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Biomedical subjects

S B Backman

Publications and source records attributed to S B Backman.

32 records · Page 2Linked to original sources
PubMed1996

Neostigmine-induced bradycardia following recent vs remote cardiac transplantation in the same patient.

PURPOSE: This report describes the effects of neostigmine on heart rate in the same patient following recent and remote cardiac transplantation. CLINICAL FEATURES: Eighty-six months following the first transplant, neostigmine 5.0 micrograms.kg-1 i.v. produced a 10% reduction in heart rate which was reversed by atropine 1.2 mg. For 24 months prior to this initial study, the patient experienced angina, suggesting cardiac afferent reinnervation. Three months after the second heart transplant, a second study showed that a six-fold increase in the dose of neostigmine, 30.0 micrograms.kg-1, only produced a 3.5% reduction in heart rate which was reversed by atropine 1.2 mg. CONCLUSIONS: These observations indicate that neostigmine produces bradycardia following cardiac transplantation, and suggest that a greater response may be observed in remotely than in recently transplanted patients.

Bradycardia↗
PubMed1996

Different properties of the bradycardia produced by neostigmine and edrophonium in the cat.

PURPOSE: The bradycardia produced by neostigmine and edrophonium was examined according to its relation to cholinesterase inhibition and to its sensitivity to block by muscarinic receptor antagonists. For comparison, the ability of muscarinic antagonists to block the bradycardia produced by electrical stimulation of the vagus nerve was determined. METHODS: Cats were anaesthetized, vagotomized and propranolol-treated. Heart rate was continuously recorded. Erythrocyte cholinesterase activity of arterial blood was measured using a radiometric technique. The right vagus nerve was isolated for electrical stimulation. The muscarinic antagonists used were atropine, glycopyrrolate, pancuronium, gallamine, and AFDX-116. RESULTS: Neostigmine produced a dose-dependent decrease in cholinesterase activity which reached a plateau at a cumulative dose of 0.16 mg.kg-1 (ED50 0.009 +/- 0.003 mg.kg-1). Neostigmine produced a dose-dependent decrease in heart rate with the dose-response relationship (ED50 0.1 +/- 0.01 mg.kg-1; P = 0.0006) shifted to the right of that for the inhibition of cholinesterase activity. In contrast to the anticholinesterase effect, the bradycardic effect did not reach a plateau and continued to increase even at doses at which the cholinesterase inhibition was maximal. The maximal decrease in heart rate when the heart was still in sinus rhythm was by 81 +/- 13 bpm (49 +/- 7% of baseline), which was produced by a dose of 0.32 mg.kg-1. Edrophonium produced dose-dependent decreases in cholinesterase activity and heart rate, which were highly correlated (correlation coefficient r = 0.99, P < 0.0001). The ED50 of the reduction in heart rate (0.9 +/- 0.18 mg.kg-1) and cholinesterase activity (0.89 +/- 0.12 mg.kg-1) produced by edrophonium were similar. Moreover, the reduction in heart rate and cholinesterase activity produced by edrophonium reached a plateau at the same dose (6.4 mg.kg-1). At this dose, heart rate decreased by 22 +/- 2 bpm (14.6 +/- 0.9% of baseline). Compared to the bradycardia produced by stimulation of the vagus nerve, that produced by neostigmine was blocked by muscarinic antagonists at significantly lower doses while that produced by edrophonium was blocked at similar doses. CONCLUSIONS: The neostigmine-induced bradycardia is poorly correlated with cholinesterase inhibition compared to that produced by edrophonium, and has a higher sensitivity to muscarinic receptor antagonists compared to that produced by edrophonium or vagus nerve stimulation. These results are consistent with the hypothesis that the neostigmine-induced bradycardia is, in part, the result of neostigmine directly activating cholinergic receptors within the cardiac parasympathetic pathway. The bradycardia produced by edrophonium may be accounted for solely by an anticholinesterase action.

Acetylcholine↗
PubMed1993

Mechanism of the bradycardia produced in the cat by the anticholinesterase neostigmine.

Neostigmine evoked bradycardia in vagotomized, propranolol-treated cats. Heart rate decreased by 50% with 0.4 +/- 0.2 mg/kg (mean +/- S.D.) i.v. of neostigmine. The bradycardia was attenuated after acetylcholine (ACh) depletion in the cardiac parasympathetic pathway suggesting ACh release within this pathway was involved. The bradycardia was unchanged after preganglionic terminal degeneration suggesting ACh release was from cardiac ganglion cells. Edrophonium produced a much weaker bradycardia suggesting the anticholinesterase effect of neostigmine may not produce the bradycardia. The neostigmine-induced bradycardia was blocked by systemic atropine (ED50, 0.005 +/- 0.001 mg/kg), pancuronium bromide (ED50, 0.033 +/- 0.021 mg/kg), pirenzepine (ED50, 74.7 +/- 7.9 micrograms/kg), hexamethonium (ED50, 8.3 +/- 1.6 mg/kg) and d-tubocurarine (ED50, 8.6 +/- 3.0 micrograms/kg). The doses of hexamethonium and d-tubocurarine that blocked the neostigmine-induced bradycardia were significantly higher than required for blocking the bradycardia produced by vagus nerve stimulation. Hexamethonium (60 mg/kg i.v.) had no effect on the bradycardia produced by the muscarinic agonist methacholine (100-300 micrograms/kg/min i.v.). The dose of pirenzepine that blocked the neostigmine-induced bradycardia was lower than required for blocking the bradycardia produced by vagus nerve stimulation. McN-A-343 ([4-hydroxy-2-butynyl]-1-trimethyl ammonium m-chlorocarbanilate chloride) (1 mg/kg i.v.) did not produce bradycardia. These observations suggest neostigmine evokes bradycardia by activation of ACh receptors on cardiac ganglion cells producing ACh release and activation of cardiac M2 receptors. The low sensitivity of the neostigmine-induced bradycardia to pirenzepine, and the failure of McN-A-343 to evoke bradycardia, suggest the receptor on cardiac ganglion cells is not an M1-type.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1990

Adrenal versus nonadrenal sympathetic preganglionic neurones in the lower thoracic intermediolateral nucleus of the cat: effects of serotonin, substance P, and thyrotropin-releasing hormone.

Adrenal and nonadrenal sympathetic preganglionic neurones (SPNs) in the intermediolateral nucleus of spinal segments T8-T10 in the cat were compared according to their responses to iontophoretic application of serotonin, substance P, and thyrotropin-releasing hormone (TRH). Responses of both types of SPN to iontophoretic application of serotonin were characterized by an increase in the rate of discharge that was slow in onset (mean +/- SD = 36 +/- 21 s) and prolonged in afterdischarge (115 +/- 70 s) following termination of application. Depression was never observed and responses were similar whether using serotonin at a pH of 3.3 or 4.5, suggesting that the absence of a depressant effect cannot be accounted for by pH, as has been reported with cortical neurones. Iontophoretic application of methysergide resulted in a decrease in the rate of discharge of both types of SPN and blocked the excitatory responses to serotonin. Adrenal and nonadrenal SPNs were excited by iontophoretic application of substance P. Responses of both types of SPN were similar and were characterized by a gradual increase in the rate of discharge that was slow in onset (42 +/- 27 s) and prolonged in afterdischarge (96 +/- 42 s). Finally, adrenal and nonadrenal SPNs were also weakly excited by iontophoretic application of TRH. These responses were slow in onset (48 +/- 27 s) and prolonged in afterdischarge (78 +/- 35 s). These data indicate that serotonin, substance P, and TRH exert excitatory effects on functionally dissimilar sympathetic preganglionic neurones and support the possibility that they may be chemical mediators of synaptic transmission in the intermediolateral nucleus. In addition, these data may be interpreted to support the notion that serotonin, substance P, and TRH are involved in global activation of the sympathetic nervous system.

Adrenal Glands↗
PubMed1990

Adrenal versus nonadrenal sympathetic preganglionic neurones in the lower thoracic intermediolateral nucleus of the cat: physiological properties.

Adrenal and nonadrenal sympathetic preganglionic neurones (SPNs) in the intermediolateral nucleus of spinal segments T8-T10 in the cat were compared according to a number of physiological properties. An SPN was classified as "adrenal" (n = 37) if it could be antidromically activated by electrical stimulation of the adrenal medulla. An SPN that could not be activated from the adrenal medulla yet could be antidromically activated by electrical stimulation of the greater splanchnic nerve was classified as "nonadrenal" (n = 123). Approximately 50% of adrenal SPNs (17 out of 37) were activated antidromically by stimulation of both the greater splanchnic nerve and adrenal medulla, suggesting that these neurones projected to the adrenal medulla via the greater splanchnic nerve, with the other adrenal SPNs taking a different route. The mean conduction velocities of adrenal (6.7 +/- 1.8 (SD) m/s) and nonadrenal (6.7 +/- 1.5 m/s) sympathetic preganglionic axons were similar. Over 80% of adrenal (31 out of 37) and nonadrenal (104 out of 116) SPNs were spontaneously active. The two types of neurone were indistinguishable in terms of the rates and patterns of discharge. Adrenal SPNs discharged with a mean rate of 1.4 +/- 1.1 spikes/s, and nonadrenal SPNs discharged with a mean rate of 1.8 +/- 1.4 spikes/s. With both types of SPN, the pattern of spontaneous activity was either irregular or phasic. With the latter pattern, periodic bursts of discharge were at the same frequency as oscillations in arterial pressure, frequency of ventilation, or phrenic nerve discharge. These data suggest that adrenal and nonadrenal sympathetic preganglionic neurones in the intermediolateral nucleus in caudal thoracic segments share a number of common physiological properties.

Adrenal Glands↗
PubMed1984

Evidence for a monosynaptic connection between slowly adapting pulmonary stretch receptor afferents and inspiratory beta neurones.

The synaptic connection between slowly adapting pulmonary stretch receptor afferents and inspiratory neurones within a region ventral to the tractus solitarius was determined using intracellular recording and spike triggered averaging techniques. When the vagus nerve was stimulated at intensities eliciting a Hering-Breuer reflex, the difference in mean latency between centrally recorded action potentials of slowly adapting pulmonary stretch receptor afferents and e.p.s.p.s of inspiratory beta neurones was 0.2 ms. This difference is indicative of a monosynaptic connection. Extracellular single unit spikes of slowly adapting pulmonary stretch receptors recorded from the nodose ganglion were used to trigger the averaging of synaptic noise recorded from inspiratory neurones. A prominent wave of synaptic depolarization was observed in all inspiratory beta neurones even when a small number of sweeps were averaged. This depolarization was absent from inspiratory alpha neurones. The shape indices of these depolarizations are consistent with a monosynaptic connection between slowly adapting pulmonary stretch receptor afferents and inspiratory beta neurones. In addition, the data raise the possibility that this connection is multiple and distributed.

Animals↗
PubMed1984

Effects of oxytocin and vasopressin on thoracic sympathetic preganglionic neurones in the cat.

When applied by iontophoresis onto single sympathetic preganglionic neurones in the intermediolateral nucleus of segments T1-T3 in the cat, oxytocin and vasopressin each had an excitatory effect. This effect consisted of a prolonged (30-300 sec) after-discharge following termination of application. These results indicate that oxytocin and vasopressin each exert excitatory effects on sympathetic preganglionic neurones and support the possibility that they may be chemical mediators of synaptic transmission in the intermediolateral nucleus, perhaps in cardioacceleratory and/or pressor pathways descending from the paraventricular nucleus of the hypothalamus.

Animals↗
PubMed1984

Effect of substance P and thyrotropin-releasing hormone on sympathetic preganglionic neurones in the upper thoracic intermediolateral nucleus of the cat.

When applied by iontophoresis onto single sympathetic preganglionic neurones in he intermediolateral nucleus of spinal segments T1-T3 in the cat, substance P and thyrotropin-releasing hormone (TRH) each had a weak excitatory effect. Two-thirds of the neurones studied were excited by substance P while one-fifth were excited by TRH. The time courses of the responses to substance P and to TRH were similar, and consisted of an increase in the rate of discharge with a latency of approximately 30 s from the onset of application. They were also prolonged (30-320 s) in afterdischarge following termination of application. These results indicate that substance P and TRH exert excitatory effects on single sympathetic pregnanglionic neurones, and support the possibility that they may be chemical mediators of synaptic transmission in the intermediolateral nucleus.

Animals↗
PubMed1984

Physiological properties of sympathetic preganglionic neurones in the thoracic intermediolateral nucleus of the cat.

Extracellular spikes were recorded from cell bodies of sympathetic preganglionic neurones in spinal segments T1-T3 of the cat. Each neurone was identified by its antidromic response to electrical stimulation of the sympathetic chain and was found in histological sections to lie within the intermediolateral nucleus. Physiological properties studied in detail included basal activity, spike configuration, and latency of antidromic activation. Also studied, in tests with paired stimuli, were the threshold interstimulus interval evoking two responses, as well as changes in amplitude and latency of the second spike which occurred at intervals near this threshold. Approximately 60% of the units studied were spontaneously active, the rest were silent. Spontaneous activity was characterized by a slow (mean = 3.1 +/- 2.6 (SD) spikes/s), irregular pattern of discharge. With approximately one-third of the cases there was a periodic pattern of discharge in phase with oscillations in blood pressure. This correlation of phasic activity suggests that many of the units studied were involved specifically in cardiovascular function. Silent and spontaneously active units could not be differentiated on the basis of latency of antidromic activation or threshold interstimulus interval; mean latency for the two groups was 7.2 +/- 4.9 ms, mean threshold interval was 6.4 +/- 4.7 ms. Thus, with the exception of basal activity, the physiological properties studied failed to indicate more than a single population of neurones. These results therefore suggest that the sympathetic preganglionic neurones in the intermediolateral nucleus subserving varied autonomic functions share overlapping physiological properties, and that functional differentiation of these neurones may be based on differences in synaptic inputs.

Animals↗
PubMed1983

Effects of GABA and glycine on sympathetic preganglionic neurons in the upper thoracic intermediolateral nucleus of the cat.

GABA (5-137 nA) and glycine (5-75 nA) each inhibit spontaneous activity and block antidromic invasion of the soma-dendritic region of single sympathetic preganglionic neurons (SPNs) in the intermediolateral nucleus of T1-T3 in the cat. These effects are rapid in onset and recovery. They are selectively blocked by bicuculline and strychnine respectively. Thus, GABA and glycine exert pharmacologically specific inhibitory effects on SPNs and this supports the possibility that they may be chemical mediators of inhibitory inputs directly onto these neurons.

Animals↗
PubMed1983

Effects of glutamate and aspartate on sympathetic preganglionic neurons in the upper thoracic intermediolateral nucleus of the cat.

Glutamate and aspartate excited all spontaneously active sympathetic preganglionic neurons (SPNs) tested in the intermediolateral nucleus of spinal segments T1-T3. Most silent neurons could be induced to discharge but the remainder showed only a decrease in antidromic spike amplitude. These effects were typically fast (on, off less than 1 s). D,L-Homocysteic acid also produced excitation; this effect was typically slower. Glutamate and aspartate were usually equipotent; 20% were differentially sensitive to aspartate, 10% to glutamate.

Animals↗