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Biomedical subjects

J B Martin

Publications and source records attributed to J B Martin.

At least 325 records · Page 18Linked to original sources
PubMed1976

Hypothalamic releasing factors: physiological evidence for a regulatory action on central neurons and pathways for their distribution in brain.

Recent observations based on single cell recordings obtained in various areas of the brain indicate that TRH, LH-RH and somatostatin have potent effects on the activity of central neurons. There is also electrophysiological evidence for the existence of a system of hypothalamic tuberoinfundibular neurons with widespread extrahypothalamic connections. These connections may indicate possible pathways for the observed widespread distribution of these peptides in the brain. These findings, coupled with behavioral studies and subcellular localization data support the postulate that hypothalamic peptides may have an important role inthe modulation of central neuronal activity.

Action Potentials↗
PubMed1976

Parallel variation of ventricular CSF tryptophan and free serum tryptophan in man.

Tryptophan was measured in the ventricular CSE and serum and the neutral amino acids leucine, isoleucine, valine, phenylalanine, and tyrosine were measured in the serum of two cases with ventricular drains. Samples were taken every two hours for 24 hours in one case and for 16 hours in the other. The CSF tryptophan was correlated significantly with the free--that is, non-albumin-bound--serum tryptophan but not with the total serum tryptophan. CSF tryptophan was not correlated significantly with the ratio of free serum tryptophan to the sum of the neutral amino acids. These data suggest that, in man, brain tryptophan concentrations are influenced by the free and not the total serum tryptophan and that physiological variations of the neutral amino acids do not appreciably influence the concentration of brain trytophan.

Adult↗
PubMed1976

Dynamic studies of growth hormone and prolactin secretion in the female rat.

Blood samples were removed via chronic intra-atrial cannulae every 15 min in female rats during the estrous cycle, the last week of pregnancy, parturition and suckling. Growth hormone (GH) secretion during the estrous cycle is characterized by episodic release, occurring approximately once hourly. The surges in GH increase during the last 3-4 days of gestation, and rise to high levels during delivery and with suckling. Prolactin (PRL) shows minimal fluctuations during the estrous cycle, except for a prominent pulsatile surge during proestrus. PRL rises 4-6 h prior to parturition and declines during delivery. These studies provide a basis for further studies on the dynamics of GH and PRL secretion in the female rat.

Animals↗
PubMed1976

Evidence for an endogenous ultradian rhythm governing growth hormone secretion in the rat.

Sequential blood samples were obtained from undisturbed freely-behaving male rats bearing chronic intracardiac venous cannulae. Blood was withdrawn every 15 min for periods of 4-24 h; plasma was separated, and saline-resuspended red cells were reinjected. Plasma GH was determined by radioimmunoassay. Pulsatile GH secretion was evident in each animal with most peak values greater than 200 ng/ml and most trough values less than ng/ml. The GH secretory episodes occurred at approximately 3 h intervals, and this rhythmic pattern of GH secretion persisted unchanged across all phases of a 12-h light-dark (L-D) cycle. Seven major episodes of GH secretion were observed during a single 24-h period. The mean period, or time interval between episodes, in 24 animals was 3.32 +/- 0.07 (SEM)h. The timing of the pulses with respect to the L-D cycle was similar in most animals, indicating that the rhythm may be entrained to the L-D cycle. The role of environmental lighting was further assessed in 14 animals exposed to constant light for 7 weeks. The results show that the basic rhythm was unchanged (mean period 3.18 +/- 0.06 h, peaks greater than 200 ng/ml, troughs less than 1 ng/ml), although entrainment to time of day was not evident. Subsequent exposure to the 12-h L-D cycle resulted in reversion to an entrained rhythm. These results suggest 1) that GH secretion in the rat is governed by an endogenous ultradian rhythm, with a periodicity of approximately 3.3 h, and 2) that the alternation of light and darkness probably serves as a Zeitgeber which sets the biological "clock" for GH secretion, but is not necessary for maintenance of the basic rhythm.

Animals↗
PubMed1976

Pulsatile growth hormone release in the rat: failure to demonstrate a correlation with sleep phases.

Concurrent 5-hour profiles of growth hormone (GH) secretion and sleep phases were obtained in 7 rats chronically implanted with right atrial cannulae, and electroencephalographic electromyographic, and electroculographic electrodes. Hormone profiles confirmed pulsatile secretion of GH. Secretory GH episodes occurred every 3 to 4 hours and peaks generally exceeded 100 ng/ml, and, in 14 of the 21 troughs recorded, GH was unmeasurable (less than 1 ng/ml). The comparison of hormone profiles and concurrent sleep patterns excluded a temporal relationship between episodic GH secretion and sleep cycles, while scattergrams of hormone values plotted against preceding sleep phase durations also failed to demonstrate a relationship.

Animals↗
PubMed1976

Ultradian growth hormone rhythm in the rat: effects of feeding, hyperglycemia, and insulin-induced hypoglycemia.

Temporal patterns of plasma GH, immunoreactive insulin (IRI), and glucose were defined by obtaining serial blood samples from freely-moving male rats bearing chronic intracardiac venous cannulae. Blood was withdrawn every 15 min for periods of 6 h. Plasma GH and IRI were determined by radioimmunoassay. The typical ultradian rhythm of GH secretion was evident in each undisturbed animal (peaks greater than 200 ng/ml; troughs less than 1 ng/ml; mean period: 3.40 +/-0.08 h). Basal plasma IRI and glucose levels fluctuated minimally. There was no significant correlation between plasma GH and IRI, GH and glucose, or IRI and glucose levels in unfed rats. The rhythmic GH secretory patterns of feeding animals (mean period: 3.12 +/-0.16 h; peaks greater than 200 ng/ml; troughs less than 1 ng/ml) were similar to those of non-feeding animals (mean period: 3.34 +/-0.15 h; peaks greater than 200 ng/ml; troughs less than 1 ng/ml) despite large fluctuations in plasma IRI levels and a wide variation in the number and size of the meals taken. No consistent relation was observed between the ingestion of meals and the bursts of GH secretion. The mean period of the GH rhythm was not significantly altered by hyperglycemia (mean period; 3.25 +/- 0.08 h), although the amplitude of the pulses of half of the hyperglycemic rats was markedly depressed. Insulin-induced hypoglycemia caused a significant depression in the amplitude of the GH pulses; however, the pattern of this response was not consistent. Despite wide variability in the GH response, the magnitude and time course of recovery of the plasma glucose levels was similar in all animals. These results suggest that GH secretion in the rat is regulated primarily by an endogenous ultradian rhythm which is not dependent on changes in plasma glucose or IRI levels, and continues to function independently of feeding behavior. It is unlikely that GH is an important physiologic regulator of glucose homeostasis in this species.

Animals↗
PubMed1975

Hypothalamic peptides: New evidence for "peptidergic" pathways in the C.N.S.

Hypothalamic peptides, discovered because of their effects on stimulation or inhibition of anterior-pituitary-hormone release, have now been shown to be distributed in many regions of the central nervous system (C.N.S.). Demonstration of their localisation in nerve terminals, of behavioural effects exclusive of anterior pituitary actions, and of depressant effects in electrophysiological experiments suggests a role in central-nervous-system function. It is postulated that a system of peptidergic neurons exists within the C.N.S. with axon terminations both on the pituitary portal system and on other neurons.

Animals↗
PubMed1975

Comparison of the effect of apomorphine and L-DOPA on serum growth hormone levels in normal men.

Apomorphine hydrochloride (0.75 mg s.c.) has been compared with L-dopa (500 mg p.o.) in their effects on growth hormone secretion in a double blind cross-over study involving nine healthy men. Apomorphine increased serum GH levels above 10 ng/ml in all nine subjects 30-60 min after injection. In contrast, only six of these subjects showed a similar elevation with L-DOPA and in only three had the level increased above 6 ng/ml by 60 min. One subject failed to respond to L-dopa and in two others the peak was less than 6 ng/ml. GH levels were significantly higher at 30, 45 and 60 min following apomorphine than following L-dopa. Apomorphine-induced GH release was not related to changes in serum cortisol or blood sugar. Benztropine mesylate (1 mg i.m.) had no effect on apomorphine-induced GH release. These results suggest: (a) apomorphine may have advantages over L-dopa as a provocative agent to assess GH secretory capacity; (b) a dopaminergic mechanism subserves GH secretion; (c) cholinergic mechanisms do not antagonize dopaminergic-related GH release.

Adult↗
PubMed1975

Relationships between tryptophan in serum and CSF, and 5-hydroxyindoleacetic acid in CSF of man: effect of cirrhosis of liver and probenecid administration.

Tryptophan was measured in the lumbar CSF and serum of patients undergoing neurological investigation (controls) and in patients with hepatic cirrhosis. Samples were taken from the fasting patients at 8:00 a.m. Under these conditions, in the controls the mean CSF, free )mpm-albumin-bound) and total serum tryptophan were in the approximate ratio 1:4:24. In this cross-sectional study, for the controls, CSF tryptophan was correlated significantly and positively with the total serum but not with the free serum tryptophan. In patients with advanced hepatic cirrhosis the mean CSF tryptophan concentration was greatly elevated. However, the mean total serum tryptophan was unchanged and the free serum tryptophan only slightly elevated. Administration of probenecid, which displaces tryptophan from binding sites on serum albumin, and thereby increases the proportion of serum tryptophan in the free form, did not affect CSF tryptophan.

Adult↗
PubMed1975

Effects of somatostatin and hypothalamic ventromedial lesions on GH release induced by morphine.

Morphine in intravenous doses ranging from 10 mug/kg to 8 mg/kg was shown to be effective in stimulating GH release in the unanesthetized rat. The response to the log of the dose was linear over a range of 10 to 1000 mug/kg. Somatostatin (GH-release inhibiting factor) administered SC in a dose of 200 mug/kg 5 min before morphine prevented the GH rise. Neither inhibitors of catecholamine or serotonin synthesis nor blockage of alpha and beta-adrenergic receptors had any effect on the response. The response was partially blocked in animals with large hypothalamic ventromedial (VMN) lesions. Such lesions completely abolished the GH response to pentobarbital. These results indicate that morphine is a remarkably potent agent for stimulation of GH release but the precise mechanism and site of action of the drug remain to be determined.

Animals↗
PubMed1975

Effectof sex, oral contraceptives, and glucose loading on apomorphine-induced growth hormone secretion.

Apomorphine-induced growth hormone (GH) secretion less in women either on or off oral contraceptives than in men. Women on oral contraceptives have a significantly greater peak GH response to apomorphine than women on no medication. The reason for these differences is unclear. Prior glucose loading in men significantly decreases the GH response to apomorphine. This suggests that stimulation of glucoreceptors antagonises dopaminergic modulation of GH secretion.

Adolescent↗
PubMed1975

Recovery from paradoxical growth hormone responses in acromegaly after transphenoidal selective adenomectomy.

A patient with acromegaly was studied before and after treatment by transphenoidal removal of a pituitary adenoma. "Paradoxical" GH responses to the dopamine agonists L-DOPA and ampomorphine disappeared after surgery, with reversion of GH responsiveness to normal. TSH-releasing hormone (TRH)-induced GH release observed pre-operatively did not occur after surgery. The findings suggest that in certain cases, acromegaly is due to pituitary dysfunction alone.

Acromegaly↗
PubMed1975

Dynamic evaluation of growth hormone (GH) and prolactin (hPRL) secretion in active acromegaly with high and low GH output.

Ten patients with active acromegaly were studied. In 9 plasma GH levels failed to suppress after glucose (OGTT), in 8 an increase in serum GH occurred after thyrotropin releasing hormone (TRH). After L-Dopa, 4 patients showed no change in serum GH, 3 exhibited a decrease and in 3 an increase in serum hGH occurred. With a combined insulin (ITT) and arginine (ATT) test, 2 patients exhibited an increase in hGH, and in 6 no change occurred. Fasting serum GH concentration was less than 11 ng/ml in 5 patients. Basal prolactin (hPRL) levels were normal in all patients including two with galactorrhea. L-Dopa suppressed and TRH stimulated hPRL secretion in all, but the responses which were seen were subnormal. Hydrocortisone infusion in two acromegalics did not affect the prolactin induced increase after TRH but blunted the GH increase after TRH.

Acromegaly↗