Impairment of cardiopulmonary baroreflex after cardiac transplantation in humans.

Mohanty, Pramod K.; Thames, Marc D.; Arrowood, James A.; Sowers, James R.; McNamara, Carolyn; Szentpetery, Szabolcs

doi:10.1161/01.cir.75.5.914

Cited by 133 publications

(45 citation statements)

References 34 publications

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“…19 The normal response of FVR at Ϫ40 mm Hg LBNP in patients with Chagas' disease indicates that when both arterial and cardiopulmonary receptors are unloaded, the reflex control of FVR is preserved. Previous studies with patients with cardiac transplantation 12 and heart failure 20,21 demonstrated a defect on reflex control of FBF and resistance during application of low and high levels of LBNP. In these studies, the reflex modulated by cardiopulmonary receptors was considered compromised, although the arterial baroreceptor reflex might also be simultaneously enrolled.…”

Section: Discussionmentioning

confidence: 91%

Decreased Cardiopulmonary Baroreflex Sensitivity in Chagas’ Heart Disease

et al. 2000

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Abstract-No study has been performed on reflexes originating from receptors in the heart that might be involved in the pathological lesions of Chagas' heart disease.Our study was undertaken to analyze the role of cardiopulmonary reflex on cardiovascular control in Chagas' disease. We studied 14 patients with Chagas' disease without heart failure and 12 healthy matched volunteers. Central venous pressure, arterial blood pressure, heart rate, forearm blood flow, and forearm vascular resistance were recorded during deactivation of cardiopulmonary receptors. By reducing central venous pressure by applying Ϫ10 and Ϫ15 mm Hg of negative pressure to the lower body, we observed (a) a similar decrease of central venous pressure in both groups; (b) a marked increase in forearm vascular resistance in the control group but a blunted increase in the Chagas' group; and (c) no significant changes in blood pressure and heart rate. To analyze cardiopulmonary and arterial receptors, we applied Ϫ40 mm Hg of lower-body negative pressure. As a consequence, (a) central venous pressure decreased similarly in both groups; (b) blood pressure was maintained in the control group, whereas in patients with Chagas' disease, a decrease in systolic and mean arterial pressure occurred; (c) heart rate increased in both groups; and (d) forearm vascular resistance increased significantly and similarly in both groups. Unloading of receptors with low levels of lower-body negative pressure did not increase forearm vascular resistance in patients with Chagas' disease, which suggests that the reflex mediated by cardiopulmonary receptors is impaired in patients with Chagas' disease without heart failure. Overall control of circulation appears to be compromised because patients did not maintain blood pressure under high levels of lower-body negative pressure. (Hypertension. 2000;36:1035-1039.)

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Section: Discussionmentioning

confidence: 91%

Decreased Cardiopulmonary Baroreflex Sensitivity in Chagas’ Heart Disease

et al. 2000

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“…[4][5][6] In contrast, prevention of carotid baroreceptor deactivation during LBNP was found to have no effect on this vasoconstrictor response, supporting the theory that, during orthostatic stress, unloading of cardiopulmonary, not sinoaortic, baroreceptors is the primary mechanism causing reflex vasoconstriction in the peripheral circulation.78 However, recent data from intraneural recordings of muscle sympathetic nerve activity (MSNA) call this theory into question. In normal humans, decreases in ventricular contractility with 8-adrenergic blockade had no effect on the reflex increases in MSNA evoked by decreases in central venous pressure,9 negating one of the principal pieces of evidence linking reflex vasoconstriction to ventricular mechanoreceptor deactivation.…”

mentioning

confidence: 99%

Relative contributions of cardiopulmonary and sinoaortic baroreflexes in causing sympathetic activation in the human skeletal muscle circulation during orthostatic stress.

Jacobsen

Morgan

Scherrer

et al. 1993

Circulation Research

102

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The aim of this study was to reexamine the hypothesis that cardiopulmonary baroreflexes are more important than sinoaortic baroreflexes in causing vasoconstriction in the skeletal muscle circulation during orthostatic stress. We recorded muscle sympathetic nerve activity (MSNA) with microelectrodes in the peroneal nerve (and forearm blood flow with venous occlusion plethysmography) in normal subjects (innervated ventricles) and in heart transplant recipients (denervated ventricles) during graded lower body negative pressure (LBNP) performed alone and in combination with intravenous infusion of phenylephrine, which was titrated to eliminate the orthostatically induced fall in blood pressure and thus the unloading of both carotid and aortic baroreceptors. The principal new findings are as follows: (1) The increases in both MSNA and forearm vascular resistance during multiple levels of LBNP were not attenuated by heart transplantation, which causes ventricular but not sinoaortic deafferentation. (2) In heart transplant recipients, a small increase in MSNA during mild LBNP was dependent on a decrease in arterial pressure, but in normal subjects, a similar increase in MSNA occurred in the absence of any detectable decrease in the aortic pressure stimulus to the sinoaortic baroreceptors. (3) In normal subjects, the large increase in MSNA during a high level of LBNP was dependent on a decrease in arterial pressure and could be dissociated from the decrease in central venous pressure. Taken together, the findings strongly suggest that sinoaortic baroreflexes are much more important and ventricular baroreflexes are much less important than previously thought in causing reflex sympathetic activation and vasoconstriction in the human skeletal muscle circulation during orthostatic stress. (Circulation Research 1993;73:367-378) KEY WORDS * sympathetic nervous system rentricular mechanoreceptors with C-fiber vagal afferents have been firmly established to reflexly inhibit sympathetic vasomotor outflow in experimental animals,1 but the role played by these afferents in the reflex control of the human cardiovascular system remains incompletely understood.Previous hemodynamic studies in humans have suggested that cardiac filling pressure and contractility, the primary determinants of ventricular mechanoreceptor C-fiber discharge in experimental animals,2,3 also are primary determinants of efferent sympathetic vasomoReceived August 6, 1991; accepted April 21, 1993. From the Department of Internal Medicine, Cardiology Division (T.N.J., B.J.M., U.S., S.F.V., R.A.L., R.G.V.), and the Department of Thoracic ventricular sensory receptors * baroreceptor reflexes tor activation during orthostatic stress.4-6 During simulated orthostatic stress with lower body negative pressure (LBNP), ,B-adrenergic blockade, which decreases ventricular contractility in normal humans, and heart transplantation, which produces ventricular deafferentation, each were found to greatly attenuate the increase in forearm vascular resistance induced by a gi...

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“…14 They also show that this is the case for the forearm vascular and plasma norepinephrine responses to leg raising. This offers additional evidence that cardiac (and also in this instance ventricular) receptors modulate systemic vascular resistance, thereby showing that cardiac receptors are involved not only in blood volume but also in blood pressure control.…”

Section: Reflex Control Of Vasomotor Tonementioning

confidence: 90%

Reflex vasopressin and renin modulation by cardiac receptors in humans.

Giannattasio

Cattaneo

et al. 1993

Hypertension

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Animal studies have shown that vasopressin secretion is modulated by arterial baroreceptors and cardiopulmonary volume receptors. Whether this is the case also in humans is controversial, however. To determine whether vasopressin is reflexly modulated by cardiac volume receptors, we studied the effect on plasma vasopressin (venous blood, radiolmmunoassay) of reducing venous return and left ventricular end-diastolic diameter (echocardiography) by producing a 20-minute lower body negative pressure in 14 healthy subjects (aged 49.3±3.8 years, mean±SEM). The data were compared with those of 14 age-matched heart-transplant recipients, i.e., subjects with cardiac denervation. In healthy subjects, lower body negative pressure at -15 mm Hg caused a modest reduction in left ventricular end-diastolic diameter (-5±3.4%) and no change in vasopressin, whereas lower body negative pressure at -37.5 mm Hg caused a more marked reduction in left ventricular end-diastolic diameter (-12±2.5%) and a small, variable, but overall statistically significant (p<0.05) increase in vasopressin (+145±46%, p<0.01). The left ventricular end-diastolic diameter changes induced by the two lower body negative pressure stimuli were similar in heart-transplant recipients, but the vasopressin increase seen with the lower body negative pressure at -37.5 mm Hg was abolished. The marked increase in plasma renin activity and forearm vascular resistance induced by lower body negative pressure in healthy subjects was also abolished or drastically attenuated in heart-transplant recipients. The abolition of the responses was not due to a generalized hyporeactivity because, in heart-transplant recipients, vasopressin, plasma renin activity, and forearm vascular resistance increased normally when stimulated by hyperosmolarity, angiotensin converting enzyme inhibition, and cold, respectively. Thus, in humans vasopressin is modulated reflexly by cardiac volume receptors, although to a limited degree and only for large changes in central blood volume. The reflex influence of cardiac receptors extends to plasma renin activity and vascular resistance, indicating a role of these receptors in both blood volume and blood pressure control. antidiuretic hormone (ADH) vasopressin is modulated not only by changes in plasma osmolality but also by changes in blood volume. '-6 They have also shown that changes in blood volume act by altering the inhibitory influences of arterial baroreceptors on ADH secretion through alterations in blood pressure.3 " 5 They act even more effectively, however, by altering a similar inhibitory influence originating from cardiopulmonary receptors through alterations of the intrathoracic blood content. 6 -8 Whether cardiopulmonary receptors and baroreceptors are involved in modulation of ADH secretion in

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Impairment of cardiopulmonary baroreflex after cardiac transplantation in humans.

Cited by 133 publications

References 34 publications

Decreased Cardiopulmonary Baroreflex Sensitivity in Chagas’ Heart Disease

Decreased Cardiopulmonary Baroreflex Sensitivity in Chagas’ Heart Disease

Relative contributions of cardiopulmonary and sinoaortic baroreflexes in causing sympathetic activation in the human skeletal muscle circulation during orthostatic stress.

Reflex vasopressin and renin modulation by cardiac receptors in humans.

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