Pulmonary vasodilator activity of prostacyclin (PGI2) in the cat.

Hyman, Albert L.; Kadowitz, Philip J.

doi:10.1161/01.res.45.3.404

Cited by 81 publications

(32 citation statements)

References 18 publications

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“…It has been reported that diverse agents such as hydralazine, isoproterenol, diazoxide, tolazoline, and phentolamine may be useful in the treatment of pulmonary hypertension (27)(28)(29)(30)(31). It has also been shown that prostacyclin and several prostacyclin-like substances have good vasodilator activity in the pulmonary vascular bed (15,(32)(33)(34) and it has recently been reported that prostacyclin produced a marked reduction in pulmonary arterial pressure in a patient with severe idiopathic pulmonary hypertension (35). The use of nitroglycerin in the treatnent of angina, and nitroprusside in the treatment of hypertensive emergencies and congestive heart failure, is well established (1-4).…”

Section: Discussionmentioning

confidence: 99%

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: 99%

Pulmonary Vasodilator Responses to Nitroprusside and Nitroglycerin in the Dog

Kadowitz¹,

Nandiwada²,

Gruetter³

et al. 1981

J. Clin. Invest.

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“…In contrast to the pressor effects of PGF2a, PGD2, and PGE2 or the PGH2 analog which may mimic the effects of TXA2 on the pulmonary vascular bed, the newly discovered bicyclic prostaglandin, PGI2, had vasodilator activity in the pulmonary vascular bed (23,24). The pulmonary vasodilator effects of PGI2 were modest under resting conditions but were greatly enhanced when pulmonary vascular resistance was increased actively by infusion of a vasoconstrictor substance (23). Although PGI2 had vasodilator activity, arachidonic acid when administered as a bolus, consistently increased pulmonary vascular resistance in the intact dog and cat and in the isolated dog lung (10,12,13,21,22).…”

Section: Discussionmentioning

confidence: 98%

“…The endoperoxide analog, PGF2a,f, and PGD2 all increased lung resistance and decreased dynamic compliance and in this regard were similar to but much more potent than arachidonic acid (17,21,26 (12). In contrast to the pressor effects of PGF2a, PGD2, and PGE2 or the PGH2 analog which may mimic the effects of TXA2 on the pulmonary vascular bed, the newly discovered bicyclic prostaglandin, PGI2, had vasodilator activity in the pulmonary vascular bed (23,24). The pulmonary vasodilator effects of PGI2 were modest under resting conditions but were greatly enhanced when pulmonary vascular resistance was increased actively by infusion of a vasoconstrictor substance (23).…”

Section: Discussionmentioning

confidence: 99%

“…We have, therefore, suggested that under resting conditions, the pulmonary vascular bed is maintained in a dilated state by production of a vasodilator product in the cyclooxygenase pathway (28). Recent evidence suggests that this vasodilator product in the cyclooxygenase pathway is a PGI2-like substance (6,23,24). It would therefore be of interest to ascertain if industrial pollutants such as NO2 or S02 have adverse effects on enzymes such as cyclooxygenase or prostacyclin synthetase which function to synthesize PGI2 which serves to maintain the pulmonary vascular bed in a dilated state under resting conditions.…”

Section: Discussionmentioning

confidence: 99%

“…It has, however, recently been reported that arachidonic acid has depressor activity in the pulmonary circulation when the prostaglandin precursor is infused (12). It has also been recently shown that the newly discovered bicyclic prostaglandin PG12 dilates that feline and canine pulmonary vascular beds (23,24). The purpose of the present report is to compare responses to primary prostaglandins (PGE2, PGF2a, and PGD2), arachidonic acid, and prostacyclin in the canine pulmonary vascular bed and the airways.…”

Section: Introductionmentioning

confidence: 89%

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Prostaglandins Evoke a Whole Variety of Responses in the Lung

Kadowitz¹,

Spannhake²,

Hyman³

1980

Environmental Health Perspectives

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Rapid intravenous (IV) injections of the prostaglandin precursor arachidonic acid (AA) increase pulmonary arterial pressure (PAP) and pulmonary vascular resistance (PVR) in a variety of species. It has recently been reported that infusions of AA decrease PAP. The purpose of this report is to contrast responses to bolus injections and infusions of AA in the anesthetized cat. In all experiments rapid IV injections of AA increased PAP and PVR; however, infusions of 68 to 680 ,ug/min produced variable responses. In 10 of 19 animals, AA infusion decreased PAP and PVR, and this response was enhanced when pulmonary vascular tone was actively increased by vasoconstrictor agents or alveolar hypoxia. In the other nine animals, the predominant response was an increase in PAP and PVR. In all experiments infusions of larger amounts of AA (1.4 to 3.4 mg/min) increased PAP. Both pressor and depressor responses to AA were inhibited by meclofenamate. This study shows that infusion of small amounts of AA dilates or constricts the pulmonary vascular bed. In contrast, infusion of larger amounts of AA always causes vasoconstriction.These data suggest that at low infusion rates, PGI2, which is a vasodilator, is the predominant metabolite formed from AA in some animals. However, at higher concentrations, the production of constrictor products predominates. These experiments also suggest that the products formed and the response observed may be dependent on a number of factors including the amount of tone present in the pulmonary vascular bed.

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Lung Circulation

Suresh

Shimoda

2016

Comprehensive Physiology

111

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The circulation of the lung is unique both in volume and function. For example, it is the only organ with two circulations: the pulmonary circulation, the main function of which is gas exchange, and the bronchial circulation, a systemic vascular supply that provides oxygenated blood to the walls of the conducting airways, pulmonary arteries and veins. The pulmonary circulation accommodates the entire cardiac output, maintaining high blood flow at low intravascular arterial pressure. As compared with the systemic circulation, pulmonary arteries have thinner walls with much less vascular smooth muscle and a relative lack of basal tone. Factors controlling pulmonary blood flow include vascular structure, gravity, mechanical effects of breathing, and the influence of neural and humoral factors. Pulmonary vascular tone is also altered by hypoxia, which causes pulmonary vasoconstriction. If the hypoxic stimulus persists for a prolonged period, contraction is accompanied by remodeling of the vasculature, resulting in pulmonary hypertension. In addition, genetic and environmental factors can also confer susceptibility to development of pulmonary hypertension. Under normal conditions, the endothelium forms a tight barrier, actively regulating interstitial fluid homeostasis. Infection and inflammation compromise normal barrier homeostasis, resulting in increased permeability and edema formation. This article focuses on reviewing the basics of the lung circulation (pulmonary and bronchial), normal development and transition at birth and vasoregulation. Mechanisms contributing to pathological conditions in the pulmonary circulation, in particular when barrier function is disrupted and during development of pulmonary hypertension, will also be discussed.

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Pulmonary vasodilator activity of prostacyclin (PGI2) in the cat.

Cited by 81 publications

References 18 publications

Pulmonary Vasodilator Responses to Nitroprusside and Nitroglycerin in the Dog

Pulmonary Vasodilator Responses to Nitroprusside and Nitroglycerin in the Dog

Prostaglandins Evoke a Whole Variety of Responses in the Lung

Lung Circulation

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