. However, subsequent to the initiation of vasodilation, an increase in the shear stress can result in an increase in the release of nitric oxide from the vascular endothelium, thus prolonging the vasodilatation obtained using each technique.
在冠状动脉床，血管舒张可由多种机制介导，包括内皮产生的一氧化氮。为了研究一氧化氮的作用，在麻醉犬身上采用了三种不同的方法来引起冠状动脉血管舒张：冠状动脉内注射1微克乙酰胆碱、突然降低主动脉血压诱导肌源性反应以及短暂阻断左旋冠状动脉后再松开引起反应性充血。在冠状动脉内给予100毫克N-硝基-L-精氨酸（一种一氧化氮合成抑制剂）之前和之后，分别进行上述每种操作。与先前的研究不同，通过使用血压补偿装置，可防止一氧化氮合成的抑制导致血压升高。在这三种技术中的每一种技术过程中观察到的结果表明，血管舒张的初始原因并非一氧化氮产生增加的结果。然而，在血管舒张开始后，剪切应力的增加可导致血管内皮一氧化氮释放增加，从而延长使用每种技术所获得的血管舒张时间。
