tein-bound iodine (P.B.I.)

No abstract

1 In normal subjects, intravenous betaxolol given in doses which inhibited the tachycardia of exercise failed to affect the peak expiratory flow rate. 2 From 2 to 48 h after administration of 150 ,ug/kg in four normal subjects, there was no significant difference between che blood levels, whether given orally or intravenously.3 At all times, heart rate and blood pressure, at rest and during exercise, were reduced equally after administration by both routes, but the area under the curve of exercise heart rate against time was significantly smaller (P<0.05) after intravenous drug. 4 The absolute bioavailability of betaxolol was 89 ± 5%.

Thyrotrophin (TSH) release in response to intravenous synthetic thyrotrophin releasing hormone (TRH) was unaltered by simultaneous corticotrophin (ACTH) and growth hormone secretion induced by hypoglycaemia or methylamphetamine in normal subjects. Secretion of growth hormone was the same whether or not TSH was secreted. While the increments in plasma corticosteroids and ACTH after methylamphetamine administration were not different whether TRH or a control injection was given, they rose more during insulin-induced hypoglycaemia when TRH was given as well. This could have been due to a slightly greater degree of stress after TRH + insulin than insulin alone. Overnight dexamethasone suppression of basal ACTH secretion did not alter the TSH response to TRH. Unlike the rat, there is no evidence suggesting competition between pituitary mechanisms involved in ACTH, growth hormone and TSH release in man.

1. Six healthy male volunteers received equivalent intravenous beta-blocking doses of propranolol, practolol and betaxolol (SL75212) or saline at weekly intervals Sixty minutes later 0.1 unit/kg insulin was given intravenously. 2. In all studies, maximum hypoglycaemia (mean 1.2 mmol/l) was reached thirty minutes after insulin. Recovery from hypoglycaemia was delayed with propranolol but practolol and betaxolol had no effect. 3. Propranolol blocked the tachycardia and widening of pulse pressure seen in saline treated subjects. It also blocked the rebound rise in free fatty acids (FFA) and glycerol concentrations that followed the nadir of hypoglycaemia. 4. Neither practolol nor betaxolol had significant effects on pulse rate or blood pressure but betaxolol resembled propranolol in blocking the rebound rise in FFA and glycerol, while practolol blocked the rise in glycerol alone. 5. The magnitude of the rise in growth hormone following hypoglycaemia was similar in all groups, but the peak was earlier after practolol and betaxolol.