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At least 991 records · Page 55Linked to original sources
PubMed1997

Clonidine-induced emesis: a multitransmitter pathway concept.

The emetic effect of clonidine injected into the cerebral ventricles through chronically implanted cannulae was investigated in unanaesthetized cats. Clonidine (0.1-300 micrograms) induced dose-dependent and shortlasting emesis. The emesis induced by the supramaximal dose of clonidine (100 micrograms) was not abolished after the ablation of area postrema. Both the alpha 2 adrenoceptor blocking agent idazoxan and the mixed alpha 1 and alpha 2 adrenoceptor antagonist phenoxybenzamine, injected intracerebroventricularly, attenuated or abolished the emesis induced by clonidine (100 micrograms). On the other hand, the alpha 2 adrenoceptor blocking agent yohimbine, the alpha 1 adrenoceptor blocking drug prazosin and the non-selective beta-adrenoceptor antagonist propranolol, injected into the cerebral ventricles, had no significant effect on clonidine-induced emesis. The antimuscarinic drug atropine injected into the cerebral ventricles prevented the clonidine-induced emesis in a dose-dependent manner. The dopamine antagonist chlorpromazine, the 5-hydroxytryptamine blocking agent methysergide and the histamine H1 and H2 receptor antagonists, antazoline and cimetidine, injected intracerebroventricularly reduced or abolished the emesis produced by clonidine. The ganglionic blocking substance mecamylamine and the opioid antagonist naloxone, all injected into the cerebral ventricles, had no significant effect on clonidine-induced emesis. In cats pretreated with the intracerebroventricular competitive inhibitor of the synthesis of catecholamines, alpha-methyl-p-tyrosine, as well as with the inhibitor of acetylcholine synthesis hemicholinium-3, the emesis caused by clonidine was depressed or abolished. The clonidine-induced emesis was also abolished when catecholamine stores were depleted by intracerebroventricular reserpine. However, the clonidine-induced emesis was not significantly changed when 5-hydroxylryptaminergic nerve terminals were damaged by 5,6-dihydroxytryptamine. It follows, therefore, that cholinergic and noradrenergic mechanisms are of basic importance for the emetic action of clonidine. With regard to receptors, the emesis induced by clonidine injected into the cerebral ventricles, is mediated at least in part through alpha-adrenoceptors, muscarinic cholinoceptors, 5-hydroxytryptamine receptors and H1 and H2 histamine receptors. These receptors appear to be located mostly presynaptically and they transmit emetic impulses to neurones integrating them into emesis. However, the direct effect of clonidine on postsynaptic receptors cannot be excluded, particularly when muscarinic and 5-hydroxytryptamine receptors are implicated. Taken together, these results point to the existence of a multitransmitter pathway/s outside the area postrema, subserving the central regulation of emesis.

Adrenergic alpha-Agonists↗
PubMed1993

Effects of blood pressure changes on the catecholamine release in the locus coeruleus of cats anaesthetized with pentobarbital or chloralose.

Effects of carotid occlusion and drugs applied intravenously on the release of endogenous catecholamines in the locus coeruleus of cats anaesthetized with pentobarbital or chloralose were investigated. The locus coeruleus was superfused bilaterally with artificial cerebrospinal fluid through push-pull cannulae inserted stereotaxically. Dopamine, noradrenaline and in some experiments also adrenaline were determined radioenzymatically in the superfusate. Under pentobarbital anaesthesia, a bilateral carotid occlusion increased the release rate of noradrenaline in the locus coeruleus, while the release of dopamine was decreased. These changes were due to the fall of blood pressure in the carotid sinus caused by the occlusion. Loading of baroreceptors by elevating blood pressure with phenylephrine (10 micrograms.kg-1 x min-1, i.v. infusion) was accompanied by a decreased release of noradrenaline in the locus coeruleus. This decrease in noradrenaline release was not detected in the caudal aspect of the locus coeruleus. Under chloralose anaesthesia, phenylephrine diminished the release rate of noradrenaline to about the same extent as under pentobarbital anaesthesia. The release rate of adrenaline was also decreased. A prolonged infusion of phenylephrine led to a prolonged pressor response associated with a sustained decrease in the noradrenaline release rate. Intravenous injection of chlorisondamine (3 mg.kg-1) did not change the release of noradrenaline, while dopamine release was reduced. It is concluded that the release of catecholamines in the locus coeruleus is influenced by signals originating from peripheral baroreceptors. The influences are similar under pentobarbital and chloralose anaesthesia. Noradrenergic neurons responding to haemodynamic signals are not uniformly distributed within the locus coeruleus.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1989

Neural mechanism generating firing patterns in jaw motoneurons during the food-induced response in Aplysia kurodai. I. Identification and characterization of premotor neurons.

1. In each right and left buccal ganglia of Aplysia kurodai, we identified 4 premotor neurons impinging on the ipsilateral jaw-closing and -opening motoneurons. Three of them (MA1 neurons) had features of multifunctional neurons. Current-induced spikes in the MA1 neurons produced excitatory junction potentials (EJPs) in the buccal muscle fibers. In addition, tactile stimulation of the buccal muscle surface produced a train of spikes in the MA1 neurons without synaptic input. The other neuron (MA2) had only a premotor function. 2. The MA1 and MA2 neurons had similar synaptic effects on the jaw-closing and -opening motoneurons. Current-induced spikes in the premotor neurons gave rise to monosynaptic inhibitory postsynaptic potentials (IPSPs) in the ipsilateral jaw-closing motoneurons. Simultaneously, spikes in one of the MA1 neurons and the MA2 also gave rise to monosynaptic excitatory postsynaptic potentials (EPSPs) in the ipsilateral jaw-opening motoneuron. 3. The IPSPs and the EPSPs induced by spikes in the premotor neurons were reversibly blocked by d-tubocurarine and hexamethonium, respectively, suggesting that the MA1 and MA2 neurons are cholinergic. 4. When depolarizing and hyperpolarizing current pulses were passed into one premotor neuron, attenuated but similar potential changes were produced in another randomly selected premotor neuron in the same ganglion, suggesting that they are electronically coupled.

Animals↗
PubMed1975

Micro-electrophoretic studies in the cat pulvinar region: effect of acetylcholine.

1. In the posterior half of the pulvinar of cats anaesthetized with halothane and nitrous oxide, the majority of neurons were fired by ACh released with small electrophoretic currents. In the anterior part of that nucleus, ACh had more variable effects: excitation, depression or none. 2. In comparison with L-glutamate, DL-homocysteic acid and DL-aspartic acid, ACh appeared to be the most potent excitant. 3. ACh-induced discharges were easily and reversibly blocked by low doses of atropine. In most cases, ACh effects could not be blocked selectively by mecamylamine or dihydro-beta-erythroidine. 4. Nicotine failed to mimic ACh, whereas carbachol was a potent excitant and was readily blocked by low doses of atropine. 5. The histochemical reaction to acetylcholinesterase was moderate in the pulvinar. 6. These observations support the view that pulvinar cells differ from other thalamic cells.

Acetylcholine↗
PubMed1996

Pharmacological manipulation of cardiovascular responses to lower body negative pressure.

To evaluate influences on blood volume distribution, atrial natriuretic peptide concentrations (ANP) and thoracic and leg electrical impedance at 2.5 (TI2.5 and LI2.5, respectively) and 100 kHz (TI100 and LI100, respectively) were monitored during administration of ketanserin, noradrenaline and trimetaphan combined with lower body negative pressure (LBNP) in 12 subjects. Administration of clinically relevant doses of ketanserin alone did not induce changes in mean arterial pressure (MAP) or in the central blood volume, as electrical impedance and ANP concentrations did not change. During continued infusion of ketanserin an increase in MAP from a mean of 90 (range 83-108) to 113 (range 98-138) mmHg was induced by noradrenaline, but TI2.5 [mean 45.6 (range 39.3-54.2)] and TI100 [mean 33.8 (range 27.5-38.5) omega] remainded stable until ganglionic blockade and LBNP were applied, when they increased by a mean of 3.1 (range 2.0-6.1) and 2.7 (range 1.1-4.2) omega, respectively (P < 0.05). Conversely, LI2.5 [mean 79.6 (range 74.1-89.4)] and LI100 [mean 56.7 (range 52.4-63.3) omega] decreased by a mean of 3.2 (range 1.2-8.0) and 2.3 (range 0.9-3.9) omega, ANP from a mean of 27.7 (range 10.2-62.7) to 12.7 (range 7.1-27.5) pmol.l-1 and MAP fell to a mean of 62 (range 42-70) mmHg (P < 0.05). The heart rate was a mean of 75 (range 69-77) beats.min-1 and did not change until LBNP, when it increased to a mean of 102 (range 78-104) beats.min-1, as presyncopal symptoms appeared. The data indicated that serotonergic blockade by ketanserin and alpha-sympathetic stimulation by noradrenaline did not affect blood volume distribution in normal humans, but that ganglionic blockade combined with LBNP reduced the central blood volume as leg volume increased; during central hypovolaemia tachycardia induced by ganglionic blockade did not prevent the fall in MAP, and thereby the appearance of presyncopal symptoms.

Adrenergic alpha-Agonists↗
PubMed1975

The influence of imipramine on dopamine-induced ganglionic inhibition and neurogenic vasodilatation in the dog.

Imipramine potentiates the dopamine-induced inhibition in the paravertebral lumbar ganglia of the dog. Potentiation by imipramine of the dopamine-induced neurogenic vasodilatation in the isolated perfused gracilis muscle, is seen in cross-circulation preparations only, where imipramine is injected into the perfusion circuit of an isolated perfused gracilis muscle, it antagonizes the dopamine-induced neurogenic vasodilatation. When imipramine is injected intravenously into a dog with an autoperfused gracilis muscle, the peripheral antagonism masks the potentiating effect at the ganglionic level, and the dopamine-induced neurogenic vasodilatation is abolished.

Action Potentials↗
PubMed1983

Channel-blocking activity is a possible mechanism for a selective ganglionic blockade.

The actions of bis-ammonium compounds (BAC) on the ionic channels activated by acetylcholine (ACh) were studied in voltage-clamped neurones of rabbit isolated superior cervical ganglion. The kinetics of binding of BAC to open channels was estimated from shortening of the decay of fast excitatory postsynaptic current. The kinetics of dissociation of BAC from open channels was estimated from the kinetics of restoring of second response to double-pulse application of ACh in presence of BAC. The ganglion-blocking activities of BAC correlated with the rate constants of their binding to open channels. It was concluded that selective ganglion-blocking actions of BAC were determined by their channel-blocking activities.

Acetylcholine↗
PubMed1984

Noncholinesterase actions of an irreversible acetylcholinesterase inhibitor on synaptic transmission and membrane properties in autonomic ganglia.

Superfusion of the organophosphorous acetylcholinesterase inhibitor soman (pinacolyl methylphosphonofluoridate; 0.01-25 microM) produced a dose-dependent reduction of extracellularly and intracellularly recorded synaptic responses in the isolated rat superior cervical ganglia at frequencies of orthodromic stimulation that do not normally produce synaptic depression. The magnitude of depression was dependent upon the frequency of stimulation (0.02-1 Hz), was maintained after the removal of soman from the superfusion solution, and recovered by over 65% during periods of inactivity. The depression of synaptic transmission produced by soman was not dependent upon the inhibition of acetylcholinesterase (AChE) activity by this agent. Transmission was increasingly depressed by doses of soman greater than those needed to inactivate all measurable ganglionic AChE activity. Dose-dependent depression of synaptic transmission in soman also occurred after pretreatment with the irreversible AChE inhibitor diisopropylphosphofluoridate (DFP; 100 microM), which inhibited greater than 98% of the AChE activity in the ganglia. Soman produced a decline in the input resistance, resting potential, spike amplitude, and spike threshold and a reduction in the hyperpolarizing afterpotential. Soman-induced depression of synaptic transmission was not due primarily to a blockade of postsynaptic nicotinic receptors. At concentrations of soman which produced significant depression in transmission, ganglionic depolarization produced by bath-applied carbamylcholine (carbachol) was either slightly depressed or facilitated. In the presence of soman, repetitive focal application of acetylcholine or carbachol did not reveal use-dependent desensitization. Muscarinic antagonists, atropine and pirenzepine, protected against the use-dependent depression of synaptic transmission induced by soman. These results suggest that a principal site of action for soman is at the presynaptic terminal and that this site is sensitive to muscarinic receptor blockade.

Animals↗
PubMed1991

Allergic manifestations of human immunodeficiency virus (HIV) infection.

Drug allergy is the most common and significant allergic manifestation of HIV3 infection. Initially described in patients treated with SMX-TMP for PCP, allergy is now known to involve a multitude of drugs. The pathogenesis of, and risk factors for, allergy in HIV infection are poorly understood, although there is evidence suggesting that allergy is more common with advancing immunodeficiency. HIV-negative subjects with sulfonamide allergy may have drug-specific antibodies and drug metabolite-induced lymphocyte cytotoxicity, abnormalities that could partly explain the allergic mechanisms and which may have future diagnostic potential; these abnormalities have not been described in HIV-infected subjects. Therapy includes avoidance, suppressive agents such as corticosteroids, and desensitization, although the appropriate role for each is not entirely clear. Serum IgE levels have been shown to rise with progressive disease; those patients with higher levels may have a worse prognosis. The mechanisms of this rise are multifactorial, probably a combination of altered T-lymphocyte regulation of IgE synthesis and of production of specific IgE directed against microbial antigens.

Acquired Immunodeficiency Syndrome↗