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 379 records · Page 21Linked to original sources
PubMed1992

Reversal of experimental hemorrhagic shock by dimethylphenylpiperazinium (DMPP).

In a rat model of hemorrhagic shock which caused the death of all control rats within 30 min, i.v. injection of the ganglion-stimulating drug dimethylphenylpiperazinium (DMPP) caused a dose-dependent reversal of the shock condition--without the need for reinfusion of the shed blood--starting from the dose of 4 ng/kg i.v. Shock reversal was associated with the mobilization of residual blood and improvement in blood flow, particularly at the carotid level. These results could influence our thinking on pathophysiology and first-aid management of shock.

Animals↗
PubMed1988

Ventricular fibrillation induced by the interaction between acute myocardial ischemia and sympathetic hyperactivity: effect of nifedipine.

Sympathetic hyperactivity plays a major role in the genesis of malignant arrhythmias during acute myocardial ischemia. An experimental model in which life-threatening arrhythmias are specifically and consistently induced by the interaction between acute myocardial ischemia and left stellate ganglion stimulation has been developed in alpha-chloralose anesthetized cats. In this preparation, drugs that share antiischemic, antiadrenergic, and specific electrophysiologic effects, such as verapamil, diltiazem, and amiodarone, were most effective. To evaluate the relative role of these different properties in mediating the effect of antiarrhythmic drugs, we used this same model to test nifedipine, a calcium channel blocker that is able to counteract the consequences of sympathetic stimulation on coronary circulation but has no electrophysiologic properties at concentrations relevant in the clinical setting. Nifedipine (15 micrograms/kg) prevented the occurrence of ventricular fibrillation in 10 of 13 animals (77%). Its efficacy was independent of changes in the peripheral hemodynamics. Plasma concentrations of nifedipine were within the therapeutic range in humans. To evaluate if this rather striking protective effect was specifically related to the prevention of the deleterious consequences of sympathetic stimulation, the effect of nifedipine on ventricular fibrillation threshold was studied in an additional group of 13 cats in the nonischemic state, during acute myocardial ischemia and during ischemia plus sympathetic stimulation. Nifedipine did not modify ventricular fibrillation threshold in nonischemic or in ischemic conditions. However, nifedipine specifically prevented the further reduction in ventricular fibrillation threshold occurring when sympathetic stimulation was superimposed on acute ischemia. These data suggest that the extension of ischemic damage by sympathetic stimulation is an important progenitor of arrhythmogenic action during acute ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1988

Smoking and mechanisms of cardiovascular control.

In humans short-term administration of nicotine, whether by smoking or intravenous injection, will typically raise blood pressure by 5 to 10 mm Hg and heart rate by 10 to 25 bpm. Smoking causes reduced myocardial contractility and left ventricular function in patients with angina pectoris or heart failure. Nicotine's mechanism of action is more complex than the classic concept of nicotinic ganglionic stimulation can account for. Nicotine exerts a potent pressor effect in the ventral lateral medulla (C-1 area). Little current data are available documenting the efficacy of centrally acting antihypertensive agents and converting-enzyme inhibitors with regard to preventing nicotine's acute cardiovascular effects.

Animals↗
PubMed1993

Effects of canine myocardial infarction on sympathetic efferent neuronal function: scintigraphic and electrophysiologic correlates.

We studied the effects of nondecentralized left stellate ganglion stimulation on regional epicardial monophasic action potential duration at 50% (APD50) and 90% (APD90) repolarization from 104 sites in 10 surviving dogs with a chronic myocardial infarction model. These effects were correlated with thallium-201 and iodine-123 metiodobenzylguanidine (MIBG) imaging to identify areas of viable but denervated myocardium. Mean infarct size was 5.2% +/- 0.8% total heart weight, and the planimetered areas of denervation were always larger (18% +/- 4% total heart area). During constant ventricular pacing, stellate stimulation tended to shorten the APD90 only in normally innervated areas (364 +/- 5 to 358 +/- 5 msec) and to increase in denervated areas (358 +/- 5 to 362 +/- 5 msec), (p value not significant (NS) for prestellate and poststellate stimulation; p < 0.05 for difference between denervated vs innervated). The APD50 significantly shortened in innervated areas from 287 +/- 5 to 270 +/- 3 msec (p < 0.05) compared with denervated areas (283 +/- 4 to 274 +/- 5 msec, p = NS). We conclude that MIBG imaging demonstration of denervation identifies areas with impaired shortening of the epicardial APD50 in response to stellate stimulation and that nontransmural myocardial infarction produces areas of denervation larger than areas of necrosis.

Action Potentials↗
PubMed1981

Extra-adrenergic mechanisms responsible for the effects of glucose-insulin-potassium solution on vulnerability to ventricular fibrillation.

In 53 chloralose-anesthetized dogs, the actions of glucose (10 mg/kg per min), insulin (0.025 U/kg per min) and potassium (0.025 mEq/kg per min) on the ventricular fibrillation and repetitive extrasystole thresholds were examined. Measurements were initially made in the control state and then repeated at 30, 60 and 120 minutes of infusion of glucose-insulin-potassium solution at a constant rate of 1.23 ml/min. The dogs received on the average 36 g of glucose, 44 U of insulin and 44 mEq of potassium over a 2 hour period. In the nonischemic myocardium, the infusion raised the threshold for ventricular fibrillation and repetitive extrasystole to a peak of 94 and 61 percent, respectively, without significantly changing serum potassium or circulating catecholamine concentration. In the ischemic myocardium, the incidence of spontaneous ventricular fibrillation during 10 minutes of coronary occlusion was reduced from 83 percent in the control state to 17 percent with glucose-insulin-potassium infusion. However, the infusion did not alter the incidence of ventricular fibrillation associated with reperfusion. Because cardio-cardiac sympathetic reflexes are elicited in response to coronary occlusion, the effect of glucose-insulin-potassium infusion on ventricular vulnerability during left stellate ganglion stimulation and norepinephrine infusion was investigated. The infusion completely prevented the reduction in the vulnerable period threshold during stellate stimulation and norepinephrine infusion. Furthermore, the peak protection afforded by the infusion was greater than that achieved with beta adrenergic blockade and was still present in catecholamine-depleted hearts. It is concluded that infusion of glucose-insulin-potassium solution protects against ventricular fibrillation in the normal and ischemic canine heart but not during reperfusion. This protection may be due in part to antagonism of adrenergic activity; however, the primary influence of the solution is mediated by extra-adrenergic mechanism.

Animals↗
PubMed1985

Extracranial vasodilation mediated by vasoactive intestinal polypeptide (VIP).

Pooled antisera to vasoactive intestinal polypeptide were used to block neurogenic extracranial vasodilatation elicited from either brainstem (locus coeruleus) or pterygopalatine ganglion stimulation in the cat. Vasodilatation was not inhibited by sham immune sera, or by antisera to bradykinin or substance P. The efferent pathway for vasodilatation from the locus coeruleus traverses the facial nerve (greater superficial petrosal branch) and the pterygopalatine and otic ganglia. Its blockade demonstrates a novel action of a peptide transmitter in the expression of a central neurogenic response.

Animals↗
PubMed1992

Effects of presynaptic alpha-adrenoceptors and neuronal reuptake on noradrenaline overflow and cardiac response.

Using an in situ perfused, innervated rat heart model, we studied the effects of presynaptic alpha-adrenergic and neuronal reuptake inhibition on evoked noradrenaline (NA) overflow and the postsynaptic response by sympathetic ganglion stimulation. NA overflow was significantly increased by neuronal reuptake inhibitors (desipramine and (+)-oxaprotiline) or by alpha-adrenoceptor antagonists (phentolamine and yohimbine), but the inotropic response was augmented only by alpha-antagonists. In the presence of desipramine, nerve stimulation induced a frequency-dependent increase in NA overflow and postsynaptic response, both were enhanced by yohimbine. In the absence of desipramine, however, postsynaptic response was potentiated by yohimbine despite an unchanged (at 2 and 5 Hz) or even reduced NA overflow (at 10 Hz). Thus, this study suggests that NA release and cardiac response are modulated by presynaptic alpha-adrenoceptors, and that the neuronal reuptake modifies the amount of NA overflow but has little effect on the postsynaptic response.

Adrenergic alpha-Antagonists↗
PubMed1992

UK-14,304, R(-)-alpha-methyl-histamine and SMS 201-995 block plasma protein leakage within dura mater by prejunctional mechanisms.

Intravenous administration of an alpha-adrenoceptor agonist, UK-14,304, a histamine H3 receptor agonist, R(-)-alpha-methyl-histamine (alpha-MeHA) or SMS 201-995 (a synthetic octapeptide analogue of somatostatin), blocked plasma protein (125I-albumin) extravasation within rat and/or guinea pig dura mater following unilateral electrical trigeminal ganglion stimulation or capsaicin administration. The extravasation caused by the administration of the neuropeptide mediator, substance P, was not inhibited by any of the three compounds. Blockade by UK-14,304 was completely antagonized by pretreatment with the highly selective alpha 2-antagonist, idazoxan, as was alpha-MeHA by pretreatment with the highly selective histamine H3 antagonist, thioperamide. Taken together, the results are consistent with blockade by prejunctional alpha 2, histamine H3 and probably somatostatin receptors which may be coupled to inhibition of neuropeptide release. Because 5-HT1-like agonists, which are useful for treating migraine and related headaches, share similar inhibitory properties in this in vivo model, the significance of prejunctional alpha 2, histamine H3 and somatostatin receptors to treatment of vascular headaches is suggested.

Adrenergic alpha-Agonists↗
PubMed1994

Developmental changes in the response of rat isolated duodenum to nicotine.

Developmental changes in the response to ganglionic stimulants, nicotine and dimethylphenylpiperazinium, were investigated in rat isolated duodenum by recording isotonic mechanical activity. The duodenal response to nicotine/dimethylphenylpiperazinium (3 x 10(-7) to 10(-3) M) in neonatal rats was contraction, which was blocked by hexamethonium, tetrodotoxin and hyoscine. The response to nicotine/dimethylphenylpiperazinium (10(-6) to 10(-4) M) in the adult duodenum was relaxation, which was blocked by tetrodotoxin and hexamethonium, but by neither guanethidine nor hyoscine. The transition of the response to nicotine/dimethylphenylpiperazinium from contraction to relaxation occurred at around the 3rd postnatal week. Nicotine-induced relaxation of adult duodenum was significantly inhibited by preincubation with alpha-chymotrypsin, a proteolytic enzyme, and a combination of nucleotide pyrophosphatase and 8-phenyltheophylline, a P1 purinoceptor antagonist. Nicotine-induced relaxation was desensitized by alpha, beta-methylene ATP, a stable P2x purinoceptor agonist. These results suggest that the contractile response of isolated duodenum to nicotine is mediated through cholinergic transmission in neonatal rats and the relaxant response is mediated through non-adrenergic, non-cholinergic transmission, which involves both peptidergic and purinergic transmission, in adult rats.

Adenosine Triphosphate↗
PubMed1985

Interaction of norepinephrine and superior cervical ganglion input in the rat pineal body.

The effects of superior cervical ganglion stimulation and the local application of norepinephrine or its antagonist propranolol were studied in 18 pineal cells. In 61% of the pineal cells, stimulation elicited excitation; the same cells also responded by excitation to norepinephrine ejection. When stimulation and norepinephrine ejection were applied together, summation (of the excitation) was observed in these cells. Several cells that failed to respond to stimulation did respond to norepinephrine ejection, but with the opposite pattern, i.e., decrease of firing rates. Propranolol prevented the norepinephrine-induced excitation and inhibition, as well as the excitation produced by stimulation. We suggest that norepinephrine regulates pineal activity by two routes: activation of the sympathetic neuronal input and inhibition by way of the circulation.

Animals↗
PubMed1991

Presynaptic modulation of release of noradrenaline from the sympathetic nerve terminals in the rat spleen.

Strips of rat spleen, loaded with [3H]NA, were superfused with Krebs' stimulated electrically at different frequencies (2, 8 and 32 Hz) with the same number of pulses and the effect of different receptor agonists and antagonists was studied on the S2/S1 ratio. Evidence has been obtained that the sympathetic nerve terminals in the spleen of the rat are equipped with presynaptic alpha 2B-adrenoreceptors, M-muscarinic, N-nicotinic and P1-purinoreceptors. Clonidine, an alpha 2-adrenoreceptor agonist, did not change the release of NA at low frequency but increased it at a high frequency of stimulation. It is suggested that clonidine is a partial agonist and reveals its antagonistic property when the biophase concentration of the full agonist, NA, released endogenously large. A novel, potent and highly selective competitive antagonist of the alpha 2-adrenoreceptor, CH-38083, enhanced significantly the release of NA, removing presynaptic negative feedback control of NA. It is suggested that the release of NA is subject to presynaptic modulation, through different presynaptic receptors and that it is involved in the communication between the central nervous system and a secondary lymphoid organ, the spleen.

Adenosine↗
PubMed1992

Evidence for inhibitory nicotinic and facilitatory muscarinic receptors in cholinergic nerve terminals of the rat urinary bladder.

Cholinergic prejunctional modulatory receptors on parasympathetic nerves in the rat urinary bladder were studied by measuring 3H-acetylcholine (ACh) release in muscle strips from the bladder body. Electrical field stimulation markedly increased 3H-ACh overflow in strips preloaded with 3H-choline. Oxotremorine (1 microM), an M2 receptor agonist and DMPP (10 microM) a nicotinic (N) receptor agonist decreased the release of ACh (50% and 55% respectively); whereas McN-A 343 (50 microM) an M1 receptor agonist increased the release (33%), indicating the presence of three types of modulatory receptors. The anticholinesterase agent, physostigmine in concentrations of 1, 5 and 25 microM and neostigmine (5 microM) increased ACh release (44-710%). However a low concentration of physostigmine (0.05 microM) decreased release. Pirenzepine, an M1 muscarinic antagonist or atropine blocked the increased ACh release in physostigmine-treated strips, but in normal strips pirenzepine did not change release and atropine increased release. McN-A 343 or prolonged application (15 min) of DMPP increased ACh release (376% and 391% respectively) in physostigmine-treated strips. The response to McN-A 343 was blocked by pirenzepine. d-Tubocurarine (DTC), a nicotinic receptor blocker, enhanced ACh release in the presence of physostigmine but proved to be ineffective in normal preparations. These findings suggest that all three cholinergic receptors (M1 facilitatory, N inhibitory and M2 inhibitory) are activated by endogenous ACh in physostigmine treated preparations whereas only M2-inhibitory receptors are activated in normal preparations. It will be important in future studies to determine whether M1 and M2 mechanisms can also be activated under more physiological conditions in the bladder and whether they are present at other cholinergic synapses.

Acetylcholine↗
PubMed1995

The opioid/anti-opioid balance in shock: a new target for therapy in resuscitation.

Teleologically, pain is of paramount importance for survival and induces the organism to cope in an active way with aggressions from a basically hostile environment. While the activation of endogenous analgesic (opioid) systems typically occurs in conditions of surrender (pre-terminal conditions, sustained tortures, etc.), the activation of endogenous anti-analgesic systems triggers mechanisms of active or passive defence (such as camouflage) aimed at survival. The distinctive features of the main anti-analgesic systems (melanocortinergic, cholecystokininergic, thyroliberinergic) and the dramatic results obtained in experimental pre-terminal conditions (hemorrhagic shock, prolonged respiratory arrest) with the administration of their neuropeptide transmitters (ACTH and several ACTH-fragments, including alpha-MSH, CCK peptides and thyrotropin-releasing hormone) are here reviewed. The study of the mechanisms underlying the resuscitating effects of these neuropeptides has led to the discovery of the (often extremely potent) resuscitating effect of other drugs (protoveratrines, nicotine, centrally-acting cholinergic agents, ganglion-stimulating drugs). It is particularly remarkable that in pre-terminal conditions these neuropeptides and drugs have highly impressive effects on cardiocirculatory parameters at doses that are almost or actually inactive under normal conditions, and that their resuscitating effect is obtained without the need for any other supportive treatment and at dose-levels well below toxic ranges. Finally, in hemorrhage-shocked animals, the treatment with anti-analgesic neuropeptides shortly after bleeding considerably extends the time-limit for an effective and definitively curing blood reinfusion. This would be of self-evident importance in clinical practice, because an extremely simple, non-toxic first-aid treatment in the field, shortly after a massive hemorrhage, could resuscitate the patient for a period sufficient to effectively set up the most appropriate in-hospital treatment.

Adrenocorticotropic Hormone↗
PubMed1976

A comparative study of the effects induced by MCN-A-343 and acetylcholine on the isolated toad rectus abdominis.

McN-A-343 (McN), a non nicotinic ganglionic stimulant, induced slow contractile responses of the toad rectus abdominis. A relaxation was also observed when large doses were added in the presence of a contraction caused by acetylcholine (Ach). The relaxation induced by McN could not be overcome by increasing Ach concentration. Bell-shaped log dose-response curves were obtained for McN. d-Tubocurarine caused an unusual change on these curves, suggesting an indirect action of the agonist. This possibility was corroborated by the fact that hemicholinium, procaine, and cold storage of the muscle caused a marked decrease of the organ sensitivity to McN but not to ACh.

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

Histochemical demonstration of nerve cell bodies in the retractor penis muscle and the penile artery of the bull.

The presence of single nerve cell bodies and small ganglia in the retractor penis muscle and the penile artery of the bull was demonstrated by using antisera to neurofilament protein and neuron specific enolase. In the retractor penis muscle the findings were confirmed by staining for acetylcholinesterase. It was also shown that relaxation of strips of the retractor penis muscle induced by 70 microM acetylcholine was totally blocked by a 2.0 microM concentration of the ganglionic blocking drug chlorisondamine. The hypothesis is presented that the relaxation of the bovine retractor penis muscle and the bovine penile artery induced by nicotinic ganglionic stimulating drugs is at least in part mediated via receptors located on the nerve cell bodies described in this study.

Acetylcholine↗
PubMed2005

The role of mast cells in migraine pathophysiology.

Mast cells are critical players in allergic reactions, but they have also been shown to be important in immunity and recently also in inflammatory diseases, especially asthma. Migraines are episodic, typically unilateral, throbbing headaches that occur more frequently in patients with allergy and asthma implying involvement of meningeal and/or brain mast cells. These mast cells are located perivascularly, in close association with neurons especially in the dura, where they can be activated following trigeminal nerve, as well as cervical or sphenopalatine ganglion stimulation. Neuropeptides such as calcitonin gene-related peptide (CGRP), hemokinin A, neurotensin (NT), pituitary adenylate cyclase activating peptide (PACAP), and substance P (SP) activate mast cells leading to secretion of vasoactive, pro-inflammatory, and neurosensitizing mediators, thereby contributing to migraine pathogenesis. Brain mast cells can also secrete pro-inflammatory and vasodilatory molecules such as interleukin-6 (IL-6) and vascular endothelial growth factor (VEGF), selectively in response to corticotropin-releasing hormone (CRH), a mediator of stress which is known to precipitate or exacerbate migraines. A better understanding of brain mast cell activation in migraines would be useful and could lead to several points of prophylactic intervention.

Animals↗