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Biomedical subjects

F M Abboud

Publications and source records attributed to F M Abboud.

At least 91 records · Page 5Linked to original sources
PubMed1987

Vasopressin facilitates inhibition of renal nerve activity mediated through vagal afferents.

We measured the effect of vasopressin (8 mU X kg-1 X min-1) on reflex inhibition of renal sympathetic nerve activity induced by volume expansion in 13 sinoaortic-denervated anesthetized rabbits. Volume expansion increased left ventricular end-diastolic pressure (LVEDP) from 5.1 +/- 0.7 to 14.1 +/- 1.4 mmHg and decreased renal nerve activity (RNA) from 57.4 +/- 6.9 to 30.2 +/- 5.6 impulses/s. Infusion of vasopressin elevated LVEDP from 6.0 +/- 1.0 to 7.3 +/- 1.1 mmHg and decreased RNA from 61.8 +/- 7.2 to 47.1 +/- 6.3 impulses/s. Heart rate fell from 243 +/- 7 to 231 +/- 9 beats/min; no other significant hemodynamic changes were seen. During the infusion of vasopressin, volume expansion increased LVEDP to 13.7 +/- 1.2 mmHg and decreased RNA to 17.0 +/- 4.2 impulses/s. The slopes relating the percent decrease in RNA to the rise in LVEDP were calculated from values of RNA recorded at several levels of LVEDP. The slope averaged -6.2 +/- 1.1%/mmHg before vasopressin and nearly doubled (-11.9 +/- 1.8%/mmHg) during vasopressin. Infusion of placebo (saline) instead of vasopressin did not alter the reflex inhibition of nerve activity. Bilateral vagotomy abolished the decrease in resting nerve activity that occurred during infusion of vasopressin as well as the reflex inhibition of RNA. These data demonstrate that vasopressin facilitates the reflex inhibition of renal sympathetic nerve activity associated with increases in LVEDP and mediated through vagal afferents.

Animals↗
PubMed1987

Inhibition of muscle sympathetic nerve activity in humans by arginine vasopressin.

Arginine vasopressin, a potent vasoconstrictor, does not raise arterial pressure in normal humans even at pathophysiological plasma levels. To examine whether the pressor effect of vasopressin in humans is buffered by baroreceptor reflex inhibition of sympathetic nerve activity, we recorded postganglionic muscle sympathetic nerve activity directly from the peroneal nerve in 12 normal men before, during, and after a 20-minute intravenous infusion of vasopressin, 4 ng/kg/min, that increased mean plasma concentrations from 6.2 +/- 0.6 to 320 +/- 68 (SE) pg/ml. During the first 5 minutes (n = 8), mean arterial pressure increased from 91 +/- 3 to 97 +/- 4 mm Hg (p less than 0.05) and integrated sympathetic nerve activity decreased from 271 +/- 45 to 156 +/- 33 units (p less than 0.05). At 15 minutes (n = 12), arterial pressure did not differ from control values whereas forearm vascular resistance fell (p less than 0.05) and central venous pressure and heart rate increased (p less than 0.05). Sympathetic nerve activity remained below control levels throughout the infusion (202 +/- 31 vs 254 +/- 40 units before infusion; p less than 0.05). An effect of vasopressin on ganglionic transmission was excluded, since the sympathoexcitatory response to apnea was not attenuated during vasopressin. Thus, pathophysiologic levels of vasopressin in humans cause inhibition of muscle sympathetic nerve activity that is not due to a ganglionic blocking action. The sympathoinhibition may be caused in part by the modest increases in mean arterial and central venous pressures and attendant stimulation of arterial and cardiac baroreceptors. The reflex decrease in sympathetic nerve activity would be expected to buffer the direct vasoconstrictor effects of vasopressin.

Adult↗
PubMed1987

Prevention or attenuation of baroreceptor resetting by pulsatility during elevated pressure.

Acute static elevation of arterial pressure increases the pressure threshold for activation of baroreceptors (acute resetting). The purpose of this study was to test the hypothesis that pulsatility during acute elevation of pressure modifies this acute resetting. Activity was recorded in 21 single baroreceptor units from the isolated carotid sinuses of dogs anesthetized with chloralose. Single-unit pressure thresholds were determined with a slow ramp increase in pressure. After a control period of static pressure at 25 to 50 mm Hg, the pressure threshold averaged 69 +/- 4 (SE) mm Hg. Three graded levels of static pressure were held for 5 to 15 minutes. The levels averaged 76 +/- 4, 115 +/- 6, and 170 +/- 5 mm Hg. The corresponding nerve activity during these periods was 0, 44 +/- 6, and 63 +/- 6 spikes per second, and the resulting increases in pressure threshold averaged 10 +/- 1, 17 +/- 2, and 26 +/- 3 mm Hg, respectively. In contrast, during equivalent elevations of pulsatile pressure, nerve activity averaged 20 +/- 3, 37 +/- 4, and 61 +/- 5 spikes per second, and the increases in pressure threshold averaged 0 +/- 4, 14 +/- 2, and 24 +/- 2 mm Hg, respectively. In some units, the pressure threshold decreased following elevation of pulsatile pressure. The results indicate that: pulsatility during elevation in pressure prevents or attenuates the acute baroreceptor resetting except at maximal pressure; upward resetting occurs with elevation of static pressure even when there is no nerve activity during the period of elevated pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Contrasting effects of static and pulsatile pressure on carotid baroreceptor activity in dogs.

The purpose of this study was to contrast the effects of static and pulsatile pressure on carotid baroreceptor activity over a wide range of mean arterial pressure. Static and pulsatile pressure were applied to the isolated carotid sinus of dogs anesthetized with chloralose. Recordings were obtained from single baroreceptor units as well as from the whole sinus nerve or a large strand of the nerve. Three observations are reported. First, in single units the pulsatile pressure threshold, which averaged 48 +/- 8 (SEM) mm Hg, was far below the static pressure threshold, which averaged 79 +/- 8 mm Hg (p less than 0.05, n = 15). Thus, pulsatility decreased the threshold by an average of 31 mm Hg in contrast to the minimal or lack of decrease in threshold reported by others in aortic baroreceptors. Second, at moderate arterial pressures a shift from static to pulsatile pressure caused a decrease in single and multiple unit activities. In single units, the decrease approximated 15% (from 42.0 +/- 2.1 to 35.5 +/- 1.9 spikes/sec, p less than 0.05, n = 25). In all units, there was no diastolic nerve activity ("silence") when diastolic pressure was 1 to 10 mm Hg above static pressure threshold; 80% of the units exhibited "diastolic silence" when diastolic pressure was 20-30 mm Hg above threshold and 40% of the units showed silence at diastolic pressures 40-50 mm Hg above threshold. In whole nerve recordings, pulsatility increased activity from 57 +/- 15 to 142 +/- 29 spikes/sec (p less than 0.05) at low mean arterial pressures (50 and 75 mm Hg), as expected from the reduction in pressure threshold noted in single units, and decreased activity by approximately 15% (from 373 +/- 69 to 320 +/- 55 spikes/sec, p less than 0.05, n = 9) at mean arterial pressures of 125 and 150 mm Hg. This decrease in activity with a shift from static to pulsatile pressure at moderate arterial pressures has not been reported previously. Third, the static pressure-activity curve was sigmoid, and its gain peaked sharply at 75-100 mm Hg; in contrast, the pulsatile pressure-activity curve was linear between 25 and 150 mm Hg, and its maximum gain was half the maximum gain during static pressure. These differences between the static pressure-activity curve and the pulsatile pressure-activity curve were noted during both increases and decreases in carotid sinus pressure; both curves exhibited some hysteresis during the decreases in pressure.

Action Potentials↗
PubMed1986

Sensitization of aortic and cardiac baroreceptors by arginine vasopressin in mammals.

Vasopressin facilitates the baroreflex control of the circulation. The peptide may act at several sites to augment the baroreflex. In this study we examined the effect of vasopressin on aortic baroreceptors in anaesthetized rabbits and on left ventricular mechanoreceptors in anaesthetized cats. Vasopressin (16 mu./kg. min) did not change resting nerve discharge in single fibres from aortic baroreceptors. Vasopressin (16 mu./kg. min) significantly enhanced the response of single aortic nerve fibre discharge to elevation in arterial pressure. The slope relating nerve activity to mean arterial pressure increased from 0.24 +/- 0.05 (mean +/- S.E. of mean) to 0.50 +/- 0.16 impulses/cardiac cycle. mmHg (P less than 0.05) in ten aortic medullated fibres and from 0.06 +/- 0.03 to 0.18 +/- 0.04 impulses/cardiac cycle. mmHg (P less than 0.05) in three non-medullated fibres. Vasopressin (16 mu./kg. min) did not change resting nerve discharge in single fibres from left ventricular mechanoreceptors. Vasopressin (16 mu./kg. min) significantly enhanced the response of single nerve fibre discharge from left ventricular mechanoreceptors in response to elevation of left ventricular end-diastolic pressure. The slope relating nerve activity to left ventricular end-diastolic pressure increased from 0.24 +/- 0.07 to 0.32 +/- 0.07 impulses/cardiac cycle. mmHg (P less than 0.05) in six medullated fibres and from 0.10 +/- 0.01 to 0.15 +/- 0.02 impulses/cardiac cycle. mmHg (P less than 0.05) in four non-medullated fibres. These data show that vasopressin sensitizes high and low pressure baroreceptors and suggest a mechanism by which vasopressin may facilitate the baroreflex control of the circulation.

Action Potentials↗
PubMed1986

Sites at which vasopressin facilitates baroreflex inhibition of lumbar sympathetic nerve activity.

We recently reported that intravenous vasopressin in anesthetized rabbits facilitates baroreflex inhibition of lumbar sympathetic nerve activity. The purpose of this study was to determine the possible sites of this facilitation. We found that intravenous infusion of vasopressin (16-32 mU X kg-1 X min-1) caused greater inhibition of lumbar sympathetic nerve activity than did phenylephrine for a given increase in aortic baroreceptor activity, suggesting a "central" action of vasopressin. A central action was supported also by the observation that the carotid baroreflex inhibition of lumbar sympathetic nerve activity was augmented by intravenous infusion of vasopressin when the carotid sinuses were isolated, filled with saline, and distended (aortic depressor and vagal nerves were cut). On the other hand, vasopressin also facilitated baroreflex inhibition of lumbar sympathetic nerve activity through an influence on arterial baroreceptors, because intravenous vasopressin caused greater afferent activity of the aortic depressor nerve per unit rise in arterial pressure than did phenylephrine. In a separate group of rabbits, intravenous infusion of vasopressin also elevated the level of afferent aortic depressor activity during increases in arterial pressure induced by intra-aortic balloon inflation. Furthermore, when vasopressin was confined to the isolated carotid sinuses, the reflex inhibition of lumbar sympathetic nerve activity during distension of carotid sinuses was augmented. We conclude that circulating vasopressin facilitates baroreflex inhibition of sympathetic nerve activity through a central nervous system action as well as through an effect on arterial baroreceptors.

Administration, Topical↗
PubMed1986

Effects of vasopressin on the circulation and its baroreflex control in healthy men.

Information on the hemodynamic effects of vasopressin (AVP) in healthy humans is very limited despite its known importance in body fluid homeostasis and release in pathologic states such as hemorrhage and trauma. Although it is a potent vasoconstrictor in vitro, it does not cause the expected rise in arterial pressure when given systemically to animals with intact baroreflexes. It has been proposed that this is because AVP facilitates baroreflex control of the circulation. In this study, we assessed the effect of infusion of AVP on resting circulatory variables and on the baroreflex control of forearm vascular resistance and heart rate in healthy men. AVP in a dose of 0.4 ng/kg/min, which raised plasma level of AVP to 24 +/- 4 pg/ml, a value known to have a significant antidiuretic effect, had little hemodynamic effect, producing only mild bradycardia and a slight increase in central venous pressure. Reflex changes in heart rate during neck suction (-15 and -30 mm Hg) and neck pressure (+15 and +30 mm Hg) were not altered. Reflex responses to lower body negative pressure and to its release were also unchanged by this dose of AVP. In contrast, a higher dose of AVP (4 ng/kg/min), which raised plasma levels to 290 +/- 41 pg/ml, a concentration known to occur as a result of hemorrhagic hypotension and circulatory stresses, did cause hemodynamic changes. There was tachycardia (from 63 +/- 2 to 68 +/- 2 beats/min), a decrease in pulse pressure (from 62 +/- 2 to 53 +/- 2 mm Hg), an increase in central venous pressure (from 2.6 +/- 0.5 to 4.1 +/- 0.4 mm Hg), and surprisingly in view of the known vasoconstrictor effect of AVP, an increase in forearm flow (from 4.4 +/- 0.7 to 5.9 +/- 1.2 ml/min/100 ml tissue) and a decrease in forearm vascular resistance (from 24 +/- 4 to 18 +/- 3 U); there was no significant change in mean arterial pressure (from 83 +/- 2 to 83 +/- 3 mm Hg). Reflex changes in heart rate were unaltered. The maximal vasoconstrictor response in the forearm attained during lower body negative pressure was not influenced by AVP, but the reflex vasodilator response to the sudden release of lower body negative pressure was significantly augmented, vascular resistance falling to 23 +/- 4 U before and 13 +/- 2 U during AVP. The unanticipated findings in this study include the biphasic changes in heart rate with increasing doses of AVP, the absence of a pressor response, and the vasodilatation in forearm vessels.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1985

Effects of chronic hypertension on vasa vasorum in the thoracic aorta.

The outer layers of the thoracic aorta receive substantial blood flow through vasa vasorum within the aortic wall. Flow delivered via these channels is functionally important because medial necrosis occurs when vasa vasorum are ligated. If flow through vasa vasorum is limited in chronic hypertension, this could contribute to medial necrosis and, perhaps, aortic dissection. In these experiments, flow and conductance in vasa vasorum were assessed in twelve awake dogs with renal hypertension (arterial pressure = 127 +/- 4 mmHg [mean +/- SE]) and nine normotensive controls (arterial pressure = 100 +/- 3 mmHg [P less than 0.001]). At rest, blood flow delivered via vasa vasorum to the thoracic aorta was similar in hypertensive and normotensive dogs (5.2 +/- 0.9 and 4.8 +/- 0.4 ml . min-1 X 100 g-1 respectively). Thus, in hypertensive dogs, conductance of the vasa vasorum decreased to maintain flow constant. During maximal dilatation induced by iv adenosine (4.7 mumol . kg-1 per min) flow delivered via vasa vasorum increased by 100% in both hypertensive and normotensive dogs. Calculations of maximum conductance indicate that vasodilator capacity was decreased by 67% in vasa vasorum of hypertensive dogs. These data suggest that vasodilator capacity of vasa vasorum in the thoracic aorta is limited in chronic hypertension. This abnormality could contribute to the pathogenesis of medial necrosis and aortic dissection in hypertensive patients.

Adenosine↗
PubMed1985

Contrasting effects of vasopressin on baroreflex inhibition of lumbar sympathetic nerve activity.

Baroreflex inhibition of lumbar sympathetic nerve activity (LSNA) during intravenous infusions of phenylephrine and vasopressin is contrasted in rats and rabbits. In rabbits, vasopressin caused smaller increases in arterial pressure and greater inhibition of LSNA than phenylephrine. In Sprague-Dawley rats, however, both vasopressin and phenylephrine caused equivalent increases in arterial pressure and reflex reductions in LSNA. The inhibition of LSNA was mediated through the arterial baroreceptors in both species because it was abolished by sinoaortic denervation. In rats, the possibility that a high level of endogenous vasopressin may have prevented the demonstration of a facilitated baroreflex with the infusion of exogenous vasopressin is unlikely since vasopressin also did not facilitate the reflex in Brattleboro rats, which lack circulating vasopressin. Further, Sprague-Dawley rats were responsive to exogenous vasopressin since infusion of increasing doses of vasopressin caused significant increases in urinary osmolality as well as progressive increments in arterial pressure. The results indicate that intravenous vasopressin given for a period of 6 min facilitates the reflex inhibition of LSNA mediated through arterial baroreceptors in rabbits, but not in rats. Vasopressin given for a period of up to 45 min to rats also fails to facilitate baroreflexes, emphasizing the difference from rabbits. In rabbits, this facilitation appears to involve a central mechanism.

Animals↗
PubMed1985

Relative contribution of aortic and carotid baroreflexes to heart rate control in man during steady state and dynamic increases in arterial pressure.

We studied the contribution of carotid vs. extracarotid baroreceptors in control of heart rate in normal humans. We measured heart interval (HI) and arterial pressure during steady-state infusion of phenylephrine (PE). PE increased mean arterial pressure (MAP) by 13 +/- 2 mmHg (mean +/- SEM; n = 10) and thus stimulated both carotid and aortic baroreceptors. Neck pressure (NP) was applied during PE infusion to counter the increase in transmural carotid sinus pressure, thus leaving only aortic baroreceptors stimulated by the increase in arterial pressure. PE infusion alone prolonged HI by 230 +/- 24 ms (P less than 0.05). Application of NP attenuated the HI response to 65 +/- 22 ms above control (P less than 0.05 vs. PE alone). During these steady-state increases in arterial pressure, elimination of the carotid baroreflex contribution reduced the HI prolongation by 41-70% in five subjects and by greater than 93% in five subjects. We also measured the HI response to dynamic ramp elevation of systolic arterial pressure (SAP) using bolus administrations of PE. Baroreflex control was calculated from the slope of the regression correlating SAP to succeeding HI for PE alone (carotid and aortic baroreceptor activation) and for PE plus superimposed dynamic NP at levels equal to the increases in SAP (aortic baroreceptor activation). During PE alone, the baroreflex slope was 20.2 +/- 2.9 ms/mmHg (n = 10). During PE plus NP, the baroreflex slope was reduced by 30% to 14.1 +/- 2.8 ms/mmHg (P less than 0.02 vs. during PE alone). Thus, during dynamic increases in arterial pressure, eliminating the carotid baroreflex contribution reduced the HI response by 30%. These studies indicate that extracarotid (presumably aortic) and carotid baroreflexes both participate in control of heart rate in humans. Extracarotid (aortic) baroreflexes appear to have the greater role in control of heart rate during dynamic increases in arterial pressure.

Adult↗
PubMed1985

Different effects of vasopressin and angiotensin II on baroreflexes.

Our data indicate that vasopressin facilitates baroreflex inhibition of lumbar sympathetic nerve activity by two mechanisms: it sensitizes baroreceptors locally and shifts the stimulus-response curve so that a lower carotid sinus pressure results in a certain level of reflex sympathetic inhibition; it also produces a corresponding shift when given i.v. and excluded from baroreceptors implicating a second, central mechanism for facilitation of baroreflexes. In contrast, angiotensin II attenuates baroreflex inhibition of peripheral sympathetic function and this is accounted for totally by a central action. Why these differences occur present challenging new questions for future investigation.

Angiotensin II↗
PubMed1984

Angiotensin II attenuates baroreflex control of heart rate and sympathetic activity.

We determined whether angiotensin II (ANG II) modulates the arterial baroreflex control of lumbar sympathetic nerve activity (LSNA) in chloralose-anesthetized rabbits. Intravenous infusion (iv) of ANG II caused significantly less reflex bradycardia and less inhibition of LSNA than iv phenylephrine (PE) for equivalent increments in arterial pressure. During a background iv infusion of ANG II, which caused a small sustained increase in arterial pressure, the reflex inhibition of heart rate (HR) and LSNA in response to further increases in pressure with graded doses of PE was attenuated, but the reflex increase in HR and LSNA in response to hypotension with graded doses of nitroprusside was unchanged. This modulation of the baroreflex by ANG II is specific since a similar background infusion of PE did not alter baroreflex responses to further increases or to decreases in arterial pressure. The frequency of aortic baroreceptors was comparable for equivalent increases in pressure caused by iv ANG II or PE. When ANG II was confined to the isolated carotid sinuses, the reflex inhibition of HR and LSNA during distension of carotid sinuses was unchanged. An excitatory effect of ANG II on the efferent limb of the baroreflex that would oppose the reflex bradycardia or inhibition of LSNA is unlikely because when the pressor effect of ANG II was prevented by nitroprusside, there were no changes in HR and LSNA. We conclude that through an effect on the central nervous system iv ANG II has a selective effect on the arterial baroreflex; it impairs reflex decreases in HR and LSNA during hypertension but not reflex increases in HR and LSNA during hypotension.

Angiotensin II↗
PubMed1984

Impaired central mediation of the arterial baroreflex in chronic renal hypertension.

After 6 wk of renal hypertension in rabbits, the arterial baroreflex control of heart rate (HR) is impaired but the baroreflex control of lumbar sympathetic nerve activity ( LSNA ) is preserved. This selective impairment may reflect a predominant abnormality in the baroreceptors. In this study, we tested the hypothesis that renal hypertension of longer duration may impair baroreflex control of LSNA through a defect in the central nervous system mediation of the reflex. Four months after induction of renal hypertension, baroreflex responses were determined during increases in arterial pressure with intravenous phenylephrine or decreases in pressure with vena caval occlusion under chloralose-urethan anesthesia. Reflex control of LSNA and HR was impaired markedly in hypertensive rabbits. Reflex inhibition of LSNA and HR in response to afferent electrical stimulation of the left aortic depressor nerve (all arterial baroreceptor afferents cut) was attenuated in hypertensive in contrast to normotensive rabbits. This attenuation was noted when the medullated fibers only were stimulated or when both medullated and nonmedullated fibers were stimulated. We conclude that baroreflex control of LSNA that is preserved after 6 wk of hypertension is impaired after 4 mo of hypertension. The impairment reflects an abnormality in the central nervous system mediation of the reflex.

Anesthesia, General↗
PubMed1984

Acute resetting of carotid sinus baroreceptors. I. Dissociation between discharge and wall changes.

The purpose of this study was to assess whether mechanical changes in the carotid sinus wall could account for acute resetting of the carotid sinus baroreceptors in chloralose-anesthetized dogs. Threshold pressure and pressure-discharge curves for single-unit baroreceptors were determined before and after the vascularly isolated carotid sinus was exposed to brief increases or decreases in base-line pressure. When intrasinus pressure was increased by 30 mmHg for 15 min, threshold pressure increased by 9 +/- 1.3 (SE) mmHg (n = 12), and when intrasinus pressure was decreased by 30 mmHg threshold pressure decreased by 14 +/- 4.2 mmHg (n = 9), with no change in gain of the pressure-discharge curves. In 14 experiments carotid sinus pressure was increased from 70 (control) to 160 mmHg for only 5 min (reset) and returned to 70 mmHg for 10 min (recovery). After exposure to the higher pressure, threshold pressure increased from 75 +/- 3.8 to 94 +/- 4.4 mmHg, and carotid sinus diameter (sonomicrometer) and calculated wall strain at each pressure increased. After the recovery period, baroreceptor threshold pressure returned to 75 +/- 4.1 mmHg, but diameter and wall strain remained elevated. We interpret our finding that baroreceptor resetting and recovery are not accompanied by reciprocal changes in carotid sinus diameter to indicate that a mechanical mechanism alone cannot explain acute resetting.

Animals↗
PubMed1984

Acute resetting of carotid sinus baroreceptors. II. Possible involvement of electrogenic Na+ pump.

In the accompanying manuscript [Am. J. Physiol. 247 (Heart Circ. Physiol. 16): H824-H832, 1984] we demonstrated that a mechanical mechanism alone cannot account for acute resetting of baroreceptors. To determine if changes in the activity of a baroreceptor electrogenic Na+ pump contributed to resetting, single-unit baroreceptor discharge was recorded from the carotid sinus nerve while resetting protocols were performed before and after exposing the vascularly isolated carotid sinus to treatments known to block the Na+ pump [ouabain and low extracellular K+ concentration ([K+]o)]. Ouabain (0.1-0.5 microgram/ml) blocked the increase in baroreceptor threshold pressure that occurred when intrasinus pressure was increased by 30 mmHg for 15 min [delta threshold = 16 +/- 3 (SE) mmHg before and 1.2 +/- 2.3 mmHg after ouabain]. In 12 experiments carotid sinus pressure was increased from 70 to 160 mmHg for 5 min and then returned to 70 mmHg for 10 min in the presence of both normal [K+]o (5.8 mM) and low [K+]o. Exposure to the low K+ solution resulted in a significantly smaller increase in threshold pressure when intrasinus pressure was increased from 70 to 160 mmHg (9 +/- 2.7 vs. 18 +/- 2.1 mmHg). When K+ was replaced, threshold pressure again increased by 18 +/- 2.3 mmHg, the increase in threshold was reversed. Thus, since ouabain blocked and low [K+]o attenuated acute resetting of the baroreceptors, we propose that changes in the activity of an electrogenic Na+ pump contribute to acute resetting.

Animals↗
PubMed1984

Selective impairment of baroreflex-mediated vasoconstrictor responses in patients with ventricular dysfunction.

Cardiac dysfunction in animals has been associated with impairment of arterial and cardiopulmonary baroreflex control of the circulation. Chronic heart failure in human beings is associated with neurohumoral excitation, which could result in part from impairment in the inhibitory influence of baroreflexes. We postulated that (1) patients with left ventricular dysfunction (LVD) have impaired baroreflex modulation of vascular resistance and (2) administration of a digitalis glycoside would immediately restore baroreflex sensitivity. Eleven patients with LVD (NYHA class, 2.8 +/- 0.2, mean +/- SEM; baseline left ventricular ejection fraction, 18 +/- 2%; cardiac index, 2.4 +/- 0.21/min/m2; and pulmonary capillary wedge pressure, 26.0 +/- 3.2 mm Hg) were compared with 17 normal control subjects. We measured forearm vasoconstrictor responses to simulated orthostatic stress with use of lower body negative pressure (LBNP) at -10 and -40 mm Hg to unload cardiopulmonary and arterial baroreceptors. Baseline forearm vascular resistance (FVR) was higher in patients with LVD than in normal subjects: FVRLVD, 68.8 +/- 15.3 U; FVRN, 23.2 +/- 2.1 U (p less than .001). During unloading of baroreceptors with LBNP -10 mm Hg, normal subjects developed vasoconstriction (delta VRN at LBNP -10 mm Hg, +5.7 +/- 1.6 U) but patients with LVD failed to have vasoconstriction and tended to develop vasodilation (delta FVRLVD at LBNP -10 mm Hg, -8.6 +/- 8.5 U) (p = .05, normals vs patients with LVD at LBNP -10 mm Hg). A more marked disparity in response was seen during unloading of baroreceptors of LBNP -40 mm Hg: delta FVRN at LBNP -40 mm Hg, +16.6 +/- 1.5 U; delta FVRLVD at LBNP -40 mm Hg, -10.3 +/- 9.6 U (p less than .001, normals vs patients with LVD). Despite high baseline values for FVR, patients with LVD developed vasoconstriction during intra-arterial infusions of norepinephrine, thereby excluding a nonspecific depression of vascular reactivity as the mechanism for abnormal responses to LBNP in patients with LVD. We also studied the short-term effects of administration of a digitalis glycoside, ouabain 0.0075 mg/kg (seven patients) or lanatoside C (Cedilanid-D) 0.02 mg/kg (three patients), on baroreflex-mediated vasoconstrictor responses to LBNP in the patients with LVD. Digitalis glycoside reduced baseline FVR from 71.8 +/- 16.6 to 48.6 +/- 12.0 U (p less than .02). Responses to LBNP tended to be normalized after administration of digitalis glycoside: delta FVR during LBNP -40 mm Hg, -11.1 +/- 10.5 U before and +7.8 +/- 5.6 U after the drug (p less than .05).(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗