Coronary Inflow and Oxygen Usage Following Cardiac Sympathetic Nerve Stimulation in Unanesthetized Dogs

Granata, L; Olsson, Ray A.; Huvos, Andrew G.; Gregg, Donald E.

doi:10.1161/01.res.16.2.114

Cited by 93 publications

(22 citation statements)

References 23 publications

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“…The concept that the coronary vasculature has the capacity to respond to sympathetic a-adrenergic activation elicited by direct electrical stimulation of sympathetic nerves to the heart (Beme et al, 1965;Granata et al, 1965;Feigl, 1967;Ross and Mulder, 1969;McRaven et al, 1971;Nayler and Carson, 1973;Feigl, 1975) or by the exogenous administration of a-adrenergic agonists Mohrman and Feigl, 1978) is firmly established. Recent evidence also indicates that a-adrenergic activation can reduce the diameter of large coronary arteries (Gerova et al, 1979;Vatner et al, 1980a).…”

Section: Discussionmentioning

confidence: 99%

“…Reflex sympathetic a-adrenergic activation has also been shown to play a significant role in the coronary vascular response to free-ranging, maximal exercise (Murray and Vatner, 1979), as well as static exercise (Aung-Din et al, 1981). Initial, transient reductions in either mean or stroke left coronary blood flow followed by pronounced coronary vasodilation have been reported in intact, conscious dogs in response to electrical stimulation of the stellate ganglion (Granata et al, 1965), noise and excitement (Rayford et al, 1965), and behavioral stress (Bergamaschi et al, 1973;Billman and Randall, 1981). However, the mechanisms responsible for the transient decrease in coronary blood flow were not investigated in those earlier studies (Granata et al, 1965;Rayford et al, 1965), and concomitant changes in heart rate and arterial pressure make it difficult to ascertain the extent to which sympathetic a-adrenergic constriction was involved in the coronary vascular response.…”

Section: Discussionmentioning

confidence: 99%

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Alpha-adrenergic-mediated reduction in coronary blood flow secondary to carotid chemoreceptor reflex activation in conscious dogs.

Murray

Lavallée

Vatner

1984

Circulation Research

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SUMMARY. We examined the late coronary vascular response to carotid chemoreceptor reflex activation in normal, conscious dogs instrumented for the measurement of right main and left circumflex coronary artery blood flows, arterial and right ventricular pressures, and arterial and coronary sinus blood gases and O 2 contents. With heart rate held constant by electrical stimulation, and with respiration controlled or allowed to vary spontaneously, carotid chemoreceptor reflex activation (induced by intracarotid nicotine) elicited a striking biphasic coronary vascular response characterized by an early dilation (previously described) and a late constriction. For example, with respiration controlled and with the autonomic nervous system intact, carotid chemoreceptor reflex activation resulted in a late increase in arterial pressure (19 ± 4%; P < 0.002), absolute reductions in right main (24 ± 4%; P < 0.002), and left circumflex (12 ± 2%; P < 0.004) coronary blood flows, and increases in right (62 ± 13%; P < 0.002) and left (26 ± 3%; P < 0.0001) coronary resistances. This carotid chemoreceptor reflex activation-induced late coronary constriction was also associated with a concomitant increase in myocardial oxygen extraction, i.e., arterial oxygen content remained constant, while coronary sinus oxygen content decreased (19 ± 6%; P < 0.04). Neither propranolol nor atropine had any significant effect on the magnitude of the right coronary constriction. However, both the absolute reduction in right coronary blood flow and increase in right coronary resistance were abolished by phentolamine. Furthermore, either total cardiac denervation or adrenalectomy significantly attenuated (P < 0.01) carotid chemoreceptor reflex activation-induced reductions in right coronary blood flow and increase in right coronary resistance. We conclude that, with autonomic nervous system activity intact, carotid chemoreceptor reflex activation can elicit an absolute reflexly mediated reduction in coronary blood flow in the normal, conscious dog, despite an increase in arterial pressure. The mechanism of this vasoconstriction involves a-adrenergic receptor stimulation mediated by both cardiac sympathetic nerves and circulating catecholamines. {Circ Res 54: 96-106, 1984) THERE NOW exists a relatively large body of experimental evidence which supports the concept that sympathetic activation can result in a-adrenergic coronary vasoconstriction. This concept is based primarily on experiments in which sympathetic activation has resulted in increases in arterial pressure which have been greater than concomitant increases in coronary blood flow, with a consequent increase in coronary resistance. It is somewhat surprising that despite recent interest in the role of coronary vasoconstriction in the pathogenesis of coronary artery vasospasm (Hillis and Braunwald, 1978;Maseri et al., 1978), there is little compelling evidence that aadrenergic vasoconstriction can mediate an absolute reduction in coronary blood flow in the presence of an intact autonomic n...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Alpha-adrenergic-mediated reduction in coronary blood flow secondary to carotid chemoreceptor reflex activation in conscious dogs.

Murray

Lavallée

Vatner

1984

Circulation Research

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“…(18)(19)(20)(21)(22)(23), but a clinically important role has not generally been ascribed to them. Hamlin et al (9) demonstrated that coronary vasoconstriction caused by intravenous digoxin could be abolished completely by previous alpha adrenergic receptor blockade with phenoxybenzamine or by ganglionic blockade with mecamylamine.…”

Section: Methodsmentioning

confidence: 99%

The Central Nervous System as a Site of Action for the Coronary Vasoconstrictor Effect of Digoxin

Garan¹,

Smith²,

Powell³

1974

J. Clin. Invest.

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A B S T R A C T Digitalis is known to have a vasoconstrictor effect in the coronary circulation. Recent studies have demonstrated that the coronary vasoconstrictor effects of acetylstrophanthidin and digoxin are neurally mediated via alpha adrenergic fibers. In the present study, experiments were done in 20 dogs anesthetized with chloralose and urethane to study the central nervous system as a possible site of action for this vasoconstrictor effect of digoxin. After the intravenous administration of 1.0 mg digoxin, cerebrospinal fluid concentrations of digoxin rose to a peak of 2.3±0.4 (SEM) ng/ml at 15 min, temporally corresponding to the peak in coronary vascular resistance change of + 20.0± 2.5% of control in the paced canine heart. Submicrogram digoxin injections into the lateral cerebral ventricle produced a significant increase in coronary vascular resistance, the latter injection producing a peak increase in coronary vascular resistance of 12.4±11.2% of control. Cross-perfusion experiments, where the isolated head of the operative dog was perfused from a donor dog receiving digoxin, thus keeping digoxin levels in the remainder of the operative dog very low, showed a similar degree of coronary vasoconstriction. Thus, the central nervous system appears to be an important site of action for the early coronary vasoconstrictor effect of digoxin.

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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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Coronary Inflow and Oxygen Usage Following Cardiac Sympathetic Nerve Stimulation in Unanesthetized Dogs

Cited by 93 publications

References 23 publications

Alpha-adrenergic-mediated reduction in coronary blood flow secondary to carotid chemoreceptor reflex activation in conscious dogs.

Alpha-adrenergic-mediated reduction in coronary blood flow secondary to carotid chemoreceptor reflex activation in conscious dogs.

The Central Nervous System as a Site of Action for the Coronary Vasoconstrictor Effect of Digoxin

Effects of Alpha Adrenergic Blockade upon Coronary Hemodynamics

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