PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Ganglionic Stimulants”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 199 records · Page 11Linked to original sources
PubMedDate not supplied

Skeletal neuromuscular and smooth muscle effects of whole venom of the green mamba, Dendroaspis angusticeps - I.

Dendroaspis angusticeps venom (75 micrograms/ml) caused an irreversible blockade of the directly as well as directly evoked contractions of the rat hemidiaphragm and indirectly evoked contractions of the chick biventer cervicis muscle. The venom itself also produced a contraction of the frog rectus abdominis muscle, rat fundal strip, rat uterus and nictitating membrane of the cat; however, it did alter responses of nictitating membrane to preganglionic electrical stimulation and to ganglion stimulant drugs. The effect was attributed to the presence of acetylcholine-like substance in the venom.

Animals↗
PubMedDate not supplied

The loss of alpha-adrenergic effect during the erectile response in the long-term diabetic rat.

The present study was designed to investigate the effect of long-term, streptozotocin-induced diabetes on the erectile response in the laboratory rat. Mean arterial blood pressure (MAP) and intracavernosal blood pressure within the erectile tissue (CCP) were continuously monitored during erection elicited by stimulation of the autonomic innervation of the penis. MAP and CCP were also measured during administration of two drugs: nitroglycerin, a nitric oxide donor drug and phenylephrine, an alpha-adrenergic agonist. The results of these studies show that during graded electrical stimulation of the ganglion, the overall magnitude of the erectile response was greater in the diabetic rats than in untreated control animals. Neither diabetic nor control animals responded significantly to infusion of nitroglycerin. However, diabetic rats and control rats responded very differently to administration of phenylephrine; in the control rats, this alpha agonist caused a sharp decline in CCP as the cavernosal vessels constricted in response to the drug. The same dose of phenylephrine had no discernible effect on CCP in the diabetic animals. This loss of alpha responsiveness may be confined to the penile circulation because MAP was elevated to approximately the same extent in both groups. Taken together, these results show that long-term diabetes leads to a failure of alpha-adrenergic responsiveness in the cavernosal circulation. The greater erectile response to ganglionic stimulation in the diabetic animals is likely due to the loss of response to endogenous norepinephrine.

Adrenergic alpha-Agonists↗
PubMed1990

Effects of increasing heart rate induced by efferent sympathetic neuronal stimulation, isoproterenol or cardiac pacing on myocardial function and oxygen utilization.

The effects of increasing heart rate by six different methods on cardiac function were investigated in 17 open-chest anesthetized dogs. Heart rate was increased approximately 30% by (1) right interganglionic nerve stimulation, (2) atrial pacing, (3) ventricular pacing, (4) atrioventricular sequential pacing, (5) right stellate ganglion stimulation, and (6) isoproterenol administration. During heart rate increases induced by atrial pacing left ventricular intramyocardial pressure, coronary blood flow, oxygen delivery per unit of myocardial oxygen consumption, and myocardial efficiency were unchanged. Ventricular pacing reduced left ventricular cavity and septal intramyocardial pressure, while circumflex coronary flow increased, resulting in reduced oxygen delivery relative to myocardial oxygen consumption. Similarly, atrioventricular sequential pacing increased circumflex coronary artery flow and myocardial oxygen consumption, and decreased septal intramyocardial pressure and oxygen delivery per unit of myocardial oxygen consumption. Right stellate ganglion stimulation and isoproterenol increased left anterior descending and circumflex coronary artery blood flow, intramyocardial pressure, and myocardial oxygen consumption. Estimated myocardial efficiency (left ventricle) was decreased by ventricular pacing and isoproterenol, and was unchanged by atrial pacing and right interganglionic nerve stimulation. Increases in heart rate induced by right interganglionic nerve stimulation did not alter myocardial oxygen consumption, or the index of cardiac efficiency. It is concluded that augmentation of heart rate by either ventricular or atrioventricular pacing impairs myocardial function so that there is a decrease of left ventricular efficiency and isoproterenol augments chronotropism and myocardial force relative to cardiac external work so there is a reduction in cardiac efficiency. In contrast, atrial pacing or right interganglionic nerve stimulation augments chronotropism such that myocardial oxygen consumption and efficiency are unchanged.

Animals↗
PubMed1984

Clonidine inhibits nicotinic effects in ganglia of the cholinergic-sympathetic system.

The electrodermal potential (EDP) recorded with surface electrodes between the palm and the shaven back of the forepaws of anaesthetized cats was taken as a measure of sudomotor activity in response to submaximal activation of cholinergic-sympathetic efferents with the nicotinic ganglionic stimulant DMPP. The intravenous injection of 30 micrograms/kg clonidine inhibited EDPs in despinalized cats and in vagotomized cats with chronic denervation of the stellate ganglion. In vagotomized cats clonidine (30 micrograms/kg i.v.) shifted the dose-response curve of DMPP (4-256 micrograms/kg i.v.) to the right. An inhibitory effect was also observed in despinalized cats upon topical application of 0.1 and 1 microgram clonidine to the stellate ganglion. In all preparations the inhibitory effect of clonidine could be antagonized by intravenous injection of 200 micrograms/kg yohimbine. As all substances used were also active when injected during arrest of blood flow to the foreleg by means of a tourniquet, actions at the level of the sweat gland could be excluded. The results lead to the conclusion that the activation of postsynaptic somadendritic alpha 2-adrenoceptors in sudomotor ganglia of the cholinergic-sympathetic nervous system inhibits the effects of nicotinic ganglionic stimulation. It is assumed that this action is due to the known ganglionic hyperpolarization induced by alpha 2-adrenoceptor stimulants.

Animals↗
PubMed1982

Captopril inhibits pressor responses to peripheral sympathetic nerve activation in cats and rats.

1. In cats, under chloralose anaesthesia, captopril (0.1-0.3 mg/kg i.v.) inhibited the potentiation of the pressor effects of the ganglion stimulant McNeil-A-343 caused by intravenous infusion of angiotensin I (0.1 microgram/min). 2. In both cats and rats under chloralose anaesthesia captopril (0.01-1.0 mg/kg i.v.) depressed pressor responses to McNeil-A-343 whilst not modifying those to bilateral occlusion of the carotid arteries, or intravenous injection of the ganglion stimulant dimethylphenylpiperazinium or adrenaline. 3. It is concluded that in the cat and rat captopril depresses cardiovascular responses to sympathetic postganglionic nerve activation, both in the presence and absence of exogenous angiotensin I by an action which is proximal to the terminal synapse.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMed1986

Autonomic nervous system regulation of epicardial coronary vein systolic and diastolic blood velocity as measured by a laser Doppler velocimeter.

The velocity of blood in a major epicardial coronary vein accompanying the left anterior descending coronary artery of dogs was measured by means of a 140-micron fiber optic probe connected to a laser Doppler velocimeter. Right atrial pressure, left ventricular intramyocardial and cavity pressures, aortic pressure, as well as peripheral and central coronary venous pressures were compared with the velocity of blood measured in the epicardial coronary vein midway between the sites of the catheters measuring proximal and distal coronary vein pressures. During control conditions, coronary vein velocity was 14-18 cm/s during systole and 1.0-2.1 cm/s during diastole. Right stellate ganglion stimulation, norepinephrine or isoproterenol increased diastolic coronary vein velocity significantly, whereas left stellate ganglion stimulation did not. Average peak systolic velocity was not affected by these interventions. During these positive inotropic interventions, the peak coronary vein velocity usually occurred later in the cardiac cycle than during control conditions. Positive inotropic interventions appeared to decrease coronary vein velocity during systole and increase it during diastole. Left vagosympathetic trunk stimulation decreased diastolic but not systolic coronary vein velocity and usually caused peak coronary vein velocity to occur earlier in the cardiac cycle than during control states. Changes induced by vagosympathetic trunk stimulation usually occurred within one cardiac cycle. It is concluded that coronary vein blood velocity can be influenced by the autonomic nervous system.

Animals↗
PubMed1984

Pressure and flow in epicardial coronary veins of the dog heart: responses to positive inotropism.

Peripheral coronary venous pressures and coronary sinus venous flow were measured in the canine heart as well as intramyocardial, intraventricular, aortic, and coronary artery pressures. Maximum coronary venous flow occurred after maximum intramyocardial and peripheral coronary artery pressures had been reached. Maximum venous flow occurred at or following the maximum peripheral coronary vein pressure. Positive inotropic changes induced by stimulation of the right or left stellate ganglia or infusing isoproterenol, norepinephrine, or dobutamine significantly increased intramyocardial pressure, systolic epicardial coronary venous pressure, and systolic coronary venous flow. Mean coronary sinus flow was augmented by all interventions except isoproterenol. The estimated systolic vein resistance was slightly increased following right stellate ganglion stimulation, but not following left stellate ganglion stimulation, isoproterenol, or dobutamine. Norepinephrine reduced this parameter minimally. These data indicate that coronary veins respond differently to a variety of different positive inotropic interventions.

Animals↗
PubMed1975

Effects of divalent cations and of catecholamines on the late response of the superior cervical ganglion.

The characteristics of the late response of the superior cervical ganglion of dogs were studied by close-arterial injection of catecholamines and divalent cations to the ganglion. 2. Dopamine, noradrenaline and adrenaline inhibit the late response as well as ganglionic activity induced by other means. The effect of dopamine is brief but that of adrenaline is prolonged. 3. Cd2+, Co2+, Ni2+, Zn2+, Hg2+ and Fe2+ markedly potentiate the late response, whereas Mn2+, Ca2+ and Mg2+ inhibit it. 4. may potentiate ganglionic activity triggered by other ganglionic stimulants. The Cd-augmented activity may be blocked by a ganglion-blocker which is specific to the stimulant. 5. CdCl2 may exhibit a direct ganglion-stimulating action on a ganglion which shows prominent late responses and has been conditioned by tetanic preganglionic stimulation. 6. CdCl2 and MnCl2 may inhibit ganglionic transmission by suppressing acetylcholine release from presynaptic nerve terminals. 7. It is concluded that the late response represents the late discharges of ganglion cells, which are very sensitive to inhibition by CaCl2 and MnCl2 and may be potentiated by CdCl2.

Animals↗
PubMed1986

Attenuation of pressor responses to sympathetic stimuli in the rat by enalapril.

Intravenous administration to pithed Wistar rats of the angiotensin converting enzyme inhibitor enalapril (0.1-1.0 mg/kg) lowered the diastolic blood pressure and reduced pressor responses occurring during electrical stimulation (1-30 Hz) of the spinal sympathetic outflow. These doses of enalapril given intravenously also attenuated pressor responses to intravenous injection of the muscarinic ganglion stimulant McNeil-A-343 (50, 100, 150 micrograms/kg) and noradrenaline (0.1-5.0 micrograms/kg). Enalapril (1.0 mg/kg, i.v.) reduced pressor responses to the nicotinic ganglion stimulant 1,1-dimethyl-4-phenyl-piperazinium (300 micrograms/kg, i.v.). These results confirmed that the actions of enalapril resemble those of captopril in the pithed rat, by causing reductions in both blood pressure and pressor responses to sympathetic stimuli.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMed1989

Functional integrity of sympathetic efferent postganglionic axons in a region of stunned myocardium.

In order to investigate whether brief, repeated episodes of acute myocardial ischemia impair the function of the intrinsic sympathetic efferent post ganglionic cardiac nerves, 12 cycles of left anterior descending coronary artery occlusions (5 mins) and reperfusions (10 mins) were successfully performed in 10 dogs. Following each brief occlusion percentage systolic shortening in the ventral myocardium was reduced, consistent with myocardial stunning. Stellate ganglion stimulation increased intramyocardial pressures in the ventral and lateral regions of the left ventricle before and after each of the artery occlusions in which stimulations were performed. Isoproterenol and tyramine also augmented intramyocardial pressures in those regions. When the coronary artery was occluded permanently in seven of the dogs tested, stellate ganglion stimulation continued to augment intramyocardial pressure in the ventral region of the left ventricle for up to 35 mins. These results indicate that following repetitive episodes of brief occlusion of a coronary artery that are reported to 'stun' the involved myocardium in a transmural distribution, sympathetic efferent post ganglionic axons can augment inotropism in the affected zone. Furthermore, when a coronary artery is totally occluded thereafter for up to 35 mins these efferent sympathetic post ganglionic nerves continue to function. It is concluded that sympathetic efferent post ganglionic neurons innervating the ventricle can augment cardiac inotropism in a region of stunned myocardium.

Animals↗
PubMed1991

Influence of reduced presynaptic myocardial norepinephrine stores on left ventricular contractility.

Many investigators have reported that myocardial norepinephrine content is decreased in congestive heart failure. However there have been no studies of how decrease in myocardial norepinephrine might influence myocardial contraction. To clarify whether decreased myocardial norepinephrine per se affects myocardial contraction, we observed the change in left ventricular contractility during 30 min of left stellate ganglion stimulation in control and acutely reserpinized dogs. We obtained left ventricular max dp/dt and left ventricular end-systolic pressure-segment length relationships as indicators of left ventricular contractility. Both parameters decreased after left stellate ganglion stimulation in reserpinized dogs (left ventricular max dp/dt: 2064 +/- 200 to 1608 +/- 168 mmHg/s, left ventricular end-systolic pressure-segment length slope 117 +/- 22 to 79 +/- 14 mmHg/mm, n = 8, P less than 0.05), while they did not change in controls. In reserpinized dogs, left ventricular norepinephrine content decreased to one-third that of controls before the stimulation, and further decreased after stimulation. These data indicate that lowered myocardial norepinephrine itself may be responsible for the negative effect on left ventricular contractility in congestive heart failure.

Animals↗
PubMed1964

A PRELIMINARY INVESTIGATION OF THE PHARMACOLOGY OF THE HUMAN ISOLATED TAENIA COLI PREPARATION.

The effects of drugs on smooth muscle strips of human taenia coli, obtained from operation specimens, were studied in vitro. Both nicotinic and muscarinic sites of action of acetylcholine were demonstrated, the nicotinic effect being a relaxation. The sympathomimetic amines, adrenaline, noradrenaline, and isoprenaline produced a relaxation of the tissue by an action on adrenaline alpha- and beta-receptors. The presence of both types of receptor was demonstrated by selective adrenergic blockade with pronethalol or Hydergine. Pronethalol in high concentrations gave a nonselective adrenergic blockade. The ganglion-stimulating agents nicotine and dimethylphenylpiperazinium produced a relaxation of the tissue in all concentrations. This relaxation was inhibited by pronethalol or physostigmine but no contractile component to ganglion stimulation was revealed when these two drugs were present together. These results indicate the presence of either sympathetic ganglia in the intrinsic nerve plexuses, or adrenergic stores in the bowel wall. There is no pharmacological evidence for parasympathetic ganglia in human sigmoid colon. Histamine produced relaxant, contractile or biphasic responses. The type of response was independent of the "tone" of the preparation. The responses were not modified by procaine, hyoscine or pronethalol, which result indicates that both the contractile and relaxant responses to histamine were due to a direct action of the drug on smooth muscle. 5-Hydroxytryptamine produced either a contraction or a relaxation of the tissue. The relaxation was due to a direct effect of the drug, since hexamethonium, procaine or pronethalol did not affect the response. No conclusions have been drawn regarding the mechanism of the contractile response to 5-hydroxytryptamine. The nature of the responses of the tissue to drugs was independent of the disease for which the specimen of colon was removed.

Acetylcholine↗
PubMed2005

Functional central nicotinic acetylcholine receptor antagonism by systemic administration of Tinuvin 770 (BTMPS).

Tinuvin 770 (BTMPS) is a non-competitive, use-dependent antagonist of nicotinic acetylcholine receptors (nAChRs). The drug is highly lipid soluble and as such it has the potential to act within the brain. Presently the ganglionic blocking drug mecamylamine is used almost exclusively to block central nAChRs upon peripheral administration. These experiments were designed to confirm the nAChR antagonism effectiveness of BTMPS in both peripheral (ganglionic stimulation) and central (locomotor activity and thermal nociceptive sensitivity) nicotinic system in vivo. BTMPS inhibited the expression of the pressor response produced by i.v. injection of the ganglionic stimulant DMPP in anesthetized rats. The inhibition dose-response profile appeared to be biphasic with the maximal inhibition occurring after administration of the 0.48 mg/kg dose of BTMPS. In rats acclimated to the test apparatus, nicotine increased different measures of locomotor activity, particularly at the 0.75 mg/kg dose. BTMPS pretreatment significantly inhibited the nicotine-induced increase in motor behaviors, again with a biphasic dose-response relationship. Lastly, nicotine elicited an antinociceptive response in rats (hot plate test). BTMPS almost completely blocked the antinociceptive responses to 1 and 1.5 mg/kg nicotine. On its own, BTMPS failed to decrease blood pressure and to decrease the nociceptive threshold. The drug also generally failed to alter locomotor activity. The use-dependent aspect of BTMPS-induced inhibition of nAChRs was evident in the drug's greater effectiveness in the presence of the highest doses of nicotine. Therefore, BTMPS can be considered as an alternative to or as a confirmatory drug for mecamylamine when inhibition of central nicotinic receptors is required.

Animals↗
PubMed1995

Sympathetic activation, ventricular repolarization and Ikr blockade: implications for the antifibrillatory efficacy of potassium channel blocking agents.

OBJECTIVES: The aim of the present study was to test, in vivo and in vitro, the influence of adrenergic activation on action potential prolongation induced by the potassium channel blocking agent d-sotalol. BACKGROUND: d-Sotalol is not effective against myocardial ischemia-dependent ventricular fibrillation in the presence of elevated sympathetic activity. Most potassium channel blockers, such as d-sotalol, affect only one of the two components of Ik (Ikr) but not the other (Iks). Iks is activated by isoproterenol. An unopposed activation of Iks might account for the loss of anti-fibrillatory effect by d-sotalol in conditions of high sympathetic activity. METHODS: In nine anesthetized dogs we tested at constant heart rate (160 to 220 beats/min) the influences of left stellate ganglion stimulation on the monophasic action potential prolongation induced by d-sotalol. In two groups of isolated guinea pig ventricular myocytes we tested the effect of isoproterenol (10(-9) mol/liter) on the action potential duration at five pacing rates (from 0.5 to 2.5 Hz) in the absence (n = 6) and in the presence (n = 8) of d-sotalol. RESULTS: In control conditions, both in vivo and in vitro, adrenergic stimulation did not significantly change action potential duration. d-Sotalol prolonged both monophasic action potential duration in dogs and action potential duration of guinea pig ventricular myocytes by 19% to 24%. Adrenergic activation, either left stellate ganglion stimulation in vivo or isoproterenol in vitro, reduced by 40% to 60% the prolongation of action potential duration produced by d-sotalol. CONCLUSIONS: Sympathetic activation counteracts the effects of potassium channel blockers on the duration of repolarization and may impair their primary antifibrillatory mechanism. An intriguing clinical implication is that potassium channel blockers may not offer effective protection from malignant ischemic arrhythmias that occur in a setting of elevated sympathetic activity.

Action Potentials↗
PubMed1985

Hypotensive actions of ketanserin in dogs: involvement of a centrally mediated inhibition of sympathetic vascular tone.

The intravenous (i.v.) administration of ketanserin (0.1-0.4 mg/kg) produced immediate and sustained decreases in systemic blood pressure and heart rate in pentobarbitone-anaesthetized dogs. These doses of ketanserin did not inhibit common carotid vasoconstrictor responses to intraarterial (i.a.) noradrenaline, pre-ganglionic stimulation of the sectioned cervical sympathetic nerve, or i.v. nicotine, thus the effects of ketanserin are not due to blockade of vascular alpha-adrenoceptors, adrenergic neurone blockade, or ganglionic blockade. Systemic pressor responses to i.v. nicotine, which produces sympathetic activation by both central and ganglionic stimulating actions, and to common carotid artery occlusion, were inhibited by 0.1-0.4 mg/kg of ketanserin i.v. These results suggest that in the anaesthetized dog, the hypotensive action of ketanserin involves a centrally mediated inhibition of sympathetic tone. Peripheral vascular 5-HT2 receptor blockade does not appear to be responsible for the hypotensive effect of ketanserin in this model, although this does not preclude the involvement of such a mechanism in its clinical antihypertensive action.

Animals↗