Effects of vasodilators on pulmonary hemodynamics and gas exchange in left ventricular failure

Pierpont, Gordon L.; Hale, Kathryn; Franciosa, Joseph A.; Cohn, Jay N.

doi:10.1016/0002-8703(80)90767-x

Cited by 57 publications

(18 citation statements)

References 12 publications

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“…The reduction in pulmo- Although vasodilator responses to nitroprusside and nitroglycerin were enhanced when pulmonary vasomotor tone was increased by an active process, responses to these agents were not enhanced when lobar vascular pressures were passively elevated by partially obstructing lobar venous outflow. These data suggest that reductions in pulmonary arterial pressure in response to nitroprusside in patients with congestive heart failure may, for the most part, be passive in nature and may be secondary to the improvement in left ventricular function which results in reductions in left ventricular end-diastolic and left atrial pressures (4,(9)(10)(11)(12). The passive nature of the pulmonary response to nitroprusside was observed in a recently published study in which this agent produced similar decreases in mean pulmonary arterial (11.7±1.5 mm Hg) and mean pulmonary arterial-wedge pressures (11.0±1.5 mm Hg) in patients with congestive heart failure (12).…”

Section: Discussionmentioning

confidence: 95%

“…Nitroglycerin is a vasodilator agent that is widely used in the treatment of anginal disease whereas nitroprusside is used in the management of hypertensive emergencies and for afterload reduction in patients with left heart failure and myocardial infarction (1)(2)(3)(4). Although the systemic vascular responses to nitroprusside and nitroglycerin have been intensively investigated (5)(6)(7)(8), the actions of these substances on the pulmonary circulation have received less attention and little, if anything, is known about the effects of these agents on the pulmonary veins (9)(10)(11)(12)(13). Nitroprusside and nitroglycerin have been reported to decrease pulmonary arterial pressure in patients with congestive heart failure (9)(10)(11)(12).…”

Section: Introductionmentioning

confidence: 99%

“…Although the systemic vascular responses to nitroprusside and nitroglycerin have been intensively investigated (5)(6)(7)(8), the actions of these substances on the pulmonary circulation have received less attention and little, if anything, is known about the effects of these agents on the pulmonary veins (9)(10)(11)(12)(13). Nitroprusside and nitroglycerin have been reported to decrease pulmonary arterial pressure in patients with congestive heart failure (9)(10)(11)(12). However, in those studies the vasodilator agents increased cardiac output and, when measured, decreased pulmonary arterial-wedge pressure so that the direct effects of these substances on the pulmonary vascular bed are uncertain (9)(10)(11)(12).…”

Section: Introductionmentioning

confidence: 99%

“…Nitroprusside and nitroglycerin have been reported to decrease pulmonary arterial pressure in patients with congestive heart failure (9)(10)(11)(12). However, in those studies the vasodilator agents increased cardiac output and, when measured, decreased pulmonary arterial-wedge pressure so that the direct effects of these substances on the pulmonary vascular bed are uncertain (9)(10)(11)(12). In a recently published study nitroprusside was reported to have no significant effect on pulmonary arterial pressure in the dog and the authors speculate that this vasodilator agent reduces pulmonary vascular distending pressure through its actions on the systemic circulation (13).…”

Section: Introductionmentioning

confidence: 99%

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Pulmonary Vasodilator Responses to Nitroprusside and Nitroglycerin in the Dog

Kadowitz¹,

Nandiwada²,

Gruetter³

et al. 1981

J. Clin. Invest.

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A B S T R A C T. The objective of this study was to determine the direct actions of nitroprusside and nitroglycerin on the pulmonary vascular bed in the intactchest dog. These widely used nitrogen oxide-containing vasodilator agents decreased pulmonary arterial pressure and increased cardiac output without altering left atrial pressure. Reductions in pulmonary arterial pressure and pulmonary vascular resistance were small under resting conditions, but were enhanced when pulmonary vascular tone was elevated by infusion of a stable prostaglandin analog that increases pulmonary vascular resistance by constricting intrapulmonary veins and upstream segments. In studies in which pulmonary blood flow to the left lower lobe was maintained constant, nitroprusside and nitroglycerin caused small but significant reductions in lobar arterial and small-vein pressures without significantly affecting left atrial pressure. With constant blood flow, lobar vascular pressures that were reduced in response to the vasodilators were more greatly reduced when lobar vascular resistance was increased by infusion of the prostaglandin analog or serotonin. However, when lobar vascular pressures were elevated by passive obstruction of lobar venous outflow, vasodilator responses to nitroprusside and nitroglycerin were not enhanced. These data suggest that nitroprusside and nitroglycerin decrease pulmonary vascular resistance by dilating intrapulmonary veins and upstream segments. These responses were minimal under control conditions but were enhanced when vascular tone was increased. This vasodilator action is independent of passive factors such as changes in pulmonary blood flow or left atrial pressure and is not secondary to an effect of these agents on the systemic circulation. Pulmonary vasodilator responses to nitroprusside and nitroglycerin were, however, found to be dependent on the existing level of vasomotor tone in the pulmonary vascular bed.

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Section: Discussionmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Pulmonary Vasodilator Responses to Nitroprusside and Nitroglycerin in the Dog

Kadowitz¹,

Nandiwada²,

Gruetter³

et al. 1981

J. Clin. Invest.

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“…Secondly, intravenous vasodilators act on all pulmonary vessels, in both ventilated and nonventilated areas. The net effect is to increase shunt fraction, which leads to a deterioration in oxygenation [58,59].…”

Section: Intravenous Vasodilatorsmentioning

confidence: 99%

Pathophysiology and pharmacological treatment of pulmonary hypertension in acute respiratory distress syndrome

Moloney

Evans²

2003

Eur Respir J

112

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Pulmonary hypertension (PH) is a characteristic feature of the acute respiratory distress syndrome (ARDS). The magnitude of PH has been shown to correlate with the severity of lung injury in patients with ARDS independently of the severity of associated hypoxaemia and has an adverse prognostic significance.Early in the histopathological evolution of ARDS, pulmonary vasoconstriction, thromboembolism and interstitial oedema contribute to the development of PH, although pulmonary vascular remodelling probably occurs eventually. Intravenous vasodilator agents lead to an increase in intrapulmonary shunting and systemic hypotension, which can limit their therapeutic use, and have not been shown to improve survival. By contrast, rapidly metabolised vasodilators administered by inhalation induce selective pulmonary vasodilatation and decrease shunting, but again do not appear to confer a survival benefit.Research aimed at further understanding the mechanisms that underlie pulmonary hypertension, a characteristic feature of the acute respiratory distress syndrome, are expected to provide improvements in pharmacological interventions for the treatment of pulmonary hypertension in the acute respiratory distress syndrome.

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