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Biomedical subjects

J T Martin

Publications and source records attributed to J T Martin.

At least 55 records · Page 3Linked to original sources
PubMed1983

Succinylcholine-induced increases in plasma catecholamine levels in humans.

Given the hypothesis that interaction of succinylcholine with nicotinic receptors releases endogenous catecholamines, plasma levels of epinephrine and norepinephrine were determined in anesthetized and manually ventilated patients immediately before and 2 min after intravenous administration of succinylcholine. Anesthesia was induced with intravenous thiopental (3-4 mg/kg) followed by the administration of nitrous oxide and oxygen (1:1) and 0.5-1.0% halothane. Stimulation of the patients was avoided. Succinylcholine (1 mg/kg) or metocurine (0.3 mg/kg) was injected intravenously and ventilation was controlled without intubation. Plasma norepinephrine levels increased from 301 pg/ml to 491 pg/ml (SEM = +/- 19 pg/ml, P less than 0.01, N = 5) 2 min after the injection of succinylcholine; the increase in plasma epinephrine was not statistically significant. The time course of catecholamine elevation was studied in three additional patients. The increase of norepinephrine occurred immediately after the injection of succinylcholine, peaked (647 +/- 67 pg/ml) around the third minute, and disappeared by the 10th min. The increase in epinephrine was less marked. Plasma levels of catecholamines did not change after the injection of metocurine (N = 2). The possibility that succinylcholine stimulates nicotinic receptors on the postganglionic sympathetic terminals is discussed. We propose that the elevation of plasma norepinephrine might contribute to the development of early adverse cardiovascular reactions to succinylcholine.

Adult↗
PubMed1982

Diurnal variation in hypothalamic monoamines and plasma corticosterone in the turkey after inhibition of tyrosine hydroxylase or tryptophan hydroxylase.

Circadian rhythms occur in hypothalamic serotonin content in the turkey. Inhibition of serotonin (5-HT) synthesis by parachlorophenylalanine (PCPA) blocks circadian variation in hypothalamic serotonin levels suggesting that the major cause of diurnal fluctuations is differing rates of synthesis of the amine. PCPA treatment also abolishes the diurnal rhythm in plasma corticosterone and elevates the basal levels of this steroid suggesting that 5-HT terminals in the hypothalamus may inhibit the release of ACTH at certain times of the day and in this fashion generate diurnal fluctuations in plasma corticosterone. Hypothalamic levels of dopamine (DA) and norepinephrine (NE) also vary diurnally, and synthesis inhibition with alpha-methyl-para-tyrosine abolishes the diurnal rhythm in NE but not DA or in plasma corticosterone. Temporal changes in release and/or degradation of DA are significant factors contributing to the diurnal rhythms of this amine in the hypothalamus. Diurnal fluctuations in plasma corticosterone do not depend on recent synthesis of catecholamines.

Animals↗
PubMed1982

Effects of testosterone, dihydrotestosterone, or estradiol administered neonatally on sexual behavior of female ferrets.

Groups of female ferrets born in the laboratory received sc Silastic capsules containing testosterone (T), 5 alpha-dihydrotestosterone (DHT), 17 beta-estradiol (E), or no steroid for 15 days beginning on the day of birth; an additional group of male ferrets received empty sc capsules neonatally. All ferrets were gonadectomized at 11 weeks of age and were subsequently tested for masculine and feminine sexual behaviors while being treated consecutively over an 8-month period with several different gonadal steroids. The ability to display masculine sexual behavior was studied in the absence of replacement hormones and during a counterbalanced sequence of treatments with Silastic capsules containing T, E, or DHT. The maximal amount of neck grip, mount, and pelvic thrusting behavior displayed, regardless of adult endocrine treatment, was significantly greater in control male and neonatally T-treated females than in females that had received no hormone, E, or DHT neonatally. Animals in all five groups displayed equivalent increments in sexual receptivity in response to daily sc injections of increasing dosages of estradiol benzoate. Polyacrylamide gel electrophoresis of plasma collected from newborn female ferrets revealed no binding of either [3H]E or [3H]T, whereas two binding peaks were found for [3H]DHT. After the administration of androgen in adulthood, equivalent clitoral growth and ossification occurred in females given either T or DHT neonatally. These results suggest that in ferrets, behavioral masculinization occurs in response to neonatal exposure to T itself and not to its major neural metabolites, E and DHT. They also show that behavioral defeminization fails to occur in ferrets even after neonatal exposure to pharmacological amounts of E, T, or DHT.

Animals↗
PubMed1981

Functions of alpha-melanotropin and other opiomelanocortin peptides in labour, intrauterine growth and brain development.

In a number of animals and in humans, factors from the fetal hypothalamus function in intrauterine growth, in labour and in brain development. Peptides of the opiomelanocortin family are produced by the pituitary, brain and placenta and are probably involved in these developmental processes. In the rat, alpha-MSH stimulates fetal growth, protein synthesis, wound healing and liver regeneration and it reduces periosteal bone resorption. In chick embryos, alpha-MSH restores the corticosteroid-induced growth retardation. Thus alpha-MSH seems to possess general trophic properties. The fetal brain in humans is involved in timing the moment of birth. This process is probably mediated by peptides of the opiomelanocortin family as suggested from observations in anencephaly and other congenital brain anomalies and from the influence of corticosteroids or ACTH on labour. The high percentage of premature deliveries in heroin addicts is worth examining endocrinologically, in this respect. The exact nature of the peptides and mechanisms involved in labour is not yet known. Some peptides of the opiomelanocortin family induce an acceleration of brain development. Neonatal treatment of rats with alpha-MSH alters their later behaviour while ACTH fragments accelerate the onset of eye-opening. Opiates and methadone inhibit brain development, and neonatal administration of beta-endorphin or naloxone causes permanent insensibility to temperature stimuli. The interrelated nature of the fetal pituitary, brain and placenta does not, at present, allow us to pin down which of these structures is primarily involved in the regulation of intrauterine growth, labour and brain development.

Adrenocorticotropic Hormone↗
PubMed1980

Cerebellar degeneration due to chronic phenytoin therapy.

Five patients developed cerebellar degeneration while being treated with phenytoin. All had high plasma levels of the drug, and none was having seizures of a type that could have caused systemic hypoxia at the time the cerebellar syndrome appeared. Cerebellar degeneration was confirmed by the finding of atrophy on CT scan and by persistence of cerebellar signs when plasma phenytoin levels were decreased. We suggest that chronic phenytoin therapy can cause cerebellar degeneration. The question of whether phenytoin or the cumulative effect of hypoxia from repeated convulsions causes cerebellar degeneration should not be posed as one of exclusive alternatives, since hypoxia is a well-known cause of cerebellar atrophy. Instead, the question should be whether or not phenytoin can also be responsible. The cases reported here suggest that it can.

Adult↗
PubMed1979

Computed tomography in cerebellar atrophic processes.

Forty-six patients with cerebellar atrophy were identified by review of CT scans of 7,500 patients. Independent examination of a separate file of the same group disclosed 49 patients whose history indicated cerebellar degeneration. Forty-three patients were in both groups indicating excellent correlation between CT abnormality and clinical cerebellar signs. Three patients with CT cerebellar atrophy failed to show clinical cerebellar signs, and 6 had clinical signs without evidence of changes on CT. Specific anatomic correlation was suggested in 10 of 13 patients with predominantly midline cerebellar CT abnormalities, and in 3 with olivopontocerebellar degeneration clinically who showed brainstem and cerebellar atrophy.

Atrophy↗
PubMed1978

Imprinting behavior: pituitary-adrenocortical modulation of the approach response.

Plasma corticosterone concentrations in newly hatched ducklings exposed to an imprinting model are inversely related to the strength of approach behavior. Injections of corticosterone before imprinting reduces following, whereas alpha1-10-adrenocorticotropin or antiserum to corticosterone augments following behavior. The sensitive period for imprinting may be regulated by changes in the pituitary-adrenocortical axis.

Adrenocorticotropic Hormone↗