Agents Acting on the Lung Circulation

Dirken, M. N. J.; Heemstra, H

doi:10.1113/expphysiol.1948.sp000931

Cited by 27 publications

(8 citation statements)

References 4 publications

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“…Most of the experiments have been carried out on laboratory animals (43)(44)(45)(46)(47)(48)(49)(50)(51)(52)(53)(54)(55)(56). A review of these papers indicates that no consistent pattern of response was obtained.…”

Section: Results Reported By Othersmentioning

confidence: 99%

The Effect of Acetylcholine on the Human Pulmonary Circulation Under Normal and Hypoxic Conditions1

Fritts¹,

Harris²,

Clauss³

et al. 1958

J. Clin. Invest.

121

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It is generally accepted that the tone of the peripheral arterioles plays an important part in regulating the systemic blood pressure in man. Whether the small vessels of the lungs exercise similar control over the pressure in the pulmonary artery is not so certain. This uncertainty has stemmed largely from the fact that the human pulmonary vessels have exhibited an erratic response to many vasoactive drugs (1-15). As a consequence, most physiologists have concluded either that the pulmonary vessels are incapable of intrinsic changes in tone, or that the effect of such changes, if they occur, is less important in determining the pulmonary arterial pressure than is the effect of mechanical factors alone.There is, however, considerable evidence to suggest that acute hypoxia increases the pulmonary vascular tone (16)(17)(18)(19)(20). This stimulus raises the pulmonary arterial pressure by a greater amount than might be expected to result from the increase in blood flow which occurs. Moreover, the pulmonary wedge and systemic pressures are not altered (19), and there is no consistent variation in the central blood volume (19,21). From these observations it may be inferred that hypoxia constricts the vessels of the lungs.Active dilatation of these vessels has not been so adequately demonstrated. Most drugs which lower the pulmonary arterial pressure have a concomitant action on the systemic pressure, and it 1 This investigation was supported by a research grant [H-2001 (C) ] from the National Heart Institute of the is difficult to determine whether the changes in the pulmonary circulation represent a primary or a secondary effect. However, one of us (P.H.) observed that a single dose of acetylcholine can lower the pulmonary arterial pressure without affecting the pressure in the systemic vessels (22,23). The response was transient, and was found only in patients with a moderate degree of pulmonary hypertension.Since it seemed possible that this fall in pressure occurred as a result of active vasodilatation, the present project was undertaken with two objectives in view: 1) to investigate the effect of a continuous infusion of acetylcholine into the pulmonary artery of normal subjects, and 2) to inquire whether the action of the drug was enhanced when the pulmonary arterial pressure in these same subjects had been raised by making them hypoxic. METHODSEach subject was studied in the unanesthetized basal state. Respiratory studies were carried out on a previous day to acquaint the subject with the laboratory personnel and to accustom him into the effects of breathing a low oxygen mixture.Catheterization of the pulmonary artery was accomplished in the usual way (24,25). The position of the catheter was adjusted so that the tip lay just beyond the pulmonic valve. In those subjects in whom the wedged pressure was also measured, a special doublelumen catheter was used which allowed the tip to be wedged while the proximal lumen opened into the main pulmonary artery. With the catheter in place, a cannula was introduced into...

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Section: Results Reported By Othersmentioning

confidence: 99%

The Effect of Acetylcholine on the Human Pulmonary Circulation Under Normal and Hypoxic Conditions1

Fritts¹,

Harris²,

Clauss³

et al. 1958

J. Clin. Invest.

121

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“…He concluded that there was no evidence of autonomic control of the pulmonary circulation. Dirken and Heemstra (2), however, in 1948 found that resection of part of the sympathetic trunk increased pulmonary blood flow in rabbits. They found that vagotomy had no effect upon pulmonary flow.…”

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confidence: 99%

Observations on Autonomic Participation in Pulmonary Arteriolar Resistance in Man 1

Fowler¹,

Westcott²,

Hauenstein³

et al. 1950

J. Clin. Invest.

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It has been generally believed that the autonomic nervous system plays an insignificant role in the regulation of pressure within the pulmonary or lesser circulation. In 1939, Hamilton (1) studied the effect of various drugs upon the pulmonary arterial and venous pressures in unanesthetized dogs. He concluded that there was no evidence of autonomic control of the pulmonary circulation. Dirken and Heemstra (2), however, in 1948 found that resection of part of the sympathetic trunk increased pulmonary blood flow in rabbits. They found that vagotomy had no effect upon pulmonary flow.Without knowledge of the pulmonary venous or "capillary" pressure, one cannot ascertain whether changes in pulmonary arterial pressure are due primarily to a change in cardiac output or to a variation in pulmonary arteriolar resistance. Until recently, the study of autonomic regulation of pulmonary blood flow in man could not be undertaken because of the lack of a satisfactory method of measuring pulmonary venous pressure, except in an occasional case of atrial septal defect. In 1948, Hellems and co-workers (3) described a method for determining pulmonary "capillary" pressure and have since given adequate proof that this pressure varies with the pulmonary venous pressure (4). When the pulmonary artery pressure, pulmonary "capillary" pressure, and cardiac output are determined simultaneously, the pulmonary arteriolar resistance may be calculated (5).With the foregoing in mind, it was decided to determine the effect of the autonomic blocking agent, tetraethylammonium chloride (TEAC), upon the pulmonary arteriolar resistance in man; this report describes the results of such studies. MATERIALIt was thought that patients having pulmonary hypertension would be more likely to show a lowering of pulmonary pressure following autonomic blockade by tetraethylammonium because the effect of such blockade is much more pronounced in the systemic circulation when hypertension is present (6). A total of 15 patients were studied. Five were normal; two had pulmonary emphysema; two, congestive heart failure; one, active pneumonia; three, hypertensive vascular disease; one, bronchiectasis; one, diaphragmatic hernia with cor pulmonale. METHODThe majority of the patients were studied in the fasting condition. Cardiac catheterization was performed by the method of Cournand and Ranges (7). A double lumen catheter was used in order that pulmonary "capillary" pressure and pulmonary arterial pressure could be measured simultaneously. Pulmonary "capillary" pressure was obtained by the method of Hellems and his associates (3). The catheter was advanced into a branch of the pulmonary artery as far as possible, so that the branch was occluded and the pressure distal to the point of occlusion was obtained. Resting cardiac outputs were obtained usually after the catheter had been in place 15 to 30 minutes or more.

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“…These data seem sufficient to support the view that anatomical factors alone cannot account for all the increase in pulmonary arterial pressure. The mechanism of this reversible elevation of pulmonary vascular resistance, therefore, needs further study.Anoxia, by producing widespread vasoconstriction in all parts of the circulation, elevates also pulmonary vascular resistance (Motley et al, 1947; LiUjestrand, 1948 ;Dirken and Heemstra, 1948; Doyle et al, 1951, etc.). Pulmonary hypertension following the administration of histamine was also observed in dogs by Dixon and Hoyle (1930).…”

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confidence: 99%

“…Anoxia, by producing widespread vasoconstriction in all parts of the circulation, elevates also pulmonary vascular resistance (Motley et al, 1947; LiUjestrand, 1948 ;Dirken and Heemstra, 1948; Doyle et al, 1951, etc.). Pulmonary hypertension following the administration of histamine was also observed in dogs by Dixon and Hoyle (1930).…”

mentioning

confidence: 99%

The Role of the Nervous System in the Maintenance of Pulmonary Arterial Hypertension in Heart Failure

Halmagyi¹,

Felkai²,

Ivanyi³

et al. 1953

Heart

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Elevation of pressure in the pulmonary veins, with a consequent elevation of pressure in the pulmonary capillaries and pulmonary artery has for many years been invoked to explain pulmonary hypertension in both mitral stenosis and left ventricular failure. Ignoring the possibility of pulmonary vasoconstriction, this hypothesis was in complete accordance with the " mechanistic " concept of the regulation of pulmonary pressure, emphasized recently by Cournand (1947Cournand ( , 1950 and Hamilton (1951). It was based mainly on the relative refractoriness of the pulmonary circulation towards substances affecting the systemic circulation.It was soon established, however, that elevation of the pulmonary venous pressure is only partly responsible for the high pressure in the pulmonary artery that is observed in heart failure. Elevation of pulmonary " capillary " pressure beyond the colloid osmotic pressure of plasma causes an increase in the pulmonary pressure gradient (Dexter et al., 1950), as a result of an increase of the pulmonary arteriolar resistance. Lewis et al. (1952), emphasize that in mitral stenosis this increased arteriolar resistance is a physiological counterpart to the anatomical changes observed in the small pulmonary arteries by Parker and Weiss (1936) and Larrabee et al. (1949). In face of this " static " theory of increased pulmonary arteriolar resistance it seems hard to understand why the presence or absence of heart failure raises or lowers the pressure in the pulmonary artery, presumably without a change in the size of the stenosed orifice (Bloomfield et al., 1949;Bayliss et al., 1951), or in the lumen of the " statically" narrowed pulmonary arterioles. Not even an increase of the circulating blood volume explains this apparent contradiction. Nor does the decrease of pulmonary arteriolar resistance following mitral commissurotomy (Draper et al., 1951; favour this theory. On the other hand, no corresponding narrowing of the pulmonary vessels can be demonstrated in hypertensive heart failure despite a similar elevation of pulmonary arteriolar resistance (Borden et al., 1950). These data seem sufficient to support the view that anatomical factors alone cannot account for all the increase in pulmonary arterial pressure. The mechanism of this reversible elevation of pulmonary vascular resistance, therefore, needs further study.Anoxia, by producing widespread vasoconstriction in all parts of the circulation, elevates also pulmonary vascular resistance (Motley et al., 1947; LiUjestrand, 1948 ;Dirken and Heemstra, 1948; Doyle et al., 1951, etc.). Pulmonary hypertension following the administration of histamine was also observed in dogs by Dixon and Hoyle (1930). The vasomotor response to both these stimuli is a consequence of their direct chemical action on the pulmonary vessels. The significance of the nervous system as a source of vasomotor stimuli affecting the pulmonary circuit is generally underestimated. Kuntz (1946)

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Agents Acting on the Lung Circulation

Cited by 27 publications

References 4 publications

The Effect of Acetylcholine on the Human Pulmonary Circulation Under Normal and Hypoxic Conditions1

The Effect of Acetylcholine on the Human Pulmonary Circulation Under Normal and Hypoxic Conditions1

Observations on Autonomic Participation in Pulmonary Arteriolar Resistance in Man 1

The Role of the Nervous System in the Maintenance of Pulmonary Arterial Hypertension in Heart Failure

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