Effects of Carotid Sinus Nerve Stimulation on Blood-Flow Distribution in Conscious Dogs at Rest and during Exercise

Vatner, Stephen F.; Franklin, Dean; Citters, Robert L. Van; Braunwald, Eugene

doi:10.1161/01.res.27.4.495

Cited by 105 publications

(51 citation statements)

References 36 publications

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“…2). In both cases cardiac output did not vary significantly, a finding in the conscious dog that we previously reported for CSNS (22) and which was noted by Fronek for carotid occlusion (29).…”

Section: Bilateral Carotid Artery Occlusionsupporting

confidence: 80%

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Extent of Carotid Sinus Regulation of the Myocardial Contractile State in Conscious Dogs

Vatner¹,

Higgins²,

Franklin³

et al. 1972

J. Clin. Invest.

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A B S T R A C T The effects of bilateral carotid artery occlusion (BCO) and carotid sinus nerve stimulation (CSNS) on left ventricular (LV) pressure (P), diameter (D), velocity of contraction (V), rate of change of pressure (dP/dt), and cardiac output were studied in conscious dogs instrumented with ultrasonic diameter gauges, miniature pressure gauges, and aortic electromagnetic flow transducers. The effects of BCO and CSNS were also studied after autonomic blockade and were compared to similar alterations in pressure produced by norepinephrine, methoxamine, and nitroglycerin. When heart rate was maintained constant with atrial stimulation, BCO had little effect on ventricular contractility, increasing isolength systolic pressure (LV Pis.) by 36% while isolength velocity of myocardial shortening (Vt..) decreased by 12% and (dP/dt)/P fell by 8%. These effects could be explained largely by vasoconstriction, since elevating systolic pressure with methoxamine produced similar results, while norepinephrine increased Vt.. by 36% and (dP/dt)/P by 56%S. CSNS produced directionally opposite results from BCO; it decreased Pi.8 by 15%, Vt.0 increased by 11%, while (dP/dt)/P remained almost constant. These effects may be explained largely by vasodilatation since reducing systolic pressure to the same level with nitroglycerin produced similar results. When peripheral vasoconstriction was minimized by phenoxybenzamine pretreatment, BCO produced a slight positive inotropic effect (Ptso increased by 8%o, Vt.. by 4%, and (dp/ This study was presented in part at the 44th Annual Scientific Sessions of the American Heart Association, Anaheim, Calif., November 1971. An

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Section: Bilateral Carotid Artery Occlusionsupporting

confidence: 80%

“…Indeed, studies in our laboratory (22) and by others (30) have shown that the aortic baroreceptors play a more important role than the carotid sinuses in the control of the chronotropic state of the heart, and similar consideration may apply to the inotropic state as well.…”

Section: Bilateral Carotid Artery Occlusionmentioning

confidence: 76%

Extent of Carotid Sinus Regulation of the Myocardial Contractile State in Conscious Dogs

Vatner¹,

Higgins²,

Franklin³

et al. 1972

J. Clin. Invest.

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“…7 Under these conditions, baroreceptor reflex impairments are transient rather than permanent, presumably because there is marked redundancy of baroreceptor afferents, particularly in the control of sympathetic nerve activity. 8 " 10 Thus, the loss of carotid baroreceptor input does not appear to cause a long-term impairment in baroreceptor reflex control of sympathetic vasoconstrictor outflow so long as the aortic baroreceptors remain intact.…”

Section: Discussionmentioning

confidence: 99%

Paroxysmal hypertension due to sinoaortic baroreceptor denervation in humans.

Aksamit¹,

Floras²,

Victor³

et al. 1987

Hypertension

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SUMMARY A 41-year-old man with a remote history of neck and mediastinal radiation was seen with severe paroxysms of hypertension, headache, and cutaneous flushing after bilateral carotid bypass surgery. Investigation revealed marked parallel fluctuations in blood pressure and heart rate and elevation of plasma norepinephrine to 1164 pg/ml during a paroxysm. We systematically evaluated his arterial and cardiopulmonary baroreceptor reflex function by assessing changes in heart rate, arterial pressure, and efferent muscle sympathetic nerve activity, which was measured directly by the microneurographic technique. Elevating resting arterial pressure from 130/88 to 164/100 mm Hg with phenylephrine or lowering it to 88/56 mm Hg with nitroprusside produced no reflex changes in heart rate or efferent sympathetic nerve activity. In contrast, decreases in cardiac filling pressures with lower body negative pressure produced a marked increase in sympathetic nerve activity. These findings indicate complete loss of the afferent limb of the arterial baroreceptor reflex but preservation of the cardiopulmonary baroreceptor reflex. They suggest that both carotid and aortic baroreceptors were impaired by the previous radiation and surgery. Despite the loss of arterial baroreceptor function, the patient did not have sustained hypertension. The paroxysms of hypertension appear to be due to spontaneous fluctuations in central sympathetic drive not buffered by arterial baroreceptors in a manner similar to that seen in sinoaortic-denervated animals. (Hypertension 9: 309-314, 1987) KEYWORDS • arterial baroreceptor reflex • microneurography • sympathetic nerve activity

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“…49 This latter point remains controversial; arterial baroreceptor reflexes of conscious dogs appear to continue to operate effectively during treadmill exercise. 50 " 52 The strong association we observed between BRS and blood pressure variability could be explained if the reflex regulation of blood pressure was preserved during physical activity but was less potent in hypertensive than in normal subjects.…”

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confidence: 90%

Factors influencing blood pressure and heart rate variability in hypertensive humans.

et al. 1988

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SUMMARY We examined the influence of baroreceptor reflex sensitivity (the increase in pulse interval in response to a phenylephrine-induced increase in blood pressure), age, blood pressure, and /3-adrenergic receptor blockade on the variability of blood pressure and heart rate in essential hypertension. Fifty-six subjects were studied before treatment; intra-arterial blood pressure was recorded outside the hospital for 24 hours. Variability was defined (from all beats occurring while subjects were awake) as the standard deviation about the average waking value for mean arterial pressure (MAP) or pulse interval. The correlation (r) between baroreceptor reflex sensitivity and blood pressure variability was -0.47 (p<0.0002). Baroreceptor reflex sensitivity was the only independent determinant of blood pressure variability on multiple regression analysis. Thirty subjects were restudied after 5 months of /3-adrenergic receptor blockade. Ambulatory blood pressure was lower during treatment, whereas pulse interval, its variability, and baroreceptor reflex sensitivity were higher. Blood pressure variability was unchanged. The variability of MAP was inversely correlated with baroreceptor reflex sensitivity before (r = -0.42, p<0.02) and during ( r = -0.45, p < 0.02) treatment, but it was unrelated to the average ambulatory MAP or to the variability of pulse interval either before or during /3-blockade. Sixteen subjects whose average waking ambulatory blood pressure was 140/90 mm Hg or less were not treated. This group of borderline hypertensive subjects had less variable MAP than did the remaining 40 subjects (12.4 ± 2.3 [SD] vs 14.5 ± 2.5 mm Hg; p<0.01). We conclude that 1) the decline in baroreceptor reflex sensitivity is the principal determinant of increased blood pressure variability in hypertension, 2) MAP and its variability are regulated independently, 3) heart rate variability is not influenced by baroreceptor reflex sensitivity and is unrelated to blood pressure variability, and 4) the blood pressure of subjects with borderline hypertension is not excessively labile. in normal and hypertensive humans, 1 but factors that might influence and regulate this variability remain imperfectly understood. Considerable experimental evidence supports the concept that the arterial baroreceptor reflex is intimately involved in the short-term regulation of arterial blood pressure. Denervation of the sinoaortic baroreceptors in rats and dogs consistently increases the beat-to-beat variation of blood pressure but has less dramatic and disputed effects on its level.2 " 5 Central interruption of the baroreceptor reflex by lesioning nucleus tractus solitarii produces hypertension, tachycardia, and increased blood pressure variability in awake animals. 6 Selective removal of the noradrenergic innervation of this nucleus does not induce hypertension, but it does cause an increase in blood pressure variability that is inversely related to a decrease in the baroreceptor reflex control of heart rate.

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Effects of Carotid Sinus Nerve Stimulation on Blood-Flow Distribution in Conscious Dogs at Rest and during Exercise

Cited by 105 publications

References 36 publications

Extent of Carotid Sinus Regulation of the Myocardial Contractile State in Conscious Dogs

Extent of Carotid Sinus Regulation of the Myocardial Contractile State in Conscious Dogs

Paroxysmal hypertension due to sinoaortic baroreceptor denervation in humans.

Factors influencing blood pressure and heart rate variability in hypertensive humans.

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