Comparison of the cardiac effects of vagus nerve stimulation and of acetylcholine infusions

Levy, M. N.; Zieske, Harrison

doi:10.1152/ajplegacy.1969.216.4.890

Cited by 64 publications

(24 citation statements)

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“…Hyperemia and hyperfunction after cessation of acetylcholine administration have been reported previously, 21 -22 but were abolished after adrenergic blockade and, thus, were most likely due to release from cholinergic inhibition of norepinephrine release. The combined a-and ^-adrenergic blockade used in the present study should prevent this effect, so the etiology of the off-response observed in baboons remains unclear.…”

Section: Lactatesupporting

confidence: 57%

Acetylcholine causes coronary vasodilation in dogs and baboons.

Winkle

Feigl

1989

Circulation Research

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Intracoronary administration of acetylcholine or efferent vagal stimulation causes coronary vasodilation in dogs. However, in baboons it has been reported that intracoronary acetylcholine results in a fall in coronary blood flow and that stimulation of the vagi is without effect. The dose response of intracoronary acetylcholine and the effect of efferent vagal stimulation on the coronary circulation were reinvestigated in closed-chest, anesthetized dogs and baboons. The left main coronary artery was cannulated and perfused at constant pressure. o-Adrenergic and 0-adrenergic receptors were pharmacologically blocked with phenoxybenzamine and propranolol. Heart rate was held constant by right ventricular pacing. In dogs, intracoronary infusion of acetylcholine (1-300 /ig/min) elicited a dose-dependent increase in steady-state coronary blood flow and coronary sinus oxygen tension, without a change in myocardial oxygen consumption. Vagal stimulation caused a coronary vasodilation that was attenuated by a metabolically mediated decrease in flow. In baboons, acetylcholine increased steady-state coronary blood flow in the dose range of 1-10 /ig/min, caused little change at 30 /tg/min, and decreased flow at 100-300 /ig/min. Coronary sinus oxygen tension increased in a dosedependent manner up to 10 /ig/min. Myocardial oxygen consumption was unchanged in the dose range of 1-10 /ig/min and declined between 30 and 300 jttg/min. Efferent stimulation of the vagi resulted in coronary dilation obscured by a metabolic reduction of flow. It is concluded that 1) low doses of acetylcholine elicit a primary coronary vasodilation in both species, but in baboons high doses of acetylcholine cause a reduction of both myocardial oxygen consumption and coronary blood flow below control values and 2) vagal stimulation causes a competition between coronary vasodilation and metabolic reduction of flow in dogs and baboons. (Circulation Research 1989;65:1580-1593 A lthough it is well established that canine cor-/ \ onary vessels vasodilate in response to -+. A . acetylcholine 1 -3 and efferent vagal stimulation, 3 " 5 there are conflicting reports regarding the response of primate coronary arteries to parasympathetic activation. Isolated epicardial coronary arteries from monkeys have been found to relax 6 and to relax or contract 7 in response to acetylcholine. Intracoronary administration of acetylcholine in intact Japanese monkeys and baboons has been reported to elicit an intense decrease in coronary blood flow. However, coronary vascular resistance is primarily determined by local metabolic factors, not direct neural control. Myocardial oxygen metabolism is affected by heart rate, systolic blood pressure, and myocardial inotropic state.1 Thus, a neural coronary vasodilation may be buffered or even masked by a metabolic vasoconstriction secondary to a decline in any of the above hemodynamic variables.The purpose of the present study was to ascertain if there is indeed a species difference between dogs and baboons in the effects of intracoron...

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Section: Lactatesupporting

confidence: 57%

Acetylcholine causes coronary vasodilation in dogs and baboons.

Winkle

Feigl

1989

Circulation Research

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“…This acetylcholine-induced dilatation of liver sinusoids is also significantly attenuated by pretreatment of the rat with the cholinergic receptor blocker atropine. [Levy and Zieske, 1969;Johansson, Johansson, I-jung anid Stage, 1972Stage, : W&atersoin, 1973. In the present in7 ritSo stuidy, the range of estimated livNer plasma acetylcholine coticentration (0-2 to 12 ng.rml -) reaching liver sinulsoids presumably by vagal impulses is comparable to studies by Liang [1975] who found that 0 5 to 2-2ng.ml--of acetylcholine was released into tle renal venous blood upon reflex stimulation of renal nerves.…”

Section: Discussionmentioning

confidence: 99%

“…Tlle local concentration of acetylcholine delivered to any region of the circulation depends on the regional blood flow and the local capillary density, and acetylcholine concentration varies along the path of capillary length of varying cholinesterase activities. None of these in vivo parameters are available in the liver sinusoids, therefore, the estimation of local acetylcholine concentration to represent in vivo physiological release of neurotransmitter substance from the vagus nerves can only be considered as an approximation, and the computation of equivalent effects is only for the purpose of comparison and does not necessarily imply that a given frequency of vagal stimulation must actually result in the calculated concentration of acetylcholine at the specific cholinergic vascular neuroeffector sites [Levy and Zieske, 1969].…”

Section: Discussionmentioning

confidence: 99%

Parasympathetic Cholinergic Vasodilator Mechanism in the Terminal Liver Microcirculation in Rats

Koo

Liang

1979

Exp Physiol

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Changes in the diameter of liver sinusoids were studied by an intravital television microscope method in pentobarbital-anaesthetized rats. Dilatation of liver sinusoids was observed during parasympathetic neural stimulation and during acetylcholine administration. Frequency-dependent stimulation-effect relationships were obtained by electrical excitation of intact vagus nerves at supramaximal intensity fr-om 2 to 8 Hz. Acetylcholine concentration-effect relationships were also obtained by intraportal venous infusions of acetylcholine 30 pil for 5 s from 10-I to 10-2 mol I -1. Systemic cholinergic receptor blockade with atropine (1 mg kg 1) markedly reduced dilatation of liver sinusoids produced by both vagus nerve stimulation and acetylcholine administration. Changes in diameter of liver sinuLsoids with frequency of neural stimulation and with concentration of administered acetylcholine were also expressed as percentage of observed maximum effect and the respective stimulation-effect curves were constructed such that at a certain percentage of diameter change, the equivalent level of vagus nerve activity was represented by a given concentration of administered acetylcholine. Liver plasma concentration of acetylcholine presumably released during electrical vagal stimulation and reaching liver sinusoids was also estimated and found to be within physiological range. It is therefore proposed that rat liver sinusoids have the capacity for parasympathetic cholinergic vasodilatation.Evidence of an autonomic sympathetic control mechanism for the calibre of liver sinusoids in rats has been demonstrated recently Cheng, 1976, 1977]. Such an adrenergic mechanism is present in many other vascular beds such as brain, stomach, kidney, heart and skeletal muscle. In coronary and cerebral circulations of dogs, there also exists a parasympathetic mechanism which has the opposite effects of sympathetic mechanism on blood flow regulation [Feigl, 1969; D'Alecy and Rose, 1977]. A similar parasympathetic mechanism could be present in the liver too. Indeed, hepatic nerves receive fibers from coeliac plexus as well as both vagus nerves [Mikhail and Saleh, 1961;Sutherland, 1964], but the role of these parasympathetic fibres in liver sinusoids is little stLidied. In the present investigation direct electrical stimulation of vagus nerves and intraportal venous infusion of the parasympathetic neurotransmitter acetyleholine were used to test for the existence of a cholinergic vasodilator mechanism in rat liver sinusoids.Also, diffiCulty exists in interpreting relationships of physiological effects of administered cholinergic substances and effects produced by neural activity, i.e., 149

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“…(b) Isoprenaline (Iso), a fladrenoceptor agonist, causes coronary vasodilatation that is completely blocked by propranolol (Klocke et al, 1965;Ross, 1974). (c) Stimulation of efferent vagal fibres to the heart or the administration of acetylcholine (ACh) in the dog results in coronary vasodilatation independent of the effects on heart rate and myocardial contractility (Berne et al, 1965;Feigl, 1969;Levy & Zieske, 1969 Recent studies have demonstrated that the vascular constrictor reaction in atherosclerotic arteries was augmented (Henry & Yokoyama, 1980;Yokoyama et al, 1983;Heistard et al, 1984). Other studies showed that after myocardial ischaemia or coronary ligation, coronary vascular responses to thrombin were changed (Ku, 1982; and the myocardial blood flow response to NA was profoundly modified (Moore & Parratt, 1973).…”

Section: Introductionmentioning

confidence: 99%

Alterations of coronary vascular responses to noradrenaline, acetylcholine and isoprenaline during acute myocardinal ischaemia in dogs

Sun

Zang

1989

British J Pharmacology

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1 The reactivity of coronary arteries to noradrenaline (NA), acetylcholine (ACh) and isoprenaline (Iso) during acute myocardial ischaemia was studied in anaesthetized, open-chest dogs. 2 The left anterior descending coronary artery (LAD) was cannulated and perfused via an extracorporal circuit at constant flow. Ischaemia was produced by decreasing the perfusion blood flow of the LAD to 50% (moderate ischaemia) and 27% (severe ischemia) of normal. A dose of each agent which had no significant myocardial effects was chosen. Heart rate was held constant by ventricular pacing during ACh administration. 3 Under normal conditions, the infusion of NA, ACh and Iso into the LAD produced significant decreases in coronary vascular resistance (P < 0.01). However, under either moderate or severe ischaemic conditions intracoronary NA resulted in a marked increase in coronary vascular resistance (P < 0.01), which was completely blocked by phentolamine, an a-adrenoceptor blocker; intracoronary ACh and Iso did not have a significant effect on coronary vascular resistance (P > 0.05). 4 These results indicate that coronary arterial responsiveness to some intrinsic vasoactive substances, such as NA and ACh, is altered during acute myocardial ischaemia. This may be important in the pathophysiology of myocardial ischaemia.

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Comparison of the cardiac effects of vagus nerve stimulation and of acetylcholine infusions

Cited by 64 publications

References 0 publications

Acetylcholine causes coronary vasodilation in dogs and baboons.

Acetylcholine causes coronary vasodilation in dogs and baboons.

Parasympathetic Cholinergic Vasodilator Mechanism in the Terminal Liver Microcirculation in Rats

Alterations of coronary vascular responses to noradrenaline, acetylcholine and isoprenaline during acute myocardinal ischaemia in dogs

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