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Results for “Ganglionic Stimulants”

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PubMed1979

Autonomic control of right atrial contractile strength in the dog.

The combined effects of parasympathetic and sympathetic stimulation on right atrial contractile strength were assessed in open-chest, pentobarbital-anesthesized dogs. A factorial experimental design was employed to quantify the percent changes in atrial contractile strength in spontaneously beating and paced hearts as a function of the frequencies of vagal and stellate ganglion stimulation. In 7 of 10 dogs, there was a substantial interaction between the two autonomic divisions; the sympathetically mediated inotropic effect became less pronounced as the background level of vagal stimulation increased. The relationship between stimulation frequencies and atrial contractile strength was not significnatly altered by pacing the hearts.

Animals↗

PubMed1994

Malignant arrhythmias and acute myocardial ischemia: interaction between flecainide and the autonomic nervous system.

The antiarrhythmic and proarrhythmic effects of flecainide were assessed in 21 anesthetized cats. Ventricular arrhythmias can be reproducibly induced in cats by the combination of acute myocardial ischemia and sympathetic stimulation. Premature ventricular contractions (PVCs), sustained (sVT) and nonsustained (nsVT) ventricular tachycardia (VT), or ventricular fibrillation (VF) may be induced by a 1-minute left stellate ganglion stimulation during a 3-minute coronary artery occlusion. After three trials yielding consistent results, flecainide (2 mg/kg intravenous bolus plus 2 mg.kg-1.hr-1 intravenous infusion) was injected and two additional trials performed. Eight cats also underwent two trials after propranolol (0.2 mg/kg) administered while flecainide infusion was maintained. Flecainide decreased heart rate and blood pressure and slightly prolonged JTc (9%, p < 0.05). It markedly augmented QRS duration (61%, p < 0.0001), which was increased by an additional 61% (p < 0.0001) during sympathetic stimulation. VF was observed in 8 animals and never after flecainide (p < 0.05). However, after drug administration all cats had VT (2 nsVT and 6 sVT), and 5 required cardiac massage. Flecainide did not prevent the occurrence of nsVT in 6 cats, and it worsened arrhythmias by inducing VT (4 nsVT and 2 sVT) in 6 cats with only PVCs or without arrhythmias in the control trials. Propranolol, administered while flecainide infusion was maintained, prevented the increase in heart rate and the marked QRS prolongation during sympathetic stimulation (4 +/- 3 vs 52 +/- 16 msec, p < 0.05) and abolished the proarrhythmic effect of flecainide in 4 of 5 animals. Thus flecainide, despite an antifibrillatory effect, does not prevent and actually may favor the occurrence of sVT during acute myocardial ischemia and enhanced sympathetic activity. Propranolol, by countering the increase in heart rate during sympathetic stimulation, prevented the rate-dependent conduction delay and abolished the proarrhythmic effect of flecainide. The exacerbation, whenever a transient ischemic episode is accompanied by elevated sympathetic activity, of the ischemia-induced conduction delay caused by flecainide may in part explain the mortality data in the Cardiac Arrhythmia Suppression Trial.

Animals↗

PubMed2004

Reticuline exposure to invertebrate ganglia increases endogenous morphine levels.

OBJECTIVES: Given the presence of morphine, its metabolites and precursors in mammalian and invertebrate tissues, it became important to determine if exposing tissues to an opiate alkaloid precursor, reticuline, would result in increasing endogenous morphine levels. METHOD: Endogenous morphine levels were determined by high pressure liquid chromatography coupled to electrochemical detection and radioimmunoassay following incubation of Mytilus edulis pedal ganglia with reticuline. Nitric oxide (NO) release was determined in real-time via an amperometric probe. Mu opiate receptor affinity for opiate alkaloid precursors was determined by a receptor displacement assay. RESULTS: Morphine is present in the pedal ganglia of Mytilus edulis (1.43 +/- 0.41 ng/mg +/- SEM ganglionic wet weight). Ganglia incubated with 50 ng of reticuline, a morphine precursor in plants, for 1 hour exhibited a statistical increase in their endogenous morphine levels (6.7 +/- 0.7 ng/mg tissue wet weight; P<0.01). This phenomenon is concentration dependent. The increase in ganglionic morphine levels occurs gradually over the 60 min incubation period, beginning 10 minutes post reticuline addition. We show that reticuline (10(-6) M) does not stimulate ganglionic NO release in a manner resembling that of morphine (10(-6) M), which releases NO seconds after its exposure to the ganglia and lasts for 5 minutes. With reticuline, there is a 3 minute delay, which is followed by an extended release period. Furthermore, in binding displacement experiments both reticuline and salutaridine (another morphine precursor) exhibit no binding affinity for the pedal ganglia mu opiate receptor subtype. This finding is further substantiated using the positive control of human monocytes where the mu3 opiate receptor subtype has been cloned. CONCLUSION: Taken together, we surmise that the morphine's precursors are being converted to morphine. The experiments strongly indicate that pedal ganglia can synthesize morphine from reticuline.

Alkaloids↗

PubMed1991

Trigeminal sensory fiber stimulation induces morphological changes reflecting secretion in rat dura mater mast cells.

Mast cells are involved in allergic reactions, but may also participate in neurogenic inflammation. The morphology of mast cells in rat dura mater and tongue was evaluated by histochemistry, as well as by scanning and transmission electron microscopy following unilateral trigeminal ganglion stimulation (5 min, 5 Hz, 5 ms, and 0.02, 0.1 or 1.0 mA). Mast cells in dura and tongue of normal animals were numerous, perivascular and often in close proximity to nerve fibers. After 5 min of electrical stimulation, mast cells contralateral to the stimulation showed histochemical characteristics of normal peripheral tissue mast cells (Safranin-positive), and by electron microscopy appeared homogeneous with numerous intact electron-dense granules. On the stimulated side, however, the staining characteristics of mast cells showed changes indicating progressive intracellular loss of their granular content. In addition, the total number of stainable mast cells decreased at all three stimulus intensities, but reached significance only at 0.1 and 0.02 mA. Ultrastructural evidence of granule changes consistent with secretion were observed although degranulation was not observed until 20 min after stimulation. There were no mast cell changes after electrical trigeminal stimulation in adult rats treated as neonates with capsaicin to destroy small caliber sensory afferent axons. These results suggest that mast cells may secrete in response to electrical stimulation of trigeminal axons, possibly mediated by antidromic release of neuropeptides, and may participate in the development of neurogenic inflammation.

Animals↗

PubMed2000

Heterogeneous sympathetic innervation influences local myocardial repolarization in normally perfused rabbit hearts.

BACKGROUND: Heterogeneity of sympathetic innervation is thought to contribute to the potential for fatal arrhythmia. However, little is known about the effects of heterogeneous innervation on repolarization. METHODS AND RESULTS: To assess this relationship, we measured activation recovery intervals (ARIs) from 64 epicardial sites in 11 rabbits studied 2 weeks after regional denervation produced by phenol and 4 sham-operated rabbits. ARI results were compared with the distribution of sympathetic innervation measured from 3D reconstructions of serial autoradiographs of [(125)I]metaiodobenzylguanidine and (99m)Tc-sestamibi. ARIs were recorded during baseline sinus rhythm, norepinephrine (NE) infusion (0.1 microg. kg(-1). min(-1)), and left stellate ganglion stimulation (SS). NE shortened ARI in 98% of electrodes in the denervated region. The degree of ARI shortening and dispersion increased (P<0.001 and P<0.01, respectively) as denervation became more severe. SS shortened ARI in 30% of electrodes in the denervated area, with increased shortening and dispersion related to increased severity of denervation (P<0.01). SS prolonged ARI in 70% of electrodes in the denervated area, with no correlation with severity of denervation. CONCLUSIONS: The magnitude and dispersion of local repolarization responses are related to the severity of denervation, as well as the type of stimulation: neural (SS) versus humoral (NE). The differences may relate to the concentration of NE released.

3-Iodobenzylguanidine↗

PubMed1975

Thermoregulatory changes induced by cholinomimetic substances introduced into the cerebral ventricles of sheep.

1 Thermoregulatory responses have been recorded from Welsh Mountain sheep exposed to warm, neutral or cold environments while injections of cholinomimetic drugs and/or their antagonists have been given into a lateral cerebral ventricle. 2. Carbachol and physostigmine inhibited panting of animals at high ambient temperature (ta), caused vasoconstriction and initiated shivering at neutral ta, and accentuated shivering at low ta. Rectal temperature (tre) invariably increased. Oxotremorine had apparently identical effects. 3. Nicotine and another ganglionic stimulant, the quaternary methyl derivative of dopamine, had no effects on thermoregulation. 4. Atropine given 10 min before injections of carbachol, physostigmine or oxotremorine completely inhibited their hyperthermic effects, but pretreatment with the ganglion-blocking drug, pempidine, caused no inhibition. The cholinergic synapses that respond to cholinomimetic drugs injected into the lateral cerebral ventricles of sheep are therefore muscarinic and not nicotinic. 5. When atropine was given to sheep exposed to cold, no detectable reduction of shivering occurred and tre decreased only slightly, even with doses of atropine far greater than needed to inhibit shivering induced by physostigmine. This may be because shivering is controlled by neural pathways unaffected by drugs administered intracerebroventricularly or because the cholinergic synapses activated by physostigmine do not carry the input from cold sensors.

Animals↗

PubMed1995

Peripheral GABAA receptor-mediated effects of sodium valproate on dural plasma protein extravasation to substance P and trigeminal stimulation.

1. The GABA transaminase inhibitor and activator of glutamic acid decarboxylase, valproic acid is being used for the treatment of migraine. Its mechanism of action is unknown. We tested the effects of sodium valproate and GABAA-agonist muscimol on dural plasma protein ([125I]-bovine serum albumin) extravasation evoked by either unilateral trigeminal ganglion stimulation (0.6 mA, 5 ms, 5 Hz, 5 min) or substance P (SP) administration (1 nmol kg-1,i.v.) in anaesthetized Sprague-Dawley rats. 2. Intraperitoneal (i.p.) injection of sodium valproate or muscimol, but not baclofen (< or = 10 mg kg-1, i.p.) dose-dependently reduced dural plasma protein extravasation caused either by electrical trigeminal stimulation (ED50: 6.6 +/- 1.4 mg kg-1, i.p., and 58 +/- 18 micrograms kg-1, i.p. for valproate or muscimol, respectively) or by intravenous substance P administration (ED50: 3.2 +/- 1.4 mg kg-1, i.p. and 385 +/- 190 micrograms kg-1, i.p. for valproate or muscimol, respectively). 3. Valproate (6.6 mg kg-1, i.p.) or muscimol (58 micrograms kg-1, i.p.) had no effect on mean arterial blood pressure or heart rate when measured for 30 min after i.p. administration. 4. The GABAA-antagonist bicuculline (0.01 mg kg-1, i.p.) completely reversed the effect of valproate and muscimol on plasma extravasation following electrical stimulation or substance P administration, whereas the GABAB-receptor antagonist, phaclofen (0.01-1 mg kg-1, i.p.) did not. Bicuculline or phaclofen, given alone, did not alter the plasma extravasation response after either electrical stimulation or SP administration. 5. Valproate decreased plasma extravasation following substance P administration in adult animals, neonatally treated with capsaicin by a bicuculline-reversible mechanism. This suggests that GABAA receptors are not found primarily on those afferent neurones or fibres which are sensitive to capsaicin treatment in neonatal rats.6. We conclude that sodium valproate blocks plasma extravasation in the meninges through GABAA mediated postjunctional receptors probably within the meninges. The dosages required are comparable to those used clinically. Agonists and modulators at the GABAA receptor may become useful for the development of selective therapeutic agents for migraine and cluster headache.

Animals↗

PubMed1980

beta-Bungarotoxin and parasympathetic nerve blocking action.

Autonomic effects of beta-bungarotoxin (beta-BuTX), a presynaptic blocking agent at the neuromuscular junction, were examined with parasympathetic (vagus), sympathetic nerve-atrial preparations isolated from guinea pigs. beta-BuTX in concentrations ranging from 0.01 to 10 micrograms/ml abolished the negative inotropic and chronotropic responses to electrical stimulation of the preganglionic trunks of the vagus nerve. This effect was time- and dose-related and was not restored by repeated washings. Such blocking action of beta-BuTX was also obtained when post-ganglionic stimulation was applied. On the other hand, beta-BuTX failed to block the positive inotropic and chronotropic responses to either pre- or postganglionic sympathetic nerve stimulation. The nicotine-induced negative, then positive inotropic and chronotropic effects, under nerve conduction block with tetrodotoxin, were little affected with the application of beta-BuTX. The negative or positive responses to exogenously applied acetylcholine or norepinephrine were also unaffected by beta-BuTX. Thus, beta-BuTX apparently blocks cholinergic transmission in the vagus nerve innervating the guinea-pig heart, probably by acting on the postganglionic nerve terminals, yet does not interfere with preganglionic cholinergic and postganglionic adrenergic transmissions in the sympathetic nerves.

Acetylcholine↗

PubMed1999

IGF-I and TGF-beta2 have a key role on regeneration of nitric oxide synthase (NOS)-containing nerves after cavernous neurotomy in rats.

The molecular mechanism of nitric oxide synthase (NOS)-containing nerve regeneration is still unknown. It is believed that growth factors are involved in this phenomenon. We investigated the change of NOS containing nerve fibers and the mRNA expression of insulin like growth factor (IGF)-I, nerve growth factor (NGF), transforming growth factor (TGF)-alpha, TGF-beta1, TGF-beta2, TGF-beta3, vascular endothelial growth factor (VEGF), endothelial NOS (eNOS) and neuronal NOS (nNOS) on the penis after cavernous nerve neurotomy in rats. Male rats were divided into four groups: (1) sham operation (n = 14); (2) unilateral neurotomy of a 5 mm segment of the cavernous nerve (n = 21); (3) unilateral neurotomy with growth hormone (n = 14); and (4) bilateral neurotomy (n = 21). Electrostimulation of the intact cavernous nerve or pelvic ganglion were performed at one, three and six months. Nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase staining and immunohistochemistry were used to identify NOS in the penis. The gene expression for growth factors, eNOS and nNOS were investigated in corporal tissue by reverse transcriptase-polymerase chain reaction (RT-PCR). One month after neurotomy, both unilateral and bilateral neurotomy groups showed significant decreases in NOS-containing nerve fibers on the dorsal and intracavernosal nerves on the side of neurotomy. Significantly lower mRNA expression of nNOS, IGF-I and TGF-beta2, higher mRNA expression of eNOS and VEGF189 were shown in these groups. At three months, the number of NOS-containing nerve fibers in the unilateral neurotomy group increased only slightly, while the GH-treated group showed a significant increase. At six months, those in the intracavernosal nerve only increased in a significant amount (P < 0.0001), however mRNA expression of nNOS, IGF-I and TGF-beta2 showed a significant increase as early as at three months. After bilateral neurotomy, the NOS-positive nerve fibers in the dorsal and intracavernosal nerve were significantly decreased at one month and remained so at six months; no erectile response could be elicited by pelvic ganglion stimulation. In the unilateral neurotomy group at six months, more NOS-positive neurons in the pelvic ganglia were found on the intact side than on the side of the neurotomy (P < 0.003), indicating that the regeneration derived from pelvic ganglion neurons on the intact side. Furthermore, electrostimulation in the unilateral neurotomy group revealed a greater maximal intracavernosal pressure and a shorter latency period at six months than at one month (P < 0.014, P < 0.001, respectively). These data suggest that IGF-I and TGF-beta2 may play a key role in the regeneration of nNOS-containing nerve fibers in the dorsal and intracavernosal nerves, and eNOS increases temporarily in the intracavernous involving VEGF189 after unilateral cavernous nerve injury.

Animals↗

PubMed1999

The role of growth factor on regeneration of nitric oxide synthase (NOS)--containing nerves after cavernous neurotomy in the rats.

Nitric oxide synthase (NOS) containing nerve regeneration can be seen six months after unilateral cavernous nerve neurotomy in rats. However, its molecular mechanism is still unknown. It is believed that growth factors are involved in this phenomenon. In this study we investigated the change of NOS containing nerve fibers and the RNA expression of insulin like growth factor (IGF)-I, nerve growth factor (NGF), transforming growth factor (TGF)-alpha, TGF-beta 1, TGF-beta 2. TGF-beta 3 and NOS on the penis after cavernous nerve neurotomy in rats. Male rats were divided into three groups: (1) sham operation (N = 10); (2) unilateral neurotomy of a 5 mm segment of the cavernous nerve (N = 15); and (3) bilateral neurotomy (n = 15). Electrostimulation of the intact cavernous nerve or pelvic ganglion was performed at one, three and six months. Nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase staining was used to identify NOS in the penile nerve fibers. The gene expression for growth factors and bNOS was investigated in corporal tissue by reverse transcriptase-polymerase chain reaction (RT-PCR) using specific oligonucleotide primers. One month after neurotomy, both unilateral and bilateral neurotomy groups showed a significant decrease in NOS-containing nerve fibers on the dorsal and intracavernosal nerves on the side of neurotomy, and a significantly lower mRNA expression of bNOS, IGF-I and TGF-beta 2. At three months, the number of NOS-containing nerve fibers in the unilateral neurotomy group increased only slightly but at six months those in the intracavernosal nerve increased in a significant amount (P < 0.0001), however mRNA expression of bNOS, IGF-I and TGF-beta 2 showed a significant increase as early as at three months. After bilateral neurotomy, the NOS-positive nerve fibers in the dorsal and intracavernosal nerve were significantly decreased at one month and remained so at six months; no erectile response could be elicited by pelvic ganglion stimulation. In the unilateral neurotomy group at six months, more NOS-positive neurons in the pelvic ganglia were found on the intact side than on the side of the neurotomy (P < 0.003), indicating that the regeneration derives from pelvic ganglion neurons on the intact side. Furthermore, electrostimulation in the unilateral neurotomy group revealed a greater maximal intracavernosal pressure and a shorter latency period at six months than at one month (P < 0.014, P < 0.001, respectively). These data suggest that IGF-I and TGF-beta 2 may play a key role in regeneration of NOS-containing nerve fibers in the dorsal and intracavernosal nerves after unilateral cavernous nerve injury.

Animals↗

PubMed1993

Pharmacological properties of nicotinic acetylcholine receptors on adrenal chromaffin cells and their modification by hypoxic exposure.

To characterize the properties of nicotinic acetylcholine receptors (nAChRs) in autonomic ganglia, we examined specific L-[3H]nicotine binding to membrane fraction prepared from cultured bovine adrenal chromaffin cells, using a modified filtration method. Binding of L-[3H]nicotine to non-treated glass fiber filters interfered with detection of specific binding to the membrane fraction. Presoaking the glass fiber filters in 3% or greater concentrations of polyethyleneimine solution (sixty times higher than the reported concentration) for more than 5 h could reduce the binding of L-[3H]nicotine to the filters to background level. Furthermore, specific L-[3H]nicotine binding to the membrane fraction was detected only when the membrane fraction was prepared in buffer containing no divalent cations such as Ca2+ and Mg2+ (EDTA and EGTA were added) and protease inhibitors. Specific binding of L-[3H]nicotine was saturable and reversible. Scatchard analysis revealed a single class of high affinity binding sites with an average Kd of 8.7 nM and a Bmax of 43.2 fmol/mg protein. Specific binding was sensitive to cholinergic agonists (carbamylcholine and L-nicotine) and ganglionic stimulating agents (lobeline and DMPP), but was resistant to neuromuscular blocking agents (alpha-bungarotoxin, d-tubocurarine) and hexamethonium. These results suggest that high-affinity nicotine binding sites on adrenal chromaffin cells are nAChRs of ganglion-type, which have properties different from nAChRs on the neuromuscular junction but similar to nAChRs in the brain.

Animals↗

PubMed1987

Ganglionic circulation and its effects on neurons controlling cardiovascular functions in Aplysia californica.

The abdominal ganglion of the mollusk Aplysia californica receives most of its blood supply through a small caudal artery that branches off the anterior aorta near its junction with the heart. Injection of an ink/gelatin mixture into the caudal artery revealed a consistent pattern of arterial branching within the ganglion and a general proximity of larger vessels to identified neurons controlling circulation in this animal. This morphological arrangement was particularly evident for the heart excitor interneuron, cell L10, which lies next to the caudal artery near its entry into the ganglion. In electrophysiological experiments, L10 was excited when blood flow or oxygen tension within the ganglion was reduced. This effect was expressed as a gradual increase in impulse frequency of L10 and conversion from tonic to bursting mode of spike discharge. L10 follower cells in the RB and LD neuron clusters were affected synaptically by the changes in L10 activity, while other follower cells (L3 and RD neurons) responded independently of L10's synaptic influence. The neurosecretory white cells (R3 to R14) that innervate the major arteries and pericardial tissues were also excited when ganglionic circulation was interrupted. In innervated preparations of the heart and respiratory organs, decreased circulation through the abdominal ganglion stimulated a transient increase in the rate and amplitude of respiratory (gill) pumping and pericardial contractions and caused a sustained increase in activity of the heart. Both responses increase cardiac output and both appear to involve a direct influence of ganglionic circulation on interneurons controlling the gill and heart. These results indicate that the cell-specific patterns of excitation and inhibition caused by fluctuations in ganglionic circulation may be important factors for maintaining circulatory homeostasis in this animal.

Animals↗

PubMed1981

A study of gastric secretion in dogs using pilocarpine.

1 Pilocarpine (40 microgram/min i.v.) stimulated acid and pepsin secretion from Heidenhain pouches but did not stimulate secretion from the innervated stomach. 2 Pilocarpine significantly increased acid secretion from the innervated main stomach after the vagal nerves were bilaterally blocked with lidocaine. 3 The effect of pilocarpine on secretion from the Heidenhain puch was depressed by ganglionic blockade (hexamethonium), by dopamine and by isoprenaline. 4 The stimulatory action of histamine on gastric secretion from either pouch or gastric fistulae was uninfluenced by dopamine. 5 The action of pilocarpine was augmented by the muscarinic ganglionic stimulant AHR 602. Considering this effect, as well as the secretory depression of isoprenaline, pilocarpine resembles pentagastrin rather than methacholine in its action.

Animals↗

PubMed2000

Actions of tachykinins within the heart and their relevance to cardiovascular disease.

Substance P and neurokinin A are tachykinins that are co-localized with calcitonin gene-related peptide (CGRP) in a unique subpopulation of cardiac afferent nerve fibers. These neurons are activated by nociceptive stimuli and exhibit both sensory and motor functions that are mediated by the tachykinins and/or CGRP. Sensory signals (e.g., cardiac pain) are transmitted by peptides released at central processes of these neurons, whereas motor functions are produced by the same peptides released from peripheral nerve processes. This review summarizes our current understanding of intracardiac actions of the tachykinins. The major targets for the tachykinins within the heart are the intrinsic cardiac ganglia and coronary arteries. Intrinsic cardiac ganglia contain cholinergic neurons that innervate the heart and coronary vasculature. Tachykinins can stimulate NK3 receptors on these neurons to increase their excitability and evoke spontaneous firing of action potentials. This action provides a mechanism whereby tachykinins can indirectly influence cardiac function and coronary tone. Tachykinins also have direct effects on coronary arteries to decrease or increase tone. Stimulation of NK1 receptors on the endothelium causes vasodilation mediated by nitric oxide. This effect is normally dominant, but NK2 receptor-mediated vasoconstriction can also occur and is augmented when NK1 receptors are blocked. It is proposed that these ganglion stimulant and vascular actions are manifest by endogenous tachykinins during myocardial ischemia.

Action Potentials↗

PubMed1977

Pharmacological analysis of the effects of metoclopramide on the guinea pig isolated stomach.

A pharmacological analysis has been made of the effects of metoclopramide on the contractile activity of isolated longitudinal muscle strips prepared from the guinea pig stomach. Metoclopramide produced up to 3-fold increases in the amplitude of the spontaneous contractions exhibited by such a preparation. This phenomenon was antagonized by hyoscine but not by tetrodotoxin nor by hexamethonium. The contractile response to transmural stimulation was also enhanced by metoclopramide, as was the response to extrinsic acetylcholine. Neural inhibitory systems were not affected by metoclopramide. The apparent sensitization to extrinsic acetylcholine was, however, prevented by tetrodotoxin and hexamethonium, implying that this effect depends upon ganglionic stimulation by acetylcholine. These results suggest that metoclopramide may act by increasing the amount of acetylcholine released at the postgangionic cholinergic nerve ending.

Acetylcholine↗

PubMed1984

Crayfish extraretinal photoreception. I. Behavioral and motorneuronal responses to abdominal illumination.

Stimulation of blinded and sighted crayfish with ventrally directed light evokes a slow tail flexion response or a tail flexion accompanied by backward walking. The response latencies and durations of sighted animals are shorter than those of blinded animals, which indicates that visual inputs can speed a response which can be released by extraretinal photoreceptors alone. Recordings from electrodes implanted in intact, freely behaving animals demonstrate that ventral illumination tonically excites abdominal postural flexor motoneurones. The motoneurone discharge occurs first in caudal segments and then spreads rostrally, as does abdominal flexion around each segmental joint. Illumination of individual abdominal ganglia (A2-A5) tonically excites a similar flexor motoneurone response in cells of the stimulated ganglion and more caudal ganglia. Swimmeret motoneurones are also tonically excited by this stimulus. These responses can be evoked in isolated abdominal nerve cords, indicating that extraretinal photoreceptors present in these ganglia activate motor circuits that are local to the abdomen. Stimulation of A6 excites the caudal photoreceptor neurones, but only excites flexor motoneurones if the abdominal ventral nerve cord is connected to the rostral part of the CNS. The motoneurones respond with repeated bursts of activity that long outlast the stimulus or the initial high-frequency burst of the caudal photoreceptor neurones. These motoneurone responses are similar to those evoked by stimulation of command fibres that also evoke backward walking (Kovac, 1974a).

Abdomen↗

PubMed1992

Prevention of life-threatening arrhythmias by pharmacologic stimulation of the muscarinic receptors with oxotremorine.

The potential antiarrhythmic efficacy of pharmacologic parasympathetic activation is still controversial. This study assessed the antiarrhythmic effect of saline solution (n = 9) and of the muscarinic agonist oxotremorine (1.5 micrograms/kg administered intravenously) (n = 17) in a feline animal model in which malignant arrhythmias were reproducibly elicited by the combination of acute myocardial ischemia and left stellate ganglion stimulation. Although saline solution had no effect, oxotremorine significantly decreased heart rate, blood pressure, the incidence of ventricular fibrillation from 47% to 0% (p = 0.004), and the incidence of malignant arrhythmias (either ventricular tachycardia or ventricular fibrillation) from 88% to 12% (p less than 0.001). When reduction in heart rate was prevented by means of atrial pacing (n = 15), the incidence of malignant arrhythmias was still significantly reduced from 87% to 27% (p = 0.001). Arrhythmias were also graded as follows: 0 = no premature ventricular contractions; 1 = 1 to 10 premature ventricular contractions; 2 = 11 to 50 premature ventricular contractions; 3 = ventricular tachycardia; 4 = ventricular fibrillation. Arrhythmia severity was 3.29 +/- 0.16 (SEM) in the control trials and was reduced to 0.76 +/- 0.26 (p less than 0.001) by oxotremorine and to 1.53 +/- 0.34 by oxotremorine and pacing (p = 0.002). Therefore a muscarinic agonist can significantly reduce malignant arrhythmias during acute myocardial ischemia and may represent a novel approach to the prevention of sudden cardiac death.

Animals↗

PubMed1996

Effects of tetrandrine on cardiac noradrenaline release evoked by electrical stimulation.

The effects of tetrandrine (TD) on endogenous cardiac noradrenaline (NA) release evoked by electrical stimulation were investigated in perfused guinea pig hearts. The overflow of cardiac NA and its intraneuronal metabolite 3,4-dihydroxyphenylethyleneglycol (DOPEG) were determined by high pressure liquid chromatography (HPLC). In the presence of TD, the release of NA evoked by either nerve ganglion-stimulation or cardiac field-stimulation was significantly reduced (P < 0.01). The overflow of DOPEG was markedly enhanced (P < 0.01). TD inhibited cardiac endogenous NA release resulting from activation of the sympathetic nerve terminals within the myocardium, and increased the release of DOPEG, indicating that TD could result in a loss of NA from storage vesicles or activate monoamine oxidase in axoplasma, which could be detected by markedly increased DOPEG release. These effects of TD may be associated with its property of calcium antagonist.

Alkaloids↗