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Biomedical subjects

B Pimstone

Publications and source records attributed to B Pimstone.

At least 19 recordsLinked to original sources
PubMed1979

Immunoreactive somatostatin release from rat spinal cord in vitro.

A calcium-dependent release of immunoreactive somatostatin from rat spinal cord in vitro in response to two depolarising stimuli (60 mM KCl and 75 micrometer veratrine) has been demonstrated. Released somatostatin immunoreactivity comprised 0.53% of total tissue content, showed parallelism when serial dilutions were compared to the immunoassay dose-response curve and eluted similarly to synthetic somatostatin on Sephadex G-25 (f) chromatography. These results provide further evidence for a neurotransmitter or neuromodulator role for somatostatin in mammalian spinal cord.

Animals↗
PubMed1979

Growth hormone release inhibitory hormone-like immunoreactivity in pancreas and gut in streptozotocin diabetes in the rat and response to insulin administration.

In streptozotocin diabetes in the rat, growth hormone release-inhibitory hormone-like immunoreactivity (GHRIH-LI) content of pancreas, gastric antrum and colon was increased. Insulin therapy significantly lowered the increased pancreatic GHRIH-LI content but did not affect that of the gastric antrum and colon at the dosage used. The relevance of these findings in relation to pancreatic and gastrointestinal function in diabetes awaits clarification.

Animals↗
PubMed1979

Metabolic clearance and plasma half-disappearance time of exogenous somatostatin in man.

The MCR and half-disappearance time of exogenously administered somatostatin have been measured during and after cessation of a constant infusion. Studies were performed on normal volunteers and patients with chronic liver disease and failure. Immunoreactive somatostatin was measured by a sensitive and specific RIA using an antiserum directed against the core of the molecule. Normal subjects had a mean MCR of 1949 +/- 250 ml/min (28.4 +/- 4.2 ml/min . kg BW) (mean +/- SEM), similar to values found in five patients with chronic liver disease. However, patients with chronic renal failure showed a highly significant (P less than 0.001) lowering of the MCR (501 +/- 32.7 ml/min or 7.8 +/- 0.6 ml/min . kg). The rate of disappearance of somatostatin after infusion was linear for 7-10 min, after which a much slower component was observed. In normal subjects, the t 1/2 of the first component varied from 1.1-3.0 min, in patients with liver disease it varied from 1.2-4.8 min, and in patients with chronic renal failure it varied from 2.6-4.9 min. Exogenously administered somatostatin is rapidly cleared in normal subjects and patients with chronic liver disease, but the MCR in end stage chronic renal failure is markedly lowered. The kidney may have a role in the metabolic clearance of exogenously administered somatostatin, or uremia may impair catabolism nonspecifically.

Adult↗
PubMed1978

Tissue growth hormone release inhibiting hormone-like immunoreactivity in experimental hypothyroidism and hypopituitarism.

Hypothyroidism in rats was associated with an increase in immuno-reactive GH-RIH in brain, pancreas and gut, although release from the latter may be diminished as portal GH-RIH-like immunoreactivity was lower than control values. Hypophysectomy resulted in a depletion of immunoreactive GH-RIH in the septum and preoptic area of the brain and gastric antrum, but an increase in pancreas; portal venous GH-RIH-like immunoreactivity was not different from control concentrations, possibly reflecting both elevated and lowered immunol-reactive GH-RIH in different regions of tissue subserved by the portal vein. Inferior vena caval GH-RIH-like immunoreactivity was always lower than in the portal vein and was not influenced by tissue pertubations in hypothyroidism and hypopituitarism which made regional blood sampling of great important in evaluating tissue changes.

Animals↗
PubMed1978

Somatostatin-like immunoreactivity in rat blood. Characterization, regional differences, and responses to oral and intravenous glucose.

Somatostatin-like immunoreactivity (SLI) has been demonstrated by radioimmunoassay (RIA) in rat serum using an antiserum specific for somatostatin and cross-reacting maximally with the biologically important area on the peptide. The RIA has a sensitivity of 35 pg/ml. SLI dilutes in parallel with synthetic somatostatin standard in the RIA and shows characteristics similar to synthetic somatostatin on Sephadex G-25 (f) gel chromatography eluting largely as a single peak with 1 M acetic acid. Significant regional differences in serum SLI are present. A positive gradient was found in paired samples from aorta (mean+/-SEM, 0.304+/-0.024 ng/ml) and portal vein (0.495+/-0.047 ng/ml) consistent with the known presence of somatostatin in gut and pancreas, and a negative gradient was noted between paired samples from portal vein (0.523+/-0.076 ng/ml) and hepatic vein (0.290+/-0.048 ng/ml) indicating hepatic clearance. No significant differences were demonstrated between aorta and confluence of cerebral venous sinuses or between aorta and inferior vena cava (IVC). After intragastric glucose, a significant and marked elevation of portal SLI was observed, maximal at 5 min (0.416+/-0.137 vs. 1.55+/-0.30 ng/ml at 5 min). A significant biphasic elevation of portal SLI also occurred after intravenous glucose. After both routes of glucose administration, the patterns of portal SLI followed closely those of portal glucose and insulin. By contrast, IVC SLI failed to reflect these changes.Thus, SLI in the rat shows chromatographic similarity with synthetic somatostatin. Regional differences in serum levels are marked; the highest concentrations being found in the portal venous effluent of pancreas and gut. Furthermore, glucose causes elevation of portal SLI in a pattern similar to portal insulin and glucose and without concomitant elevation in IVC. This differential elevation of SLI after glucose is consistent with a hormonal action within the portal system as a direct effect of somatostatin on the liver has previously been demonstrated. In addition, the liver is important in the clearance of portal SLI, possibly to prevent extraportal effects in response to gut and pancreatic stimulation. Finally, it is clear that regional sampling of serum for SLI measurement may be critical in the investigation of the putative physiological roles for somatostatin.

Animals↗
PubMed1977

The effects of TRH on prolactin, plasma renin activity, water and electrolyte excretion in normal males.

The effect of TRH induced secretion of TSH and prolactin (hPrl) on plasma renin activity (PRA), water and electrolyte excretion, was studied in 7 normal males before and after an intravenous injection of 2 ml normal saline or 200 microgram TRH. Plasma hPrl and TSH rose significantly (p less than 0.01) in all 7 subjects after TRH but not after saline injection. No significant differences in the hourly excretion of sodium, potassium and free water clearance were noted before and after either saline or TRH injection. Mean PRA values of the 7 subjects were similar after either the 2 ml saline of TRH injection. Our results indicate that despite a correlation between basal hPrl and sodium excretion as well as free water clearance, acute TRH induced elevation of hPrl is not associated with changes of urinary sodium and potassium excretion, free water clearance and PRA in normal males. These findings provide some evidence against a direct osmoregulatory role of hPrl in man.

Adult↗
PubMed1977

Metabolic clearance and plasma half disappearance time of exogenous gonadotropin releasing hormone in normal subjects and in patients with liver disease and chronic renal failure.

The metabolic clearance rate (MCR) and half disappearance time (t 1/2) of gonadotropin releasing hormone (GnRH) has been measured during and after cessation of constant infusion of exogenous GnRH. Studies were performed on normal subjects and patients with severe renal and liver disease. GnRH was quantified by a sensitive and specific radioimmunoassay which does not measure GnRH fragments. The MCR of GnRH in normal subjects was 1640+/-59.7 ml/min (23.7+/-1.8 ml/min/kg), similar to values found in 4 patients with liver disease. However in chronic renal failure an MCR of only 631+/-62 ml/min (9.1+/-0.7 ml/min/kg) was obtained. The t1/2 of GnRH after infusion was linear for 8-10 min, after which a much slower component was observed. The t1/2 of the first component ranged from 5.5 to 8 min in normal subjects, 6.5-8 min in patients with liver disease but prolonged (12-16.5 min) in patients with renal failure. It would appear that GnRH is cleared rapidly in normal subjects, that moderate liver dysfunction does not alter this, but that impaired renal function significantly prolongs the t1/2 and lowers the MCR. The kidney might be an important catabolic organ for infused GnRH; alternatively, uremia might impair catabolism non-specifically.

Adult↗
PubMed1977

Pancreatic islets of malnourished rats: quantitative histologic and electron microscopic findings.

Young rats were maintained for three weeks on a low-protein diet. These animals developed many of the features of human protein-calorie deficiency, including dextrose intolerance and diminished insulin release. Quantitative histologic and ultrastructural studies showed that malnourished rats had (1) a reduced total pancreatic islet volume, and (2) a preponderance of pale granules in the B cells. It is suggested that pale B granules may contain increased amounts of insulin, which accumulate in the cells because of defective insulin release. The mechanism responsible for this has not been elucidated.

Animals↗
PubMed1975

The effect of prolonged lithium carbonate administration on the thyrotrophin and prolactin response to thyrotrophin-releasing hormone.

Thyrotrophin (TSH) and prolactin (PRL) responses to intravenous thyrotrophin-releasing hormone (TRH) were measured in euthyroid patients suffering from psychiatric disease on long-term lithium carbonate (LC) and phenothiazine therapy. These responses were retested after oral tri-iodothyronine (T3) 120 mug/day had been given for a week. The raised basal TSH and the suppression of the exaggerated responses to TRH by T3 found in some of the patients suggest a mild disturbance of thyroid function in patients on long-term LC therapy, even in the face of clinical euthyroidism and otherwise normal thyroid function. Basal serum PRL levels and the responses to TRH were elevated in 2 of 5 patients, probably associated with phenothiazine administration. In all 5, a moderate blunting of the PRL responses after TRH was produced by T3. The suppressive effect of T3 on TRH-induced PRL responses was unexpected and suggests a modifying role of thyroid hormones on PRL secretion, although further studies are needed to confirm this possibility.

Female↗
PubMed1975

A specific radio-immunoassay for gonadotrophin-releasing hormone.

A specific antiserum has been made to synthetic gonadotrophin-releasing hormone (GnRH) conjugated to keyhole limpet haemocyanin and appears to be directed against amino acids 6-8 of this decapeptide. This has allowed the development of a radio-immunoassay for GnRH sensitive to 5 picograms per tube. Although it is easily measurable in hypothalamic extracts, we have failed to detect GnRH in plasma and urine from normal subjects and menopausal women.

Animals↗