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Results for “Ganglionic Blockers”

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PubMed2000

Involvement of central and peripheral cannabinoid receptors in the regulation of heart resistance to arrhythmogenic effects of epinephrine.

Intravenous injection of the selective cannabinoid receptor agonist HU-210 in doses of 0.05 and 0.25 mg/kg increased heart resistance to arrhythmogenic effects of epinephrine, while intracerebroventricular infusion of this substance had no effect on the incidence of epinephrine-induced arrhythmia. The selective antagonist of type I cannabinoid receptors SR141716A in a dose of 3 mg/kg and ganglion blocker hexamethonium in a dose of 10 mg/kg did not modify the antiarrhythmic effect of HU-210. This effect of HU-210 is probably related to activation of type II peripheral cannabinoid receptors.

Animals↗

PubMed1996

Rat exocrine pancreatic secretion by vagal stimulation occurs via multiple mediators.

The vagus is a mixed nerve containing cholinerrgic and non-cholinergic neurons. Vagal fibers interact with peptidergic neurons of the enteric nervous system which stain immunohistochemically for cholecystokinin, vasoactive intestinal polypeptide, and gastrin releasing peptide. The contribution of these peptidergic neurons in the pancreatic response to vagal stimulation is unknown. We tested the effect of specific inhibitor of these stimulants against vagally mediated exocrine secretion in rats. The response to vagal stimulation was blocked significantly by each of the following: the ganglionic blocker hexamethonium (100% inhibition); the muscarinic, cholinergic blocker atropine (85% inhibition); the specific cholecystokinin-A receptor blocker (91% inhibition); and a vasoactive intestinal polypeptide polyclonal antibody (89% inhibition). This observation is consistent with the hypothesis that potentiating interactions among several agonists mediate the vagal response. Our study, however, dose not exclude acetylcholine as the final common mediator.

Amylases↗

PubMed1994

Parasympathetic-mediated reflex salivation and vasodilatation in the cat submandibular gland.

The aim of the present study was to compare and characterize the secretory and vasodilator effects induced by chorda lingual nerve (CLN) stimulation (i.e., direct parasympathetic stimulation) and reflex parasympathetic stimulation in the submandibular gland (SMG) of sympathectomized cats. The increase in blood flow and salivary secretion in response to electrical stimulation of the central cut ends of the vagus and inferior alveolar nerves, as well as to stimulation of the CLN at a site approximately 5 mm distal to the intersection of the CLN and the SMG duct (site D) was completely abolished by section of the chorda tympani nerve (CTN). Neither response to CLN stimulation at a site nearly 5 mm proximal to the intersection of the CLN and the SMG duct (site C) was affected by CTN section. Section of the CLN at a site approximately 5 mm distal to the intersection of the CTN and the CLN abolished the submandibular salivary and vasodilator responses elicited by CLN stimulation at site D but had no effect on the two responses evoked by CLN stimulation at site C. The blood flow increases evoked by electrical stimulation of the CLN at site D were greatly reduced by prior treatment with the autonomic ganglion blocker hexamethonium, but the vasodilator responses evoked from site C were reduced much less. These data suggest that the secretory and vasodilator responses elicited by CLN stimulation at site D and those by vagus and inferior alveolar nerve stimulation are mediated largely via a parasympathetic reflex mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1997

Effects of adenosine and adenosine analogues on mean circulatory filling pressure and cardiac output in anesthetized rats.

The effects of adenosine and adenosine analogues, 2-[p-(2-[carboxyethyl) phenethylamino]-5'-N-ethylcarboxamidoadenosine (CGS 21680) and N6-2-(4-aminophenyl)-ethyladenosine (APNEA), on mean arterial pressure, cardiac output, mean circulatory filling pressure, arterial resistance, venous resistance and heart rate in untreated or treated (with ganglion-blockers mecamylamine and atropine) pentobarbital-anesthetized rats were examined. Infusion of adenosine (100, 300 and 900 microg/kg/min), CGS 21680 (0.1, 0.3 and 0.9 microg/kg/min) or APNEA (1.0, 3.0 and 9.0 microg/kg/min) reduced mean arterial pressure and arterial resistance in all groups. Adenosine and APNEA also reduced mean circulatory filling pressure, venous resistance and heart rate in untreated animals. Furthermore, APNEA but not adenosine reduced cardiac output. In contrast, CGS 21680 increased cardiac output and heart rate but did not have any effect on mean circulatory filling pressure or venous resistance. In ganglion-blocked rats, APNEA reduced cardiac output, mean circulatory filling pressure and heart rate, while adenosine did not have any effect on these parameters. In addition, APNEA and adenosine reduced arterial resistance but were unable to alter venous resistance while CGS 21680 reduced mean circulatory filling pressure and arterial resistance but did not further affect cardiac output, heart rate and venous resistance in ganglion-blocked animals. The results of the present study suggest that adenosine and APNEA dilate arterioles and vein, whereas CGS 21680 causes arterial dilatation but not venodilatation in untreated animals due to hypotension-induced sympathetic activation. A possible explanation for the present observations could be differences in the distribution of vascular A2 versus A3 adenosine receptors in the venous circulation.

Adenosine↗

PubMed2001

Is compensatory vasoconstrictor tone in the hindquarter vascular region induced by hemorrhage in conscious spontaneously hypertensive rats?

We investigated whether a compensatory vasoconstrictor action would be induced by a hypotensive intervention in the hindquarter vascular region of conscious spontaneously hypertensive rats (SHRs). Mean arterial pressure and hindquarter blood flow were recorded. After hemorrhage (withdrawing blood, 0.3 ml/100 g body weight), hindquarter resistance (HQR) was increased significantly. The decrease in HQR induced by the administration of a ganglionic blocker (C6; 25 mg/kg, i.v.) was significantly greater in SHRs with hemorrhage than in those without hemorrhage. The present results suggest that a detectable hindquarter compensator tone occurs due to hemorrhage in SHRs, although an abnormal substantial vasoconstrictor tone already exists in the hindquarters.

Animals↗

PubMed1994

The pharmacology of the nicotinic antagonist, chlorisondamine, investigated in rat brain and autonomic ganglion.

1. A single administration of the ganglion blocker, chlorisondamine (10 mg kg-1, s.c.) is known to produce a quasi-irreversible blockade of the central actions of nicotine in the rat. The mechanism of this persistent action is not known. It is also unclear whether chlorisondamine can block neuronal responses to excitatory amino acids and whether chronic blockade of nicotinic responses also occurs in the periphery. 2. Acute administration of chlorisondamine (10 mg kg-1, s.c.) to rats resulted in a blockade of central nicotinic effects (ataxia and prostration) when tested 1 to 14 days later, but caused no detectable cell death in tissue sections sampled throughout the rostrocaudal extent of the brain which were stained in order to reveal neuronal degeneration. 3. Long-term blockade of central nicotinic effects by chlorisondamine was not associated with significant alterations in the density (Bmax) of high-affinity [3H]-nicotine binding to forebrain cryostat-cut sections. 4. In cultured dissociated mesencephalic cells of the foetal rat, chlorisondamine and mecamylamine inhibited [3H]-dopamine release evoked by N-methyl-D-aspartate (NMDA, 10(-4) M), but only at high concentrations (IC50 approx. 600 and 70 microM, respectively). A high concentration of chlorisondamine (10(-3) M) had no effect on responses to quisqualate (10(-5) M) and only slightly reduced responses to kainate (10(-4) M). Mecamylamine (10(-3) M) was ineffective against both agonists. 5. In adult rat hippocampal slices, chlorisondamine depressed NMDA receptor-mediated synaptically-evoked field potentials, but again only at high concentrations (10(-4)-10(-3) M). Synaptic responses that were mediated by non-NMDA excitatory amino acid receptors were less affected. 6. In rat isolated superior cervical ganglion, electrically-evoked synaptic transmission was reduced 1 h after acute in vivo administration of chlorisondamine (0.1 mg kg-1, s.c.). However, in vivo administration of a higher dose (10 mg kg-1, s.c.) did not significantly affect ganglionic transmission when tested two weeks later, despite the continued presence of central nicotinic blockade.7. These results indicate that the persistent CNS nicotinic blockade by chlorisondamine is not accompanied by changes in nicotinic [3H]-nicotine binding site density or by neuronal degeneration in the brain; that at doses sufficient to produce nicotinic receptor blockade, chlorisondamine acts in a pharmacologically selective manner; and that chronic central blockade is not accompanied by long-term peripheral ganglionic blockade.

Amino Acids↗

PubMed1989

Characterization of the muscarinic and serotoninergic receptors of the intestine of the rainbow trout (Salmo gairdneri).

The ability of carbachol and 5-hydroxytryptamine (5-HT) to contract isolated segments of rainbow trout intestine in a concentration-dependent manner indicates the presence of muscarinic and serotoninergic receptors in this tissue. The activity of these agonists appears to be directly on the smooth muscle, since ganglionic blockers and inhibitors of neurotransmission did not inhibit contractions. The carbachol-induced contractions were selectively inhibited by atropine and (+-)-3-quinuclidinyl xanthene-9-carboxylate hemioxalate hydrate, an M-2 muscarinic receptor antagonist. However, the inhibition was not competitive. McN-A-343, an M-1 muscarinic agonist had no effect on intrinsic tone. The 5-HT-induced contractions were selectively inhibited by methysergide and the 5-HT2 receptor blockers, ketanserin and 1-(1-naphthyl)piperazine. Again, the inhibition by these agents was not competitive. 5-HT1 and 5-HT3 receptor antagonists did not inhibit contractions. The results thus suggest that the smooth muscle of the rainbow trout intestine contains M-2 muscarinic and 5-HT2 receptors.

Animals↗

PubMed2005

Intravenous adenosine protects the myocardium primarily by activation of a neurogenic pathway.

Endogenous adenosine is a trigger for ischemic myocardial preconditioning (IPC). Although intravascular administration of adenosine has been used to further unravel the mechanism of protection by IPC, it is questionable whether adenosine and IPC employ the same signaling pathways to exert cardioprotection. We therefore investigated whether the active metabolic barrier of the endothelium prevents an increase in myocardial interstitial adenosine concentrations by intravenous adenosine, using microdialysis, and also the role of NO and activation of a neurogenic pathway in the cardioprotection by adenosine. In pentobarbital-anesthetized rats, area at risk and infarct size (IS) were determined 120 min after a 60-min coronary artery occlusion (CAO), using trypan blue and nitro-blue-tetrazolium staining, respectively. IPC with a single 15-min CAO and a 15-min adenosine infusion (ADO, 200 microg min(-1) i.v.) limited IS to the same extent (IS = 41 +/- 6% and IS = 40 +/- 4%, respectively) compared to control rats (IS = 63 +/- 3%, both P < 0.05). However, IPC increased myocardial interstitial adenosine levels seven-fold from 4.3 +/- 0.7 to 27.1 +/- 10.0 microM (P < 0.05), while ADO had no effect on interstitial adenosine (4.1 +/- 1.2 microM), or any of the other purines. The NO synthase inhibitor N(omega)-nitro-L-arginine (LNNA), which did not affect IS (IS = 62 +/- 3%), attenuated the protection by ADO (IS = 56 +/- 3%; P < 0.05 vs ADO, P = NS vs LNNA). The ganglion blocker hexamethonium, which had also no effect on IS (IS = 66 +/- 3%), blunted the protection by ADO (IS = 55 +/- 4%; P < 0.05 vs ADO and vs hexamethonium). These observations demonstrate that cardioprotection by ADO is dependent on NO, and is primarily mediated by activation of a neurogenic pathway.

Adenosine↗

PubMedDate not supplied

Effects of ganglionic blockade on noradrenaline release and cell injury in the acutely ischemic rat myocardium.

We investigated the mechanisms responsible for ischemia-induced myocardial noradrenaline release in pentobarbitone-anaesthetized rats with left coronary artery occlusion. By means of tissue analysis of catecholamines and the Hillarp-Falck fluorescence histochemical technique for visualizing catecholamines in tissues, we studied the effect of a ganglionic blocker (chlorisondamine 0.1 mg/kg i.v.) on the ischemia-induced changes of the myocardial adrenergic nerve endings. In addition, the myocardial creatine kinase activity and potassium content were determined to estimate the extent of ischemic cell injury. In rats treated with either saline or chlorisondamine, the tissue noradrenaline content of the ischemic left ventricle was markedly reduced after 2.5 h of coronary ligation. In saline-treated rats 0.5 h of ischemia caused a slight decrease in left ventricular noradrenaline content, and this tended to be even less marked in chlorisondamine-treated animals. The changes in catecholamine fluorescence of the acutely ischemic myocardium seen after ganglionic blockade were essentially the same in both groups, but the size of the regions with reduced catecholamine fluorescence was more variable in the chlorisondamine-treated rats. Chlorisondamine caused a reduction in arterial blood pressure and heart rate and tended to reduce the degree of ischemic cell damage. We conclude that in our model the decrease in myocardial noradrenaline content after 2.5 h of ischemia is largely due to a local, nerve impulse--independent release of noradrenaline caused by ischemic changes in the tissue. The acute release of noradrenaline seen during 0.5 h of ischemia may be the combined result of local, ischemia-induced release of noradrenaline and an increased sympathetic nerve activation of the heart.

Animals↗

PubMed1993

5-HT1C/5-HT2 receptor blockade prevents 1-(2,5-dimethoxy-4-iodophenyl)2-aminopropane-, but not stress-induced increases in brain tryptophan.

We have previously shown that acute administration of the 5-HT1C/5-HT2 receptor agonist, 1-(2,5-dimethoxy-4-iodophenyl)2-aminopropane (DOI), elevates brain tryptophan levels. The present work aimed to investigate the mechanisms responsible for this elevation. Acute s.c. administration of a 2-mg/kg dose of DOI increased brain tryptophan levels but did not affect either plasma free tryptophan, plasma total tryptophan, brain 5-HT, or brain 5-hydroxyindoleacetic acid. Pretreatment with the 5-HT1C/5-HT2 receptor antagonist, LY 53857, prevented the DOI-induced increase in brain tryptophan levels, whilst the increase was reduced by the 5-HT2 receptor/alpha 1-adrenoceptor antagonist, ketanserin, and to a lesser extent, by the ganglionic blocker, chlorisondamine. On the other hand, pretreatment with either the peripherally acting 5-HT1C/5-HT2 receptor blocker, BW 501C67, the 5-HT uptake enhancer, tianeptine, the 5-HT uptake blocker, paroxetine, or the beta 2-adrenoceptor antagonist, ICI 118.551, proved ineffective. Lastly, pretreatment with LY 53857 did not affect the immobilization-induced elevation in brain tryptophan levels. It is concluded that the elevation in brain tryptophan levels induced by DOI but not that induced by stress is due to central 5-HT1C and 5-HT2 receptor stimulation.

Adrenergic beta-Antagonists↗

PubMed1992

Reflex cardiovascular response to exercise is modulated by circulating vasopressin.

Peripheral vasopressin (AVP) can act centrally to sensitize the arterial baroreflex and/or peripherally to attenuate regional blood flow by a direct vascular effect. Because plasma concentrations of AVP increase during exercise, this study examined the possibility that AVP is capable of modulating the reflex cardiovascular response to static muscle contraction. Thus, in anesthetized cats, the pressor [mean arterial pressure (MAP)], myocardial contractile (dP/dt), and heart rate responses to 30-45 s of electrically induced static contraction of the hindlimb muscles were compared before and after intravenous injection of the V1 receptor antagonist d[CH2)5Tyr(Me)]-AVP (V1-x, n = 7), V1-x plus the V2 receptor antagonist [d(CH2)5,D-Phe2,Ile4,Arg8,Ala9]vasopressin (V2-x, n = 5), or the ganglionic blocker hexamethonium chloride (n = 5). In three additional cats, the contraction-induced cardiovascular response was monitored before and after injection of V1-x + V2-x and after hexamethonium. Subsequent to treatment with V1-x, the MAP and dP/dt responses to contraction were augmented by 18 +/- 5 and 22 +/- 10%, respectively (P < 0.05). After injection of V1-x + V2-x, the MAP and dP/dt responses were augmented to a similar extent (32 +/- 6 and 40 +/- 17%, respectively; P < 0.05). However, there was no difference in the magnitude of augmentation of these responses between the two conditions. The heart rate response was not altered by either treatment. Ganglionic blockade eliminated the cardiovascular responses to contraction. Last, when the pressor and contractile responses to contraction were initially augmented by administration of V1-x + V2-x, subsequent ganglionic blockade abolished the entire cardiovascular response.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2006

Central action of increased osmolality to support blood pressure in deoxycorticosterone acetate-salt rats.

To test the hypothesis that increased osmolality contributes to hypertension in deoxycorticosterone acetate (DOCA)-salt-hypertensive rats by acting in the brain, DOCA-salt and Sham-salt rats were instrumented with bilateral, nonoccluding intracarotid and femoral catheters. Two weeks prior, rats were uninephrectomized and received subcutaneous implants with or without DOCA (65 mg) and began drinking salt water (1% NaCl and 0.2% KCl). DOCA-salt rats (n=28) exhibited elevated blood pressure (159+/-4 mm Hg; P<0.05) and heart rate (392+/-10 bpm; P<0.05) compared with Sham-salt animals (n=5; blood pressure: 107+/-5 mm Hg; heart rate: 355+/-10 bpm). Bilateral intracarotid infusion of hypotonic fluid (osmolality: approximately 40 mOsm/L), which lowers osmolality of blood to the brain by approximately 2%, rapidly decreased blood pressure in DOCA-salt rats (-22+/-4 mm Hg after 15 minutes; P<0.05; n=7) but not Sham-salt rats (2+/-2 mm Hg; n=5). Hypotonic fluid infused intravenously did not lower blood pressure (0+/-2 mm Hg) in DOCA-salt rats (n=7). In DOCA-salt rats pretreated with a V(1) vasopressin antagonist (Manning compound, 5 microg, IV), intracarotid hypotonic infusion still decreased blood pressure (-10+/-3 mm Hg; P<0.05; n=9), but the response was smaller (P<0.05). Finally, in DOCA-salt rats (n=4) pretreated with the V(1) antagonist and the ganglionic blocker hexamethonium, decreasing osmolality of blood to the brain did not reduce blood pressure. These data indicate that, in DOCA-salt rats, hypertonicity acts in the brain to support blood pressure, in part by stimulating vasopressin secretion and in part by stimulating another rapidly reversible mechanism, likely the sympathetic nervous system.

Animals↗

PubMed1993

Neuroleptics induce penile erection in the rabbit.

1. Intramuscular (i.m.) administration of the neuroleptics chlorpromazine, haloperidol and spiperone at doses ranging from 0.1 to 0.4 mg/kg in male rabbits induced a dose-dependent penile erection. 2. The i.m. administration of the alpha 1-adrenoceptor antagonists prazosin and bunazosin (0.1-0.4 mg/kg), induced a dose-dependent penile erection. However, that of the peripheral dopamine receptor antagonist domperidone (0.4-4.0 mg/kg) and the dopamine receptor agonist apomorphine (0.1-1.0 mg/kg) did not. Penile erection was not induced by i.m. injection of chlorpromazine in combination with intrapenile administration of the alpha 1-adrenoceptor agonist methoxamine. 3. Penile erection was induced by the administration of chlorpromazine (0.25-1.00 mg/body) into the lateral cerebral ventricle. At a low dose, however, the administration of chlorpromazine into the lateral ventricle induced a less notable penile erection than that induced intramuscularly. 4. Penile erection was induced by i.m. injection of the ganglionic blocker hexamethonium (5-20 mg/kg). When chlorpromazine was given after pretreatment with hexamethonium, penile erection was more notable than that induced by either drug given alone. 5. These results suggest that neuroleptics could act locally in the penile structure to cause penile erection by alpha 1-adrenoceptor-blocking actions.

Adrenergic alpha-Agonists↗

PubMed1993

Reflex vasodilatation in the cat lip elicited by stimulation of nasal mucosa by chemical irritants.

Local application of capsaicin (threshold dose 150 microM) or nicotine (threshold dose 15 mM) to the nasal mucosa as well as electrical stimulation (threshold intensity 10 V) of the nasal mucosa elicited dose- or intensity-dependent blood flow increases in the ipsilateral lower lips of the anesthetized cats. Pretreatment with 3 mM capsaicin applied locally to the nasal mucosa abolished or reduced the vasodilation in response to capsaicin, nicotine, and ammonia vapor but not to light mechanical or electrical stimulation of the nasal mucosa. The blood flow increases elicited by all above stimuli were greatly reduced by pretreatment with hexamethonium, an autonomic ganglion blocker. These results suggest that stimulation of the nasal mucosa by chemical (capsaicin, nicotine, ammonia), mechanical, or electrical methods elicits the autonomic reflex vasodilatation in the cat lower lips. Furthermore, there seem to be at least two types of afferent fibers in the nasal mucosa of the cats: one type is capsaicin-sensitive fibers, while another type is capsaicin-resistant fibers involved in reflex vasodilatation.

Ammonia↗

PubMed2006

Esophageal-gastric relaxation reflex in rat: dual control of peripheral nitrergic and cholinergic transmission.

It has long been known that the esophageal distension produced by swallowing elicits a powerful proximal gastric relaxation. Gastroinhibitory control by the esophagus involves neural pathways from esophageal distension-sensitive neurons in the nucleus tractus solitarius centralis (cNTS) with connections to virtually all levels of the dorsal motor nucleus of the vagus (DMV). We have shown recently that cNTS responses are excitatory and primarily involve tyrosine hydroxylase-immunoreactive cells, whereas the DMV response involves both an alpha1 excitatory and an alpha2 inhibitory response. In the present study, using an esophageal balloon distension to evoke gastric relaxation (esophageal-gastric reflex, EGR), we investigated the peripheral pharmacological basis responsible for this reflex. Systemic administration of atropine methyl nitrate reduced the amplitude of the gastric relaxation to 52.0+/-4.4% of the original EGR, whereas NG-nitro-L-arginine methyl ester (L-NAME) reduced it to 26.3+/-7.2% of the original EGR. Concomitant administration of atropine methyl nitrate and L-NAME reduced the amplitude of the gastric relaxation to 4.0+/-2.5% of control. This reduction in the amplitude of induced EGR is quite comparable (4.3+/-2.6%) to that seen when the animal was pretreated with the nicotinic ganglionic blocker hexamethonium. In the presence of bethanechol, the amplitude of the esophageal distension-induced gastric relaxation was increased to 177.0+/-10.0% of control; administration of L-NAME reduced this amplitude to 19.9+/-9.5%. Our data provide a clear demonstration that the gastroinhibitory control by the esophagus is mediated via a dual vagal innervation consisting of inhibitory nitrergic and excitatory cholinergic transmission.

Animals↗

PubMed1998

Enhanced hemodynamic response to [D-ALA2,D-MET5]-methionine enkephalin (DAME) in streptozotocin-induced diabetic rats is reversed by insulin replacement.

The present study examined the alterations of hemodynamic responses to [D-ala2,D-Met5]-methionine enkephalin (DAME) in diabetic animals. Male Sprague-Dawley rats (12 weeks old) were used for this study. Diabetes was induced by a single injection of streptozotocin (65 mg/kg, i.v.). After 7 days, blood glucose levels were determined to confirm the diabetic state. Animals were anesthetized and instrumented to monitor mean arterial pressure, hindlimb bloodflow and hindlimb vascular resistance. Administration of DAME produced a significantly greater reduction in blood pressure, increase in hindlimb bloodflow and decrease in hindlimb vascular resistance in diabetic vs. control rats. These effects were blocked by naloxone. All hemodynamic changes were attenuated after pretreatment with the ganglionic blocker, hexamethonium, indicating that the responses were mediated either within the central nervous system or at the ganglia. Insulin reversed the exaggerated depressor effect of DAME on streptozotocin-treated rats. Collectively, these results suggest that diabetic rats have altered opioidergic hemodynamic responses to DAME due to mu receptor alterations in the CNS or in autonomic ganglia. These effects were reversed by replacement of insulin.

Animals↗

PubMed2002

Central Orexin-A stimulates pancreatic exocrine secretion via the vagus.

INTRODUCTION: Digestive organs are controlled from the central nervous system, and the vagus nerve plays an important role. Orexins are recently purified neuropeptides localized in neurons within the lateral hypothalamus. AIM: To examine the effects of centrally injected Orexin-A and B on pancreatic exocrine secretion in conscious rats. METHODOLOGY: Rats were prepared with cannulae draining bile and pancreatic juice separately. The experiments were conducted without anesthesia on day 4 or 5 after the operation. RESULTS: Intracerebroventricular administration of Orexin-A (0.25, 0.5, and 1.0 nmol) significantly increased pancreatic fluid and protein output in a dose-dependent manner. A significant stimulatory effect of Orexin-B was not observed. Pretreatment with the ganglion blocker hexamethonium and with atropine completely abolished the stimulatory effect of central Orexin-A. Central Orexin-A significantly increased pancreatic secretion after pretreatment with omeprazole. Intravenous injection of Orexin-A had no effect. Centrally administered Orexin-A stimulated the vagal efferent nerve in anesthetized rats. CONCLUSIONS: Centrally administered Orexin-A stimulates pancreatic exocrine secretion through the vagal efferent nerve, and the stimulatory action is independent of gastric acid secretion.

Animals↗

PubMedDate not supplied

[Ganglion block in cardiopulmonary bypass surgery].

Ganglion blockers increase the antinociceptive defense in anesthesiological support of cardiopulmonary bypass operations for mitral and aortic valve failure. Benzohexonium decreased total peripheral vascular resistance, increased cardiac and stroke indexes, and increased systolic potency of the heart. Ganglionar blocking was associated with an increase of systemic oxygen transport, arrhythmias developed rarely, blood concentrations of epinephrine, norepinephrine, ACTH, vasopressin, and leukinferon were lower.

Adrenocorticotropic Hormone↗