Reflex pulmonary vasoconstriction due to stimulation of the aortic body by nicotine

Stern, Shlomo; Ferguson, Richard; Rapaport, Elliot

doi:10.1152/ajplegacy.1964.206.6.1189

Cited by 15 publications

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“…However, with the concomitant tachycardia, the over-all flow did not change significantly. The systemic vascular resistance increased significantly after stimulation of the aortic chemoreceptors, similar to the results obtained in our previous investigation (16) and with the recent results of Daly and Ungar (6). This rise in peripheral vascular resistance appears to be effectively opposed by the enhanced ventricular performance and, thus, flow is maintained without significant change.…”

Section: Discussionsupporting

confidence: 92%

“…If the strain gauge arch had been sutured to the right rather than the left ventricle, we would have obviated the difficulties in interpretation occurring as a result of simultaneous changes in arterial pressure. However, this would have been countered by the disadvantage that the right ventricle also faces an increased impedance within the pulmonary circulation as a result of reflex aortic chemoreceptor stimulation (16). Further evidence for immediate enhancement of ventricular performance is suggested by the fact that the over-all flow did not decrease during a period when nicotine evoked a significant rise in peripheral vascular resistance.…”

Section: Discussionmentioning

confidence: 99%

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Comparison of the Reflexes Elicited from Combined or Separate Stimulation of the Aortic and Carotid Chemoreceptors on Myocardial Contractility, Cardiac Output and Systemic Resistance

Stern

Rapaport

1967

Circulation Research

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Changes in left ventricular performance, stroke volume, and peripheral vascular resistance were studied in dogs after combined and separate stimulation of the aortic and carotid chemoreceptors. Selective stimulation of the aortic chemoreceptors produced an immediate increase in myocardial contractility as judged by the force developed by a strain gauge arch sewn into the left ventricular myocardium and by changes in the first derivative of the left ventricular pressure. Similar results were seen when heart rate changes were prevented by prior administration of atropine, when changes in outflow impedance were prevented by previous blockade of the alpha-adrenergic receptors, and when there was combined chemoreceptor stimulation. Betaadrenergic blockade prevented the increase in myocardial contractility observed after chemoreceptor stimulation. With selective carotid chemoreceptor stimulation there was no significant change in contractility. Aortic chemoreceptor stimulation increased the heart rate and peripheral vascular resistance, while stroke volume decreased; carotid chemoreceptor stimulation slowed the heart rate and increased the stroke volume, but not change peripheral vascular resistance.ADDITIONAL KEY WORDS ventricular performance chemoreflexes hemodynamics adrenergic receptor blockade sympathetic fibers anesthetized dogs • Recent reports on the effect of chemoreceptor stimulation on myocardial performance seemingly differ. Using anoxia as the stimulus to the carotid chemoreceptors, several investigators (1-3) described a negative inotropic effect. Using combined anoxic stimulation of the carotid and aortic chemoreceptors, other workers (4) described a positive inotropic effect. These opposing findings led us to reevaluate the effects of chemoreceptor stimulation on the performance of the left ventricle. Data indicate that the hemodynamic responses to stimulation of the aortic and carotid chemoreceptors differ (5, 6); therefore, we were careful to separate the effects arising from each of these receptors. We were also able to separate any changes in myocardial contractility induced by direct sympathetic stimulation from those induced by reflex peripheral vasoconstriction and resultant increase in outflow impedance (7, 8) by using drugs to produce separate and combined blockade of the alpha-and beta-adrenergic receptors. We also studied the immediate changes in stroke volume following chemoreceptor stimulation, since measurements of cardiac output in pre- 214

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Comparison of the Reflexes Elicited from Combined or Separate Stimulation of the Aortic and Carotid Chemoreceptors on Myocardial Contractility, Cardiac Output and Systemic Resistance

Stern

Rapaport

1967

Circulation Research

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“…Stimulation of the carotid bodies and of the aortic bodies caused increases in systemic vascular resistance of 28x9 + 4x5 0/ and 23-5 + 4-2 %, respectively, which, in contrast with the effects observed in the spontaneously breathing animal, are not significantly different from each other (P > 0.1). These responses obtained under conditions of controlled pulmonary ventilation and perfusion of the systemic circulation confirm those of previous workers (Bernthal, 1938;Daly & Daly, 1959;Daly & Scott, 1963;Stern, Ferguson & Rapaport, 1964;, indicating that systemic vasoconstriction represents the primary vascular response to stimulation of the carotid and aortic bodies.…”

Section: Dogs Breathing Spontaneouslysupporting

confidence: 89%

Comparison of the reflex responses elicited by stimulation of the separately perfused carotid and aortic body chemoreceptors in the dog

Daly¹,

Ungar²

1966

The Journal of Physiology

111

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1. In dogs under chloralose and urethane anaesthesia, the carotid and aortic bodies were isolated from the circulation and separately perfused with blood, the composition of which could be controlled at will. The remainder of the systemic circulation was perfused at constant blood flow, thereby enabling the reflex vascular responses to be determined. The systemic venous blood was oxygenated in the isolated perfused lungs of a second dog and the P(O2) and P(CO2) of the systemic arterial blood was maintained constant.2. Using hypoxic hypercapnic blood to stimulate the arterial chemoreceptors, carotid body excitation in spontaneously breathing animals caused an increase in respiratory minute volume approximately seven times larger than that evoked by stimulation of the aortic bodies. Whereas the hyperpnoea of carotid body origin is due to an increase in rate and depth of breathing, that from the aortic bodies is due predominantly to an increase in respiratory frequency.3. Stimulation of the carotid bodies in spontaneously breathing animals caused small variable changes in systemic vascular resistance, whereas stimulation of the aortic bodies invariably increased the vascular resistance.4. When pulmonary ventilation was maintained constant, the vascular response to stimulation of the carotid bodies was considerably modified in that constriction invariably occurred; that from the aortic bodies, however, was little affected. There was now no significant difference in the size of responses from the two groups of chemoreceptors. These constrictor responses represent the primary vascular effects.5. A similar modification of the carotid body vascular response occurred in the spontaneously breathing animal after denervation of the lungs, and is due to abolition of a lung-inflation vasodilator reflex.6. The size of the primary vasoconstrictor responses from the carotid and aortic bodies is reduced by lowering the arterial blood P(CO2).7. The results indicate that there is a fundamental difference in the functions of the carotid and aortic bodies. They exert a quantitatively similar primary control of the ;vasomotor centre' which is in striking contrast to the relatively more powerful influence on respiration by the carotid bodies. In the spontaneously breathing animal, however, the primary vasoconstrictor response from the carotid bodies is offset to a varying degree by the lung-inflation vasodilator reflex initiated by the concomitant hyperpnoea. This is not evident with the aortic bodies because of the relatively weaker respiratory response they evoke.

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“…It also has been shown that if serotonin is injected into the ascending aorta, stimulation of the aortic body and carotid body chemoreceptors plays a part in evoking the haemodynamic responses (Braun & Stern, 1961). In our study, the onset of the systemic response generally occurred within two or three beats after injection; possibly reflex stimulation of the chemoreceptors may be involved in this effect, similar to that produced after injections of nicotine and other chemostimulants (Stern, Ferguson & Rapaport, 1964). However, unlike the persistence of the systemic response to serotonin after a-adrenergic blockade, this procedure decreased markedly the systemic hypertensive response after nicotine injection into the base of the aorta (Stern & Rapaport, 1967).…”

Section: Discussionsupporting

confidence: 70%

The role of adrenergic receptor blockade in serotonin‐induced changes in the pulmonary circulation.

Rapaport¹,

Rolston²,

Stern³

1977

The Journal of Physiology

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SUMMARY1. In dogs, i.v. injection of serotonin caused a rise in pulmonary artery pressure and pulmonary arteriocapillary resistance that persisted even after ax-and fl-adrenergic receptor blockade; pulmonary venous resistance also increased, but this was abolished by pretreatment with either propranolol or phenoxybenzamine.2. The injection of serotonin into the ascending aorta produced an immediate rise in systemic, pulmonary arterial and pulmonary venous pressures and pulmonary venous resistance. After phenoxybenzamine, the rise in systemic and pulmonary arterial pressures remained unchanged, but previously observed increases in pulmonary venous pressure and resistance were blocked. In contrast, propranolol failed to abolish the rise in pulmonary venous resistance after serotonin injection into the ascending aorta.3. These results confirm the observation that the vasoconstrictor effect attributed to intravenously injected serotonin on the arterial side of the pulmonary circulation is independent of the known sympathetic pathways. The data suggest that the pulmonary venoconstriction induced by intravenous serotonin is of reflex origin, abolished by alpha and beta receptor blockade, whereas the efferent arm of the reflex pulmonary venoconstriction following injection of serotonin into the ascending aorta is mediated via alpha-adrenergic receptors.

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Reflex pulmonary vasoconstriction due to stimulation of the aortic body by nicotine

Cited by 15 publications

References 0 publications

Comparison of the Reflexes Elicited from Combined or Separate Stimulation of the Aortic and Carotid Chemoreceptors on Myocardial Contractility, Cardiac Output and Systemic Resistance

Comparison of the Reflexes Elicited from Combined or Separate Stimulation of the Aortic and Carotid Chemoreceptors on Myocardial Contractility, Cardiac Output and Systemic Resistance

Comparison of the reflex responses elicited by stimulation of the separately perfused carotid and aortic body chemoreceptors in the dog

The role of adrenergic receptor blockade in serotonin‐induced changes in the pulmonary circulation.

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