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Results for “Ganglionic Blockers”

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At least 1,117 records · Page 62Linked to original sources
PubMed1994

Neuronal involvement in the intestinal effects of Clostridium difficile toxin A and Vibrio cholerae enterotoxin in rat ileum.

BACKGROUND/AIMS: Activation of intestinal mast cells and neurons is involved in intestinal inflammation and diarrhea. This study compared the effects of neuronal inhibitors and inhibition of intestinal sensory afferent nerves on the intestinal actions of Clostridium difficile toxin A, an inflammatory enterotoxin, and cholera toxin, a noninflammatory enterotoxin. METHODS: The effects of lidocaine, hexamethonium, atropine, and long-term pretreatment of capsaicin on fluid secretion, mannitol permeability, myeloperoxidase (MPO) activity, and release of rat mast cell protease II (RMCPII) were measured in toxin A- and cholera toxin-exposed loops in vivo. RESULTS: Lidocaine, hexamethonium, and capsaicin, but not atropine, inhibited toxin A-mediated secretion and MPO activity, but only capsaicin reduced mannitol permeability. Lidocaine, but not capsaicin, reduced secretion and permeability caused by cholera toxin. Toxin A caused release of RMCPII from rat ileum in vivo and in vitro; this was inhibited by lidocaine or capsaicin, whereas cholera toxin had no effect on release of RMCPII. CONCLUSIONS: Neuronal mechanisms are important in the in vivo effects of these two enterotoxins. Capsaicin-sensitive sensory afferent neurons and mast cells are involved in the intestinal mechanism of toxin A, but not cholera toxin.

Animals↗
PubMed1986

Actions of cimetidine and ranitidine at some cholinergic sites: implications in toxicology and anesthesia.

Cimetidine and ranitidine are specific and potent H2-receptor antagonists widely used in the effective therapy of peptic ulcer disease. The drugs also possess other pharmacological properties unrelated to H2-receptor antagonism. More recently large experimental doses of cimetidine or ranitidine were found to have anticholinesterase, ganglion blocking and neuromuscular blocking activities. Actions of the drugs at such cholinergic sites may account for some of their clinically documented adverse effects. The toxicological implications of these findings including the potential for drug interactions to occur, especially during some anesthetic procedures, are discussed.

Anesthesia↗
PubMed1993

A study on the vasopressin induced delay in the gastrointestinal transit in mice: possible mechanism of action.

The effect of arginine vasopressin (AVP) on the gastrointestinal (GI) transit and its possible mechanism were studied using charcoal meal test in mice. A dose related inhibitory effect was recorded. The effect appears to be independent of the time allowed between AVP administration and testing. The studies on the mechanism reveal that AVP acts without involving V1 and V2 vasopressin receptors. An almost complete reversal of the effect by physostigmine and potentiation by atropine indicate that AVP might act through an inhibition of the release of acetylcholine. However, the neural nicotinic receptors mechanisms do not seem to contribute since hexamethonium failed to modify the AVP action. Further, a partial antagonism by naloxone or prazosin pretreatment indicates that opioid and alpha 1 adrenergic systems also contribute to this action of AVP. However, the effect appears to be independent of alpha 2 and beta adrenergic systems since yohimbine and propranolol failed to modify the same.

Animals↗
PubMed1990

Insulin and glucagon secretion in swimming mice: effects of autonomic receptor antagonism.

To study the regulation of islet hormone secretion in exercise-stress, we developed a swimming mouse model. Mice swam for 2, 6, or 10 minutes whereafter blood was sampled for analysis of plasma levels of insulin, glucagon, and glucose. Plasma insulin levels, which were not different from resting controls after 2 or 6 minutes of swimming, were slightly lower after 10 minutes of swimming (P less than .05). Plasma glucagon levels were increased after 2, 6, and 10 minutes of swimming (P less than .001), and plasma glucose levels were lower after 6 and 10 minutes of swimming (P less than .05). Glucose (5.6 mmol/kg)-stimulated insulin secretion was inhibited by 52% +/- 9% by the swimming (P less than .001). The mechanisms behind this inhibition of glucose-stimulated insulin secretion and the increase in basal plasma glucagon levels induced during 2 minutes of swimming were investigated by the use of autonomic receptor antagonists, administered intraperitoneally 20 minutes before the swimming period. The ganglionic antagonist hexamethonium (56 mumols/kg) prevented the swimming-induced inhibition of glucose-stimulated insulin secretion, indicating involvement of nerves in the inhibition. Also the nonselective alpha-adrenoceptor antagonist phentolamine (6.0 mumols/kg) and the alpha 2-adrenoceptor antagonist yohimbine (3.6 mumols/kg) prevented the inhibition of glucose-stimulated insulin secretion induced by swimming, whereas the beta-adrenoceptor antagonist L-propranolol (9.6 mumols/kg) had no effect. The swimming-induced increase in plasma glucagon levels was partially inhibited by hexamethonium by (58% +/- 24%, P less than .05). Phentolamine and yohimbine totally prevented the increase in plasma glucagon levels, whereas L-propranolol had no effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Role of the baroreflex in beta 2-sympathomimetic induced tachycardia in male rats.

The aim of the study was to determine whether tachycardia which is associated with the use of beta 2-sympathomimetic tocolytic agents is caused by baroreflex activation or by direct stimulation of cardiac beta-adrenoceptors. In conscious male rats, tachycardiac responses following intravenous injection of hexoprenaline, ritodrine and fenoterol were compared following (i) bilateral sinoaortic denervation (SAD) or (ii) sham-operation, and (iii) ganglionic-blockade using hexamethonium. Dose-ranges were chosen to result in similar reductions in diastolic blood pressure (DAP). Furthermore, following ganglionic blockade, the relative contribution of beta 1-adrenoceptor stimulation was assessed using the selective beta 2-receptor antagonist ICI 118,551. In intact rats, increases in HR induced by all beta-adrenoceptor agonist were comparable. In SAD and ganglion-blocked rats, DAP fell more pronounced at even lower doses. The corresponding increases in HR were approximately 3 times smaller than in intact rats but not different between agents. During ganglionic blockade ICI 118,551 significantly inhibited HR responses to fenoterol and hexoprenaline but not ritodrine. The conclusion is that in intact male rats, baroreflex activation is the major determinant of tachycardia following injection of ritodrine, fenoterol or hexoprenaline. Increasing the beta 2-selectivity of these drugs will not limit the tachycardic effects.

Adrenergic beta-Agonists↗