HEMODYNAMIC-EFFECTS OF NITROGLYCERIN AND LONG-ACTING NITRATES
HEMODYNAMIC-EFFECTS OF NITROGLYCERIN AND LONG-ACTING NITRATES
复制标题
DOI：
10.1016/0002-8703(85)90490-9
复制
发表时间：
1985-01-01
影响因子：
4.8
通讯作者：
ABRAMS, J
中科院分区：
文献类型：
--
作者：
ABRAMS, J
硝酸甘油 (NTG) 和硝酸异山梨酯 (ISDN) 是血管平滑肌的有效扩张剂。有机硝酸盐在非常低的剂量下产生静脉舒张作用，随着剂量的增加，静脉循环几乎没有额外的血管舒张作用。硝酸盐在低至中等剂量时会增加动脉直径并改善动脉电导，而在高剂量时这些药物会使身体的小动脉或阻力血管扩张。对硝酸盐施用的总体血流动力学反应将通过交感神经反射放电的程度、充血性心力衰竭的存在或不存在、所施用的硝酸盐的剂量以及硝酸盐耐受性的存在或不存在来调节。有机硝酸盐的局部循环作用包括降低血管阻力和增加流向手臂和腿部的动脉血流量。静脉扩张也发生在四肢。在内脏和肠系膜循环中，硝酸盐诱导最初的血管舒张反应，随后反射性血管收缩。正常状态下肝脏血流量变化不大。服用硝酸盐后，肺血流量减少，肺动脉和静脉压力下降。 NTG给药后肾血流量基本保持不变或略有减少，但反射性交感神经活动可能引起继发性血管收缩。长期以来，人们一直认为硝酸盐的抗心绞痛作用与其全身或外周作用有关，通过降低左心室前负荷和后负荷来减少心肌需氧量。然而，大量证据表明硝酸盐对正常心脏和缺血心脏的冠状动脉循环都有重要的直接影响。这些作用包括扩张冠状动脉、增加侧支血流量以及增强缺血区域的氧合和营养灌注。最近的研究表明，有机硝酸盐可以扩张一些冠状动脉粥样硬化狭窄。人们早就知道这些药物可以逆转或预防冠状血管痉挛。因此，心肌缺血和心绞痛的作用是复杂的。硝酸盐治疗充血性心力衰竭的功效主要来自于左心室前负荷的降低（表现为肺毛细血管楔压的降低）以及肺动脉、右心室和右心房压力的降低。此外，NTG 和 ISDN 在充血性心力衰竭中的动脉-小动脉扩张作用可能会导致左心室后负荷或射血阻抗降低，随后每搏输出量和心输出量增加。
Nitroglycerin (NTG) and isosorbide dinitrate (ISDN) are potent dilators of vascular smooth muscle. The organic nitrates produce venodilation at very low doses, with little additional vasodilation of the venous circulation with increasing dosage. Nitrates increase arterial diameter and improve arterial conductance at low to moderate doses, and at high doses these agents produce dilation of the arteriolar or resistance vessels of the body. The overall hemodynamic response to nitrate administration will be modulated by the degree of sympathetic reflex discharge, the presence or absence of congestive heart failure, the dosage of administered nitrate, and the presence or absence of nitrate tolerance. Regional circulatory effects of the organic nitrates include a decrease in vascular resistance and an increase in arterial blood flow to the arms and legs. Venodilation also occurs in the extremities. In the splanchnic and mesenteric circulations, nitrates induce an initial vasodilative response followed by reflex vasoconstriction. Hepatic blood flow changes little in the normal state. Pulmonary blood flow decreases and pulmonary artery and venous pressures fall after nitrate administration. Renal blood flow remains essentially unchanged or decreases slightly after NTG administration, although reflex sympathetic activity may cause secondary vasoconstriction. The antianginal effects of nitrates have long been thought to be related to their systemic or peripheral actions, which reduce myocardial oxygen requirements through decreases in left ventricular preload and afterload. There is, however, considerable evidence that nitrates have important direct effects on the coronary circulation in both the normal and the ischemic heart. Such actions include coronary artery dilation, increased collateral blood flow, and enhanced oxygenation and nutrient perfusion to zones of ischemia. Recent work indicates that organic nitrates dilate some coronary atherosclerotic stenoses. These drugs have long been known to reverse or prevent coronary vasospasm. Thus the actions in myocardial ischemia and angina are complex. The efficacy of nitrates in congestive heart failure primarily arises from a decrease in left ventricular preload, manifested by a fall in pulmonary capillary wedge pressure, and from decreases in pulmonary artery, right ventricular, and right atrial pressures. In addition, the arterial-arteriolar dilating effects of NTG and ISDN in congestive heart failure may result in a decrease in left ventricular afterload or impedance to ejection, with a subsequent increase in stroke volume and cardiac output.