Biomedical subjects
Publications and source records attributed to W J Kalk.
Furosemide, in combination with breast binding and milk fluid restriction, seems to inhibit postpartum lactation effectively, but has no effect in reducing serum prolactin levels. Inhibition of milk secretion must therefore be mediated by other mechanisms.
The effect of the sulphonylureas gliclazide (S 852) and glibenese on platelet function, blood lipid levels and the control of diabetes, was prospectively evaluated in 12 maturity-onset diabetic subjects by means of a double-blind crossover study. Including the pretrial period, platelet aggregation in response to collagen was uniformly lower than in matched normal controls, but neither drug produced any additional effect on platelet function. Control of blood glucose levels was no better than with comparable agents, and no measurable changes occurred in blood lipid levels. The drugs had no significant side-effects and were well tolerated. It is concluded that neither agent offers special advantages over other sulphonylureas, particularly in regard to platelet function.
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A 48 year old premenopausal woman presented with galactorrhea and amenorrhea associated with chest wall burns. Basal serum prolactin levels were raised, and were further elevated by the administration of L-dopa, chlorpromazine and TRH. Intercostal nerve block and bromocryptine treatment reduced prolactin levels to normal, but did not noticably reduce milk secretion.
Repeated intensive pancreatic beta-cell stimulation was carried out in 42 subjects, comprising 22 normal controls, 10 mild to "severe" maturity-onset diabetics, and 10 chronic pancreatitis patients. Each subject received 75 gm. oral glucose twice and 1 mg. glucagon plus 0.5 gm. tolbutamide intravenously three times at short intervals. Each of the three combined stimuli caused almost equivalent marked spikes of insulin release in all experimental groups. The total calculated output of insulin was equivalent to the total daily insulin output in normal subjects. Pancreatitics and those with severe diabetes (fasting blood sugar greater than 120 mg./100 ml.) had qualitatively similar but a quantitatively smaller response. Those with mild diabetes were similar to the normal subjects but had an exaggerated response to the second oral glucose dose, suggesting overactivity of the enteroinsular axis. Despite the inordinate insulin levels, hypoglycemia did not occur.
Thyrotropin (TSH) responses to intravenous thyrotropin-releasing hormone (TRH) were studied in 9 men after 12 and 36-h fasts separated by more than a week and performed in random order. The TSH, basally and in response to TRH, was significantly lower after the 36-h fast compared to that after 12 h. The mechanism for this effect is not clear, but may be related to the altered hormonal or fuel status associated with prolonged fasting.
The effects of repeated injections of 75 U crude cholecystolinin-pancreozymin (CCK-PZ) at increasing plateau glucose concentrations achieved by glucose infusion were studied in 15 controls, 8 chronic pancreatitics and 8 mild maturity onset diabetics. In control subjects CCK-PZ alone caused minor insulin release but proportinally greater secretion with increasing blood glucose concentrations. Chronic pancreatitis patients who had normal responses to intravenous glucose responded normally to the CCK-PZ but at significantly higher plateau glucose levels. Diabetics had no response to IV glucose boluses of 5 g or 10 g, but with glucose infusions of 250-500 mg/min had almost normal insulin responses to CCK-PZ. The responses to CCK-PZ plus glucose were greater than either stimulus alone, indicating an interaction between these and the beta cell. These studies suggest that the gut homone-receptor in the beta cell is intact in maturity onset diabetes and chronic pancreatitis, whether the glucose receptor is normal or defective. The peptide-responsible in the crude CCK-PZ is not secretin, glucagon or gut glucagon, but may be gastric inhibitory polypeptide (GIP) since pure CCK-PZ has no insuli releasing properties.
The effects of tolbutamide infusion (1 gm. over forty minutes) on plasma pancreatic glucagon-like immunoreactivity (PGLI), serum insulin, and blood glucose were studied in six patients with chronic pancreatitis and six matched controls.asal PGLI levels were significantly higher in the patients, despite higher fasting glucose concentrations. Tolbutamide infusion had no significant effect on mean PGLI levels in controls but was associated with significant elevation in pancreatitis patients, despite higher circulating glucose levels in the latter. The data suggest that chronic calcific pancreatitis patients hypersecrete immunoreactive glucagon, possibly from a nonpancreatic source and that this immunocreactive material may be stimulated by sulfonylureas.
Arginine, administered intravenously, was a more potent stimulus to gastrin release than oral Oxo-feeding, while oral arginine failed to elicit a response in normal subjects. Intravenous arginine stimulated a rise in serum gastrin only in normal subjects but not in antrectomized or vagotomized patients. The gastric antrum appears to be the major site of production of heptadecapeptide gastrin and 'mini' gastrin, as measured by the anti-serum used in our radio-immunoassay.
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