Effects of Carotid Sinus Nerve Stimulation on the Coronary Circulation of the Conscious Dog

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

doi:10.1161/01.res.27.1.11

Cited by 95 publications

(36 citation statements)

References 30 publications

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“…We have previously shown that coronary flow is maintained in the conscious dog during CSNS when pressure declines and that a significant coronary vasodilatation occurs (21). Feigl has found that coronary blood flow increases with carotid occlusion (36) and this was confirmed for the conscious dog in two experiments in the present study.…”

Section: Bilateral Carotid Artery Occlusionsupporting

confidence: 80%

“…It is unlikely that significant chemoreceptor effects occurred since we have previously measured arterial blood gases and found no significant change in Po., Pco2, and pH with CSNS (21). Furthermore, chemoreceptor stimulation is considered to cause no change (31) or to decrease myocardial contractility (32), and therefore could not have masked the observed response.…”

Section: Bilateral Carotid Artery Occlusionmentioning

confidence: 99%

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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%

Section: Bilateral Carotid Artery Occlusionmentioning

confidence: 99%

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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“…29 ' 30 Electrical stimulation of the carotid sinus nerve, which mimics increased carotid sinus pressure, produces inhibition of coronary sympathetic constrictor tone. 31 ' 32 In the present experiments a restriction of flow and oxygen delivery was observed before a-receptor blockade but not afterwards; the most probable interpretation of these results is that an a-receptor vasoconstrictor mechanism limits coronary blood flow during reflex sympathetic activation from the carotid sinus baroreceptors.…”

Section: Neural Controlsupporting

confidence: 47%

Competition between sympathetic vasoconstriction and metabolic vasodilation in the canine coronary circulation.

Mohrman¹,

Feigl²

1978

Circulation Research

248

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Before a-receptor blockade, either intracoronary norepinephrine infusion or reflex sympathetic activation from the carotid sinus resulted in an increase of only 0.85 ml/100 g mirr' in oxygen delivery for each increase of 1 ml/100 g min" 1 in cardiac oxygen consumption. Under these circumstances, myocardial oxygen extraction increased and coronary venous oxygen content fell. After a-receptor blockade, either intracoronary norepinephrine infusion or a carotid sinus reflex resulted in an increase of 1.23 ml/100 g min ' in oxygen delivery for each increase of 1 ml/100 g min' 1 in cardiac oxygen consumption. Myocardial oxygen extraction and coronary venous oxygen content changed only slightly after a-receptor blockade. The greater coronary vasodilation and lesser change in cardiac oxygen extraction after a-receptor blockade were significantly different (P < 0.001) from the values before blockade. It is concluded that the coronary a-receptor constrictor mechanism competes with metabolic vasodilation during sympathetic activation even when there are large increases in myocardial metabolism. The net effect of the a-receptor constrictor influence is to restrict the metabolically related flow increase by about 30%, thus increasing oxygen extraction and decreasing coronary venous oxygen content.IT HAS LONG been known that stimulation of the sympathetic innervation of the heart results in tachycardia and augmented contractility, accompanied by increased myocardial oxygen consumption, increased coronary blood flow, and decreased coronary sinus oxygen content. A previous study in this laboratory demonstrated that sympathetic a-receptor coronary vasoconstriction is capable of competing with local metabolic control and lowering coronary sinus oxygen tension after adrenergic /3-receptor blockade. 17 In that study the positive inotropic and chron-

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“…In the stable state, metabolic regulators such as adenosine and prostaglandins are thought to be more important than neurogenic and myogenic factors (1)(2)(3)(4), though neurogenic mechanisms have been shown to alter coronary flow in awake and anesthetized animals as well. Both sympathetic and parasympathetic activation in animals produce coronary vasoconstriction and vasodilation (5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21), with a recent study suggesting the presence of alpha adrenergic tone on the coronary vasculature in the resting state (15). In man, reflex coronary vasoconstriction in response to a cold stimulus, mediated through an alpha adrenergic mechanism, has also been demonstrated (22).…”

Section: Introductionmentioning

confidence: 99%

Effects of Alpha Adrenergic Blockade upon Coronary Hemodynamics

Orlick¹,

Ricci²,

Alderman³

et al. 1978

J. Clin. Invest.

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A B S T R A C T The effect of alpha adrenergic blockade on coronary blood flow regulation at rest was studied in 11 normally innervated patients and 8 cardiac allograft recipients by measuring arterial pressure and coronary sinus blood flow by thermodilution before and after alpha adrenergic blockade with phentolamine. Coronary vascular resistance was calculated by using coronary sinus blood flow and mean arterial pressure, and metabolic demand was estimated by the product of systolic arterial pressure and heart rate. In addition, the coronary sinus blood flow response to tachycardia was examined in 9 innervated patients and 12 denervated patients, with measurements repeated after phentolamine in 8 of the 9 innvervated patients and 6 of the 12 denervated patients. There was a 7.3+4.4% increase in coronary sinus blood flow in the innervated patients in response to alpha blockade, whereas the transplanted patients had an 8.2±1.8% fall in coronary sinus blood flow, despite equivalent changes in rate pressure product. The innervated patients also demonstrated a significantly greater increase in coronary sinus blood flow than did the transplanted patients during the first 5 s of an abrupt increase in heart rate (26±4 vs. 8±2.5 ml/min, P < 0.001). This early response was blunted after alpha adrenergic blockade. We conclude that there is basal alpha adrenergic tone present on the coronary vasculature in man that is withdrawn by a sudden increase in heart rate.

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Effects of Carotid Sinus Nerve Stimulation on the Coronary Circulation of the Conscious Dog

Cited by 95 publications

References 30 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

Competition between sympathetic vasoconstriction and metabolic vasodilation in the canine coronary circulation.

Effects of Alpha Adrenergic Blockade upon Coronary Hemodynamics

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