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Biomedical subjects

J B Martin

Publications and source records attributed to J B Martin.

At least 289 records · Page 16Linked to original sources

Hypothalamic-pituitary responses to intracranial self-stimulation in the rat.

The effects on pituitary and adrenal hormones of intracranial self-stimulation (ISS) and forced stimulation in rewarding (PS) and non-rewarding (NSS) sites were investigated in adult male rats. Growth hormone (GH) was suppressed during periods of ISS and PS and rose sharply to a peak within 15 min of cessation. The interval between GH secretory episodes was significantly shortened during all 3 types of stimulation when compared to the normal rhythmic discharge observed in freely behaving baseline (BL) sampled rats. ISS, PS and NSS resulted in a rapid rise in prolactin (Prl), which returned to normal by the end of each hourly period of stimulation. There was a significant reduction of Prl elevation in the second and third periods of stimulation, suggesting that the first exposure to ISS had a greater stimulatory effect than subsequent stimulations. There was a rapid and sustained release of corticosterone (CS) during ISS and PS. As with Prl, the initial period of either ISS or PS caused a greater effect that subsequent periods. These studies provide data to compare the relationship between ISS and neuroendocrine responses. The hormonal responses, with minor exceptions, were similar under all experimental conditions, and could not be clearly dissociated from previously described stress responses. Neural pathways and substrates involved in GH, Prl and CS secretion are discussed in relation to pathways activated by LH-MFB stimulation. Potential differential functions of monoamines and hypothalamic neuropeptides in behavioral and neuroendocrine regulation are hypothesized.

Animals↗

Neuropharmacological regulation of episodic growth hormone and prolactin secretion in the rat.

The effects on GH and PRL secretion of several pharmacological agents known to modify central neurotransmitter action were determined in unanesthetized male rats. Phenoxybenzamine, an alpha-adrenergic blocker (5 mg/kg iv), abolished episodic GH secretion and caused elevation of serum PRL levels. Propranolol, a beta-adrenergic blocker (5 mg/kg iv), had no effect on GH secretion and caused a small but significant depression in PRL levels. Parachlorophenylalanine methyl ester, an inhibitor of tryptophan hydroxylase (300-350 mg/kg ip), resulted in significant inhibition of GH pulsatile secretion and suppressed PRL levels. Methysergide hydrogen maleinate (25 mg/kg iv), a serotonin receptor antagonist, also inhibited GH secretion, but produced a transient stimulation in PRL levels. Atropine sulfate (2 mg/kg iv) caused significant suppression in GH secretion, but had no effect on PRL. Picrotoxin, a gamma-aminobutyric acid antagonist, in a subconvulsive dose of 1-3 mg/kg iv, also depressed GH episodic secretion but did not affect PRL levels. These results indicate that several neurotransmitters, i.e., norepinephrine, serotonin, acetylcholine, and gamma-aminobutyric acid, found in high concentration in the hypothalamus, influence GH and PRL secretion.

Animals↗

Antiserum to somatostatin reverses starvation-induced inhibition of growth hormone but not insulin secretion.

The role of SRIF in starvation-induced inhibition of GH and insulin secretion was assessed by passive immunization with anti-SRIF serum. Six-hour secretory profiles obtained from chronically cannulated male rats deprived of food for 72 h showed marked suppression of GH secretory bursts and significant depression of plasma insulin levels. Administration of 1 ml SRIF antiserum (SRIF AS) iv to starved rats resulted in rapid (within 15 min) restoration of high amplitude GH pulses (600-800 ng/ml) and sighificant elevation of GH trough values. The mean 6-h GH level of starved SRIF, AS-treated rats (189.2 +/- 23.9 ng/ml) was significantly higher than that of starved, normal sheep serum-treated control animals (62.8 +/- 5.8 ng/ml) (P less than 0.005). In contrast to the effects on GH, plasma insulin levels in starved rats administered SRIF AS remained low. No significant difference was observed in the mean 6-h plasma insulin level of starved-SRIF, AS-treated rats when compared to starved, normal sheep serum-treated controls. These findings suggest that circulating SRIF is a physiological regulator of starvation-induced GH suppression but is not involved in mediating the inhibition of insulin.

Animals↗

Surgical demand scheduling: a review.

This article reviews the literature on scheduling of patient demand for surgery and outlines an approach to improving overall performance of hospital surgical suites. Reported scheduling systems are categorized into those that schedule patients in advance of the surgical date and those that schedule available patients on the day of surgery. Approaches to estimating surgical procedure times are also reviewed, and the article concludes with a discussion of the failure to implement the majority of reported scheduling schemes.

Appointments and Schedules↗

Parameters affecting hospital occupancy and implications for facility sizing.

Simulation is used to investigate the effects on hospital occupancy of the number of beds in the facility, the percentage of patients who are emergencies, the percentage of elective patients who are scheduled, and the average lengths of stay of emergency and elective patients. A practical method is presented for estimating the optimum size of a short-term hospital on the basis of expected demand, and use of the results in planning is discussed.

Admitting Department, Hospital↗