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Hemodynamic effects of nitroglycerin and long-acting nitrates

Abrams, Jonathan

The American heart journal, 1985-07, Vol.110 (1), p.217-224 [Periódico revisado por pares]

United States: Mosby, Inc

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  • Título:
    Hemodynamic effects of nitroglycerin and long-acting nitrates
  • Autor: Abrams, Jonathan
  • Assuntos: Angina Pectoris - physiopathology ; Arteries - drug effects ; Arterioles - drug effects ; Blood Circulation - drug effects ; Coronary Circulation - drug effects ; Coronary Disease - physiopathology ; Extremities - blood supply ; Heart Failure - physiopathology ; Hemodynamics - drug effects ; Humans ; Isosorbide Dinitrate - pharmacology ; Lung - blood supply ; Nitroglycerin - pharmacology ; Regional Blood Flow - drug effects ; Splanchnic Circulation - drug effects ; Sympathetic Nervous System - drug effects ; Time Factors ; Veins - drug effects
  • É parte de: The American heart journal, 1985-07, Vol.110 (1), p.217-224
  • Notas: ObjectType-Article-2
    SourceType-Scholarly Journals-1
    ObjectType-Feature-3
    content type line 23
    ObjectType-Review-1
  • Descrição: 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.
  • Editor: United States: Mosby, Inc
  • Idioma: Inglês
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