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PubMed1994

Effects of berberine on delayed afterdepolarizations in ventricular muscles in vitro and in vivo.

The effects of berberine on delayed afterdepolarizations in ventricular muscles in vitro and in vivo were investigated to help explain the mechanisms for its antiarrhythmic action. Berberine 3 mumol reduced the amplitude of delayed afterdepolarizations induced by ouabain or posthypoxic reoxygenation and abolished subsequent triggered activity in isolated guinea pig right ventricular papillary muscles. At 30 mumol, it decreased the incidence of delayed afterdepolarizations, associated with a further decrease in the amplitude of delayed afterdepolarizations. In rabbit left ventricular (LV) muscles in vivo, berberine 1 mg/kg intravenously (i.v.) decreased the amplitude of delayed afterdepolarizations evoked by ouabain and calcium gluconate from 9.6 +/- 1.9 to 6.8 +/- 0.8 mV and left stellate ganglion stimulation from 9.4 +/- 2.1 to 6.2 +/- 0.7 mV and blocked ventricular arrhythmias. After a 4-mg/kg i.v. bolus, the drug inhibited and even completely abolished development of delayed afterdepolarizations, yet still reduced maximal velocity of depolarization in isolated and in vivo ventricular muscles. Therefore, one of the important mechanisms for antiarrhythmic action of berberine may be suppression of delayed afterdepolarizations, which may be attributable in part to a decrease in Na+ influx.

Animals↗
PubMed1991

Cholinergic and noncholinergic submucosal neurons dilate arterioles in guinea pig colon.

Outside diameter of isolated submucosal arterioles in guinea pig colon were monitored to examine vasodilator innervation to these gastrointestinal microvessels. Electrical stimulation of intrinsic submucosal ganglia dilated submucosal arterioles that had been preconstricted with vasopressin or norepinephrine. In approximately 50% of arterioles examined, the muscarinic receptor antagonist 4-diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP, 10 nM) abolished nerve-evoked vasodilations; 4-DAMP (500 nM) only partially inhibited the response in the other 50%. No significant differences in the nerve-evoked vasodilations were observed after extrinsic denervation of sympathetic and sensory fibers and removal of myenteric neurons by surgical myectomy. Immunohistochemistry demonstrated both substance P (SP) and vasoactive intestinal polypeptide (VIP) fiber projections to arterioles after sensory denervation and myectomy. Superfusion with muscarine and SP, but not with VIP or calcitonin gene-related peptide (CGRP), also dilated the arterioles; concentrations of muscarine and SP producing half-maximal responses were 35 and 6 nM, respectively. However, local pressure ejection of both CGRP and VIP dilated the arterioles. The SP receptor antagonist [D-Arg1,D-Phe5,D-Trp7,9,Leu11]SP reduced vasodilations in response to ganglionic stimulation as well as to pressure ejection of both SP and VIP. This study demonstrates that submucosal arterioles in the guinea pig distal colon receive a cholinergic as well as a noncholinergic vasodilator input from neurons in the submucosal plexus. SP and VIP are both likely candidates as the noncholinergic vasodilator transmitter to colonic gastrointestinal microvessels.

Animals↗
PubMed1985

Optical recording of membrane potential responses from early embryonic chick ganglia using voltage-sensitive dyes.

Changes in absorbance of voltage-sensitive merocyanine-rhodanine dyes were used to monitor electrical responses in the semilunar ganglion of 4-10-day-old developing chick embryos. The electrical responses were simultaneously recorded from many positions in the ganglion. Stimulation of the afferent nerve fibers (the ophthalmic division of cranial nerve V) with a suction electrode led to changes in light absorption of the stained ganglia. With both the depolarizing and hyperpolarizing pulses, the change was largest at 700 nm and was eliminated at a wavelength of 620 nm where the voltage-dependent absorption change of the dyes disappears. In the 4-10-day-old embryonic ganglia, two types of optical membrane potential responses, 'non-conducted' and 'conducted' responses, were identified. The non-conducted response varied with the intensity of the stimulus and had the nature of an electrotonic spread. Furthermore, this non-conducted response exhibited an 'initial upstroke-response' followed by the steady-state plateau evoked by larger depolarizing pulses. The conducted responses were blocked by tetrodotoxin (TTX) or by high external potassium concentration. The incidence of the conducted responses increased as development proceeded from the 5th to the 10th day of age. Thus, the TTX-sensitive action potential activity is probably generated initially in the semilunar ganglion during the 5-10-day-stage of development. These data represent the first demonstration of membrane potential responses in early embryonic intact nervous system. Furthermore, these studies demonstrate the usefulness of voltage-sensitive dyes in the analysis of the organizing process of embryonic neuronal functions during these early stages of development.

Animals↗
PubMed1980

Absence of stellate ganglion influence on alveolar-duct constriction.

Previous work has shown decreased lung compliance with high wash fluid surface tensions, but normal ratios of lung weight to body weight during stellate ganglion stimulation (SGS) in cats and monkeys. In the present study, effects of SGS on diameters of alveolar ducts were determined in spontaneously breathing cats under ketamine anesthesia. Compliance and pulmonary resistance were also measured. A fluorocarbon cooled to - 100 degrees C was poured onto an exposed lung lobe after rapidly opening the chest after sham operation and during SGS. Examination of the outer 2 mm of the lungs by light microscopy revealed no alveolar-duct constriction by SGS, although compliance decreased by 15%. Pulmonary resistance was unchanged. Alveolar-duct diameters were 157 +/- 4.3 micron (mean +/- SEM) in control animals and 163 +/- 4.6 micron in SGS cats. Absence of alveolar-duct constriction suggests that peripheral airway constriction did not contribute to the decrease in compliance during SGS.

Airway Resistance↗
PubMed1986

Suppression of pain in trigeminal neuropathy by electric stimulation of the gasserian ganglion.

Lesions of the peripheral part of the trigeminal nerve may cause trigeminal neuropathy associated with severe pain. Such pain usually does not respond to carbamazepine and analgesics, and it is continuous and lacks the characteristic paroxysmal character of tic douloureux. These patients often present with complex changes of facial sensibility in the form of dysesthesia, hyperalgesia, and allodynia. The pain sometimes responds favorably to transcutaneous nerve stimulation, but direct stimulation of the trigeminal ganglion and rootlets via an implanted electrode provides a greater likelihood of pain relief. Fourteen patients diagnosed as having painful trigeminal neuropathy received implants of a gasserian ganglion-stimulating electrode. The mean follow-up period is 4 years (range, 1 to 7 years). Eleven of the patients have retained the pain-relieving effect, and 1 had pain disappear without further stimulation. Eight of the patients estimated their pain relief to be complete or very good. There were no serious complications, but in several of the patients the electrode had to be exchanged because the insulation of the lead wires broke. For the selection of patients for permanent electrode implantation, a method has been developed for trial stimulation via a percutaneous electrode introduced into the trigeminal cistern. Temporary trial stimulation can be performed for several days. It is concluded that stimulation of the trigeminal ganglion and rootlets with the aid of an implanted electrode may effectively relieve certain forms of trigeminal pain that are otherwise extremely difficult to manage.

Adult↗
PubMed1981

Stellate ganglion influence on static compliance and surface layer lipids in cat lungs.

In order to determine the effects of stellate ganglion stimulation (SGS) on static lung compliance, pressure-volume relationships were measured on lungs in situ in cats anesthetized with ketamine. The lungs were inflated with 100% oxygen to 100, 93.75, 87.5, 81.25, 75, 50, and 25% TLC as determined at 20 cm H2O transpulmonary pressure. After a maximal filling, lungs were inflated twice to each volume, alternating unstimulated and SGS conditions. Static lung compliance was decreased by SGS at 93.75 (5.7 +/- 0.4 (SE) vs. 5.4 +/- 0.4 ml/cm H2O; P less than 0.05) and 87.5% TLC (6)6 +/- 0.6 vs 6.0 +/- 0.5 ml/cm H2O; P less than 0.05). In order to assess possible effects of SGS on surfactant that might be related to the loss of compliance, lung lipids and proteins obtained during SGS were quantitated. Total phospholipid (TPL) increased from 3.22 +/- 0.33 to 4.16 +/- 0.23 mg/g lung after 1 min 7V SGS (P less than 0.05) and to 4.58 +/- 0.61 mg/g lung after 4 min 20V (P less than 0.05). The ratio of cholesterol (chol) to disaturated phosphatidylcholine (DSPC) decreased after 4 and 6 min, and may have resulted in increased surface tension forces at high lung volumes. The data from this study lend support to previous findings which showed that the compliance decrease during SGS may be related to increased surface tension forces.

Animals↗
PubMed1998

Blockade of the reward-potentiating effects of nicotine on lateral hypothalamic brain stimulation by chlorisondamine.

Chlorisondamine, a quarternary nicotinic antagonist, was given in a dose that crosses the blood-brain barrier, is taken up and concentrated intracellularly by dopaminergic neurons, and induces long-term blockade of the locomotor stimulant and rewarding effects of nicotine. This treatment had no effect on the rewarding effects of lateral hypothalamic brain stimulation, failing to shift the function that relates reward strength to rate of responding (rate-frequency function). That the treatment regimen was sufficient to block nicotinic receptors in the reward system was confirmed by the fact that it completely blocked the ability of normally effective nicotine to potentiate the rewarding effects of stimulation (shift this function to the left). These data add evidence that the direct, endogenous cholinergic contribution to brain stimulation reward is muscarinic and fit with other evidence that the potentiation of brain stimulation reward by exogenous nicotine involves actions on nicotinic receptors native to dopaminergic neurons.

Animals↗
PubMed2006

Nicotine prevents stress-induced enhancement of long-term depression in hippocampal area CA1: electrophysiological and molecular studies.

Nicotine treatment prevents chronic psychosocial stress-induced impairment of hippocampus-dependent spatial memory and long-term potentiation (LTP). In this study, we investigated the effect of chronic nicotine treatment on stress-induced enhancement of long-term depression (LTD). After paired-pulse stimulation, LTD was evoked in area CA1 of anesthetized control, stressed, nicotine-treated, and nicotine-treated stressed rats. In stressed rats, a significantly greater LTD magnitude was seen than in control rats. Stress also facilitated the induction of LTD. Nicotine treatment of stressed rats prevented stress-induced enhancement and facilitation of LTD. For chronically stressed rats, we previously reported marked decreases in the basal levels of brain-derived neurotrophic factor (BDNF), CaMKII, P-CaMKII, and calmodulin as well as a significant increase in calcineurin basal levels. Herein, Western blot analysis conducted 1 hr after induction of LTD by paired-pulse stimulation showed that the levels of calcineurin and P-CaMKII were increased in the stressed group compared with the other groups and were normalized by chronic nicotine treatment. Additionally, after paired-pulse stimulation, the levels of total CaMKII were increased in all groups with no change in the levels of BDNF and calmodulin. Therefore, the increase in the levels of calcineurin and P-CaMKII during expression of LTD in area CA1 may explain the enhanced magnitude of LTD in chronically stressed rats.

Analysis of Variance↗
PubMed1993

Alterations of immune status induced by the sympathetic nervous system: immunomodulatory effects of DMPP alone and in combination with morphine.

The aim of the present study was to explore the involvement of the sympathetic nervous system (SNS) in the immunomodulatory effects of morphine in Lewis rats and to assess the effects of alterations in SNS activity on immune status. In the first experiment, sympathetic tone was elevated by administering the ganglionic stimulant 1,1-dimethyl-4-phenylpiperazinium (DMPP) in doses of 0, 0.01, 0.1, and 1.0 mg/kg, sc, 5 min before the sc administration of 15 mg/kg morphine or saline. Animals were sacrificed 1 h after the morphine injection and multiple in vitro immune assays were then conducted. Although DMPP did not significantly enhance morphine's suppressive effects in the spleen and blood mitogen stimulation assays or the splenic natural killer (NK) cell assay, DMPP alone produced effects on immune status in saline-treated animals. Therefore, a second experiment was conducted to examine the immunomodulatory effects of increasing peripheral sympathetic outflow in greater detail. Animals were administered a wider dose range of DMPP (0, 0.005, 0.05, 0.5, and 5.0 mg/kg, sc) 30 min prior to sacrifice and an expanded repertoire of immune assays was conducted. DMPP dose-dependently suppressed the mitogenic responsiveness of splenic T lymphocytes, splenic NK cell activity, and interleukin-2 (IL-2) and gamma-interferon production by stimulated splenocytes. DMPP did not alter the total number of splenic leukocytes or the proliferative response of splenic B lymphocytes. In the mesenteric lymph nodes, DMPP had no effect on mitogenic responsiveness, the production of IL-2 or the total number of leukocytes. In the blood, however, DMPP increased mitogenic responsiveness at intermediate doses and decreased proliferation at higher doses. DMPP also dose-dependently decreased the number of blood leukocytes/ml. Taken together, these results indicate that increasing peripheral sympathetic outflow results in profound effects on immune status that depend upon the degree to which SNS activity is altered, the compartment of the immune system, and the lymphocyte subtype.

Adjuvants, Immunologic↗
PubMed2000

The significance of nitric oxide for parasympathetic vasodilation in the eye and other orbital tissues in the cat.

The role of nitric oxide formation in the vasodilation in the eye and other orbital tissues caused by pre-ganglionic stimulation of the facial nerve was studied in cats under alpha-chloralose anaesthesia. Regional blood flows were determined with radioactive microspheres during unilateral stimulation of the facial nerve before and after inhibition of nitric oxide synthase (NOS), alone or in combination with muscarinic blockade.N(omega)-nitro-L-arginine (L-NA), a non-selective NOS-inhibitor, caused a significant increase in mean arterial blood pressure (MABP) and a decrease in cardiac output (CO). Concomitantly, local blood flows on the non-stimulated control side were reduced in most of the investigated tissues, indicating marked vasoconstriction. An inhibitor selective for neuronal NOS, 7-nitro-indazole (7-NI), had no significant effect on MABP, CO or local blood flows. During facial nerve stimulation at 5 Hz (n =6), choroidal blood flow on the stimulated side was 108+/-41% (P</=0.05) higher than on the non-stimulated side during control conditions, an effect that was completely abolished by L-NA. During stimulation at 10 Hz (n =8), the choroidal blood flow was 171+/-38% (P</=0.01) higher on the stimulated side during control conditions. The corresponding values after L-NA and subsequent administration of atropine were 97+/-21% (P</=0.05, compared to control conditions) and 50+/-14% (P</=0.05, compared to control conditions), respectively. Atropine alone had no significant effect on the increase in choroidal blood flow caused by stimulation at 10 Hz (n =7), whereas subsequent administration of L-NA caused a statistically significant reduction. Administration of 7-NI had no significant effect on the choroidal vasodilation at 10 Hz (n =7), whereas subsequent administration of L-NA caused significant reduction, at least as compared to control conditions. These results suggest that nitric oxide is of greater significance for the choroidal vasodilation, caused by facial nerve stimulation, in the cat than it is in the rabbit. However, no definitive conclusions can be made concerning the source of the nitric oxide. Direct release of nitric oxide from the parasympathetic nerve fibres could contribute as well as nitric oxide formed in the vascular endothelium, secondary to the release of acetylcholine and/or VIP. At high frequencies, a part of the choroidal vasodilation seems to be independent of nitric oxide.

Animals↗
PubMed1990

Alpha 1-adrenergic coronary constriction during exercise and ischemia.

This paper reviews work primarily from our laboratories, examining an alpha 1-adrenergic receptor-mediated coronary constriction during exercise and myocardial ischemia in dogs. It was demonstrated that in the quiescent conscious dog, the coronary circulation is devoid of an alpha 1-coronary constriction. Furthermore, it was shown by the intracoronary injection of selective agonists that both alpha 1- and alpha 2-receptor subtypes are present in coronary vessels. However, during exercise or ischemia only the selective alpha 1-antagonist prazosin caused an increase in coronary inflow, indicating that only alpha 1-receptors were activated. During both conditions, the increase in flow caused by alpha 1-blockade was associated with an increased contractile function in subendocardium. In experiments on anesthetized dogs, it was shown that prazosin caused an equal increase in perfusion of subepicardial and subendocardial layers during stellate ganglion stimulation. However, contractile function was increased only in subendocardium. It was proposed that only in deeper muscle layers does an alpha 1-coronary constriction impose a flow-limitation on contractile function. Finally, recent results indicate that myocardial ischemia, produced either by partial coronary stenosis or by maintenance of coronary inflow at the resting level during exercise, may initiate a vicious cycle with a further increase in alpha 1-adrenergic coronary constriction. Abolition of this positive feedback mechanism may partially explain the anti-infarction effects of chronic ventricular sympathectomy, as previously observed in our laboratories.

Animals↗
PubMed1989

Inhibition of the 5-HT-induced cardiogenic hypertensive chemoreflex by the selective 5-HT3 receptor antagonist ICS 205-930.

We investigated the effect of ICS 205-930 [(3 alpha-tropanyl)-1H-indole-3-carboxylic acid ester], a selective antagonist at 5-HT3 receptors, on the cardiogenic hypertensive chemoreflex in the anaesthetized dog. The reflex was elicited by injection of 5-HT (12.5-1600 micrograms) into the left cardiac ventricle and consisted of a dose-dependent systemic hypertension associated with a decrease in heart rate. ICS 205-930 (10, 30, and 100 micrograms/kg i.v.) caused a displacement to the right of both the dose-response curves of 5-HT-induced blood pressure increase and heart rate reduction. Its blocking effects upon the action of 5-HT could be surmounted by increasing the dose of the agonist. The selective 5-HT2 receptor antagonist, ketanserin (0.1 mg/kg i.v.) and the combined 5-HT1 and 5-HT2 receptor antagonist, methiothepin (0.1 mg/kg i.v.) had no influence on the hypertensive reflex. When the reflex was elicited by the ganglionic stimulant, 1,1-dimethyl-4-phenyl-piperazinium (DMPP; 100-1600 micrograms), ICS 205-930 had no blocking effect. The results suggest that the 5-HT-induced cardiogenic hypertensive chemoreflex is mediated by 5-HT3 receptors.

Animals↗
PubMed1985

Release of cholecystokinin-immunoreactivity into the vascular bed of the guinea-pig small intestine during peristalsis.

The release of cholecystokinin-immunoreactivity (CCK-IR) into the venous effluate of the isolated and vascularly perfused guinea-pig small intestine was measured. Raising the intraluminal pressure by 5 mbar for 8 min initiated peristalsis and was associated with an increased release of CCK-IR. The ganglion stimulant dimethylphenyl-piperazinium failed to alter the release of CCK-IR. The results are discussed in the light of a possible involvement of CCK-containing neurones in intestinal peristalsis.

Animals↗
PubMed1980

Effects of McN-A-343, a cholinomimetic drug, on endplate currents in the frog.

The muscarinic ganglion stimulating agent, McN-A-343 has unusual blocking actions on endplate currents (EPCs) at frog neuromuscular junctions. McN-A-343 caused depolarization by a curare-sensitive process, blocked neuromuscular transmission, depressed EPCs and reduced the time for EPC decay. These results are explained best by a nicotinic agonist action of McN-A-343 on the acetylcholine receptor to cause ion flow and the blockade by McN-A-343 of the open ion channels. The actions of McN-A-343 are similar to those of decamethonium (C-10) described by others. Unlike C-10, however, McN-A-343 did not alter the exponential character of the EPC or alter the voltage dependency of the EPC. The prototypical nicotinic agonist, dimethylphenylpiperazinium had no effect on EPC parameters of endplate clamped at -90mV.

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

Effects of ryanodine on the spike after-hyperpolarization in sympathetic neurones of the rat superior cervical ganglion.

Effects of ryanodine on sympathetic neurones of the rat superior cervical ganglion were investigated by means of intracellular recording. Ryanodine (1 microM) significantly shortened the after-hyperpolarization (AH) following the spike evoked by current injection or pre-ganglionic stimulation without affecting the configuration of the spikes. The shortening of AH caused by ryanodine was dose-dependent at concentrations between 0.1 and 1 microM and was slowly recovered by washing the tissue over 1 h. A partial inhibition of the apamin-sensitive slow component of AH was the maximal effect obtained at 1 microM. Although the input membrane resistance was not changed, ryanodine evoked repetitive discharges at long intervals in response to long depolarizing current pulses applied across the cell membrane. Ryanodine (5 microM) did not depress the Ca-spike but shortened the following AH in a lesser degree than that following the normal spike. Spontaneous small fluctuations of the resting membrane potential were occasionally observed under normal conditions. They were facilitated by caffeine and abolished by ryanodine. Caffeine also enhanced the slow component of the AH but did not affect it in the presence of ryanodine. These results suggest that ryanodine inhibits Ca release from intracellular store sites. The released Ca may contribute to generating the long-lasting AH and to regulating the excitability of rat sympathetic neurones.

Action Potentials↗
PubMed1993

Effects of compound U74500A in animal models of gastric and duodenal ulceration.

Pretreatment with U74500A (up to 0.65 mg/100 g) failed to affect gastric lesions induced by 100% EtOH gavage in Sprague-Dawley rats. Topical application of U74500A did not reduce lesions induced by 40% EtOH in ex vivo gastric chamber preparations. However, pretreatment of rats with U74500A (0.65 g/100 g per os) reduced the incidence and severity of experimental duodenal ulcer induced by cysteamine HCl, and duodenal ulcer induced by cysteamine-HCl plus GABA. These results show U74500A to have powerful and specific antiduodenal ulcer actions. Pharmacologic analysis of organ-bath preparations of the small intestine show this compound to reduce intestinal contractility to applied cholinergic and serotonergic agonists. However, relaxations induced by electrical or nicotinic ganglionic stimulation were unaffected. U74500A itself caused concentration-dependent contractions.

Analysis of Variance↗
PubMed1991

Pharmacology of antimigraine drugs.

The drugs used in migraine therapy can be divided into two groups: agents that abort an established migraine attack and agents used prophylactically to reduce the number of migraine attacks. Both groups have drugs that are specific for migrainous headaches and that are non-specific, and are used to treat the accompanying headache (analgesics), vomiting (anti-emetics), anxiety (sedatives and anxiolytics), or depression (antidepressants). The main drugs with specific action on migraine include ergot alkaloids (ergotamine, dihydroergotamine), agonists (sumatriptan) or partial agonists (methysergide) at a specific subtype of 5-HT1-like receptors, beta-adrenoceptor antagonists (propranolol, metoprolol), calcium antagonists (flunarizine) and anti-inflammatory agents (indomethacin). The pharmacological basis of therapeutic action of several of these drugs is not well understood. In the case of the ergot alkaloids and 5-HT1-like receptor agonists, however, it is likely that the antimigraine effect is related to the potent and rather selective constriction of the large arteries and arteriovenous anastomoses in the scalp and dural regions. In addition, these drugs inhibit plasma extravasation into the dura in response to trigeminal ganglion stimulation, but it is possible that this effect is related to the selective vasoconstriction in the extracerebral vascular bed. The selectivity of the pharmacological effects of these antimigraine drugs (constriction of the extracerebral arteries and arteriovenous anastomoses, poor penetration into the central nervous system and the absence of an antinociceptive effect even after intrathecal administration) strongly suggests that excessive dilatation in the extracerebral cranial vasculature, probably initiated by a neuronal event, is an integral part of the pathophysiology of migraine.

Analgesics↗