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Biomedical subjects

A M Snyder

Publications and source records attributed to A M Snyder.

11 recordsLinked to original sources
PubMed2000

An assessment of desflurane for use during cardiac electrophysiological study and radiofrequency ablation of supraventricular dysrhythmias in children.

Desflurane has several properties making it a desirable agent for use in electrophysiological studies (EPS) for diagnosis and treatment of cardiac dysrhythmias. We studied 47 children, mean age 12.8+/-4.6 years, mean weight 52.9+/-24.0 kg, with clinical history of supra- ventricular tachycardia (SVT) during EPS using desflurane in a crossover comparison with fentanyl. The patients served as their own controls. All received oral premedication with lorazepam, and intravenous induction with thiopentone, rocuronium, and oxygen. Group 1 (n=24) were administered fentanyl 10 microg.kg-1 bolus i.v. with an infusion of 3 microg.kg-1.h-1 during initial EPS. Fentanyl was discontinued and desflurane, 6% endtidal, was administered and the EPS repeated. Group 2 (n=23) were initially administered 6% desflurane after induction, and following EPS the desflurane was discontinued and the patients administered fentanyl 3 microg.kg-1 bolus and EPS repeated (explanations of EPS abbreviations are provided). Desflurane reduced the mean arterial pressure (MAP) in all patients. In Group 1, desflurane shortened the sinus cycle length (SCL), i.e. increasing the heart rate, and atrial effective refractory period (AERP) while Group 2 demonstrated no such effect on AERP. There were no other significant differences between fentanyl or desflurane techniques in terms of EPS measurements. SVT was inducible with both agents in both groups. Desflurane seems an acceptable agent for use during EPS procedures.

Administration, Oral↗
PubMed1997

Use of extinction and reinforcement to increase food consumption and reduce expulsion.

Extinction and reinforcement contingencies were used to treat 2 children with feeding disorders. Positive reinforcement and avoidance extinction effectively increased food acceptance but also increased food expulsion. Reduced expulsion and increased swallowing were achieved by repeated presentation of expelled food, a second extinction component

Behavior Therapy↗
PubMed1989

Analgesic effects of phencyclidine-like drugs in rhesus monkeys.

Analgesic and discriminative stimulus effects of phencyclidine (PCP), ketamine, dextrorphan, (+)-N-allyl-normetazocine [(+)-SKF 10,047] and (+)-5-methyl-10,11-dihydro-5H-dibenzo(a,d) cyclohepten-5,10-amine maleate (MK-801) were studied in rhesus monkeys. All five compounds increased in a dose-related manner the latency for monkeys to remove their tails from warm water with the order of potency being MK-801 greater than PCP greater than ketamine greater than (+)-SKF 10,047 greater than dextrorphan. Moreover, these effects were temperature-dependent with larger doses required to produce a maximum response when higher temperatures (i.e., 55 degrees C) were studied. The effects of PCP, ketamine, dextrorphan, (+)-SKF 10,047 and MK-801 were not attenuated by a dose (1.0 mg/kg) of the opioid antagonist quadazocine that antagonized the analgesic effects of the opioid mu agonist alfentanil and kappa agonist U-50,488. MK-801, PCP, (+)-SKF 10,047 and dextrorphan also substituted in a dose-related manner for the ketamine discriminative stimulus (1.78 mg/kg) and their relative potency as discriminative stimuli was the same as their relative potency in the tail withdrawal procedure. The apparent analgesic effects of PCP-like drugs occurred at doses 2- to 8-fold larger than doses required for discriminative stimulus effects and 3- to 10-fold smaller than doses required for anesthesia. These results support the notion that PCP-like drugs produce analgesic effects at subanesthetic doses. Moreover, the analgesic effects of PCP and related drugs in rhesus monkeys were not mediated by actions at the opioid receptors known to be associated with analgesia.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1986

Sprouting of serotoninergic afferents into striatum after dopamine-depleting lesions in infant rats: a retrograde transport and immunocytochemical study.

Intraventricular injections of 6-hydroxydopamine in 3-day-old rats resulted in the near-total loss of tyrosine-hydroxylase-immunoreactive processes in the striatum when examined 2-6 months later. This destruction of dopamine (DA) afferents was accompanied by an increase in the density of serotonin (5-HT)-immunoreactive fibers in the striatum. The hyperinnervation was most striking in the rostral striatum, an area containing few 5-HT-immunoreactive fibers in control rats. Retrograde tracing, with either horse-radish peroxidase or rhodamine-labelled microspheres, indicated a significant increase in the number of neurons projecting to the rostral striatum from the dorsal raphe nucleus of lesioned animals. The increase was largely confined to the rostral extent of the dorsal raphe, and overlapped the distribution of cells labelled after injections of HRP into caudal striatum of control and lesioned animals. In sections additionally processed for immunocytochemistry, 80-90% of retrogradely labelled raphe neurons in both groups of animals were found to be 5-HT-immunoreactive. None of changes encountered in infant-lesioned rats were observed 2-4 weeks after 6-HDA was given to adult animals. These findings demonstrate that removal of DA afferents during development leads to an enlargement of the serotoninergic projection from the raphe nucleus to the striatum.

Animals↗
PubMed1985

Stress-induced neurological impairments in an animal model of parkinsonism.

Adult rats were given the neurotoxin 6-hydroxydopamine (6-HDA) by means of cerebrospinal fluid to produce large dopamine-depleting brain lesions. Although the animals behaved normally in their home cages, they became akinetic after such treatments as glucoprivation, tail shock, and exposure to severe cold. The neurological impairments were related both to the extent of dopamine depletion and to the intensity of the stress. Drugs known to enhance dopaminergic function were found to reverse the stress-induced neurological deficits, while dopaminergic antagonists potentiated the debilitating effects of stress. After focal lesions were produced by injecting 6-hydroxydopamine directly into specific brain regions, stress-induced akinesia was found to correlate best with dopamine depletion in the corpus striatum, especially the lateral portion of that structure. These and other findings suggest that the acute emergence of parkinsonian symptoms during stress may reflect extensive damage to the dopaminergic nigrostriatal pathway that had been concealed in a preclinical phase, owing to compensatory neurochemical changes in the dopaminergic neurons that yet remain intact.

Animals↗
PubMed1984

Apparent sprouting of striatal serotonergic terminals after dopamine-depleting brain lesions in neonatal rats.

Near-total dopamine-depleting brain lesions produced in 3-day-old rats by intracerebroventricular injection of the neurotoxin 6-hydroxydopamine led to pronounced increases in striatal serotonin (5-HT) and 5-hydroxyindoleacetic acid contents 1-8 months later. This effect was associated with an increase in in vitro high affinity 5-HT uptake, suggesting that proliferation of new serotonergic terminals had occurred within the striatum. No such effect was obtained when comparable brain lesions were produced in adult rats.

Animals↗
PubMed1984

Effect of dopamine-depleting brain lesions on suckling and weaning in rats.

Rats given large dopamine-depleting brain lesions as adults exhibit severe impairments in ingestive behavior and sensorimotor function. In contrast to these well-known effects, virtually complete destruction of central dopaminergic neurons produced no such dysfunctions when it occurred in neonates. Indeed, rats continued to suckle and grow, albeit somewhat more slowly, and they could be weaned readily when they were 27 days old. Although most brain-damaged animals did not survive weaning when they were 18 days old, whereas controls exhibited no difficulty, this failure appears to be the consequence of their reduced body weight and related inability to maintain body temperature in a relatively cool environment (22 degrees C). Such premature weaning occurred more successfully when growth was stimulated by rearing brain-damaged pups in small litters or when ambient temperatures were raised to 31 degrees C so as to minimize heat loss. These results demonstrate that the effects of near-total dopamine-depleting brain lesions are considerably less severe when they occur in infants than when they occur in adults, and, consequently, they reveal a capacity for neural plasticity during development that is no longer present at maturity.

Animals↗