Studies of Pulmonary Hypertension. Ix. The Effects of Intravenous Hexamethonium on Pulmonary Circulation in Patients With Mitral Stenosis1

Yu, Paul N.; Nye, Robert E.; Lovejoy, Frank W.; Schreiner, Bernard F.; Yim, Bernard J. B.

doi:10.1172/jci103598

Cited by 31 publications

(5 citation statements)

References 26 publications

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“…It is equal to the difference between total pulmonary and pulmonary vascular resistances. 16 Changes in hemodynamic data during methoxamine infusion were considered "individually significant" when they exceeded the range of variation of 2 successive determinations at rest as previously reported for this laboratory. 17 When the patient's ventilation became stable, determination of the cardiac output was carried out by the Fick procedure.…”

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confidence: 99%

Hemodynamic Effects of Methoxamine in Mitral Valve Disease

Stanfiled

1960

Circulation Research

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The hemodynamic changes following elevation of systemic arterial pressure and total systemic resistance by methoxamine were studied by right heart catheterization in 18 patients with mitral valve disease and 4 patients with no significant cardiovascular abnormality. This is the first detailed report of the circulatory effects of this drug in man. Changes in oxygen consumption, arterial oxygen saturation, stroke index and pulmonary artery to pulmonary "capillary" mean pressure gradient were insignificant. Forward cardiac index and heart rate decreased significantly while arteriovenous oxygen difference increased markedly in all groups of patients. The hemodynamic mechanisms involved in the changes observed during methoxamine infusion are discussed. Characteristic of patients with mitral insufficiency were significant increments of pulmonary arterial mean, pulmonary "capillary" mean, and pulmonary "capillary" V peak pressures. These subjects also had significantly greater increments in "left heart" resistance than patients without mitral insufficiency. An elevation of pulmonary "capillary" V peak pressure of 35 per cent or more of the elevation of systemic arterial systolic pressure was found to be a useful index of the presence of mitral insufficiency. Study of the pulmonary "capillary" pressure records during methoxamine infusion may obviate the necessity of left heart catheterization in the detection of significant mitral insufficiency.

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Hemodynamic Effects of Methoxamine in Mitral Valve Disease

Stanfiled

1960

Circulation Research

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“…First, injection of hexamethonium in the intact animal was followed by a highly significant fall in pressure in the femoral artery and a significant fall in the pulmonary veins while the pulmonary arterial pressure and the pulmonary arteriovenous gradient were unchanged. These results are mentioned since, while the hypotensive action of ganglioplegics on the pulmonary circulation in cases of pulmonary hypertension has been demonstrated (Gilmore et al, 1952;Freis et al, 1953;Halmagyi et at., 1953;Davies et at., 1954;Storstein and Tveten, 1954;Sancetta, 1955;Wade et al, 1956;Balchum et at., 1957;Yu et at., 1958), the effect of such substances on pulmonary pressure in man and animals in normal conditions is still not clear. Fowler et at.…”

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confidence: 99%

Mechanism of Pulmonary Vasoconstriction After Injection of 5-Hydroxytryptamine in the Dog

Vitolo¹,

Obbiassi²,

Zocche³

et al. 1962

Heart

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The hypertensive action of 5-hydroxytryptamine (5-HT) on the pulmonary circulation of the dog has been studied by a number of workers during the past few years. They all agree that pulmonary hypertension of this origin is due to arteriolar vasoconstriction (McCanon and Horvath, 1954;Borst et al., 1956;Vitolo et al., 1957;Bracco and Curti, 1958;Carlier et al., 1958; GomezFerrer, 1958;Kabins et al., 1959;Shepherd et al., 1959;Fowler, 1960). In fact, according to some authors, 5-HT is the most powerful pulmonary vasoconstrictor there is (Ginzel and Kottegoda, 1953;Borst et al., 1957; Attinger, 1957 Attinger, , 1959Gilbert et al., 1957Gilbert et al., , 1958 Rose and Lazaro, 1958).Very little is known about the mechanism whereby pulmonary vasoconstriction is produced. Rose (1957), using a system of partial extracorporeal circulation, injected 5-HT in such a way that it came into contact only with the pulmonary vascular bed; the hypertension thus elicited was attributed to a direct action on the pulmonary vessels. Rudolph and Paul (1957) similarly came to the conclusion that 5-HT acts directly on the pulmonary arteriolar tone. Finally, bilateral cervical vagotomy, alone (Rose and Lazaro, 1958) or combined with section of the spinal cord (Nahas, 1958; Nahas and McDonald, 1959), has been shown to be incapable of modifying the pulmonary pressor response to 5-HT in the dog. However, as far as we know, the classical methods of studying circulatory physiopathology (adrenalectomy, section of the spinal cord, interaction with metabolites, sympatholytics and adrenolytics, etc.) have not so far been applied sufficiently for conclusive results to be obtained. Furthermore these experiments have largely been aimed at discovering the action of 5-HT on the peripheral circulation in various animal species, but we know that the effects of this substance vary to a considerable degree according to the species of animal, the dosage, the means, and the route of administration. These considerations prevent us from accepting the results so far obtained from experiments on other species of animals or in other regions of the canine circulation as valid for the action of 5-HT on the pulmonary circulation of the dog.The lack of studies on the subject, the powerful action of 5-HT on the pulmonary circulation, and the fact that it is the only substance so far known which will act on the pulmonary circulation in a dose insufficient to influence the systemic circulation (Rose, 1957) all led us to continue our studies of the mechanism by which 5-HT produces pulmonary vasoconstriction in the dog.The object of the present study was to discover whether 5-HT produces pulmonary vasoconstriction by increasing the nervous tone through stimulation of the sympathetic nerves or by releasing vaso-active substances originating in the adrenal medulla. To study the first possibility, the changes in pulmonary haemodynamics following injection of 5-HT in the dog in basal conditions were compared with those following ganglionic block of sympathetic impulses wit...

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“…The intravenous infusion of angiotensin (Hypertensin) into 15 patients with normal systemic and pulmonary artery pressures caused an increase in PVR averaging 42 per cent. 59 Mean pulmonary artery pressure rose slightly more than wedge pressure, increasing the value of II p, while there was no change in cardiac output. Segel, Harris, and Bishop41 also noticed an increase in PVR, averaging 28 per cent, in 7 normal subjects infused with angiotensin IIY In this case cardiac output fell and there was little change in II p, as both pulmonary artery and wedge pressures were elevated by about 8 mm.…”

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confidence: 88%