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Biomedical subjects

H Keen

Publications and source records attributed to H Keen.

At least 181 records · Page 10Linked to original sources
PubMed1980

Human insulin produced by recombinant DNA technology: safety and hypoglycaemic potency in healthy men.

Human insulin synthesised by recombinant DNA technology was compared with highly purified porcine insulin in healthy men. Intracutaneous injection over a wide range of concentrations of both insulins into five subjects gave rise to no local reactions over a 48 h period. The glycaemic response to standard subcutaneous injection at high and low dose levels was measured with both insulins in each of six men. Plasma glucose decrement with the two insulins was similar but human insulin was perhaps slightly more potent than porcine insulin at the low dose, and slightly less so at the high. The glycaemic response to the isulins, each infused intravenously at high and low concentrations for 1 h in a further six subjects, showed a similar trend. Depression of glycaemia with human insulin slightly exceeded that with porcine insulin at the low concentration infusion and fell slightly short of it at the high. Genetically synthesised human insulin seems to be safe and effective in man. Its dose-response relationship may differ from that of porcine insulin.

Adult↗
PubMed1980

Coronary-heart-disease risk and impaired glucose tolerance. The Whitehall study.

In the Whitehall Study of 18,403 male civil servants aged 40--64 years, 7 1/2 year coronary-heart-disease (CHD) mortality has been examined in relation to blood-sugar concentration 2 h after a 50 g oral glucose load. CHD mortality was approximately doubled for subjects with inpaired glucose tolerance (IGT), defined as a blood-sugar above the 95th centile (greater than or equal to 96 mg/dl). There was no trend of CHD mortality with blood-sugar below the 95th centile. Within the IGT group, age, systolic blood-pressure, and ECG abnormality (Whitehall criteria) were significantly predictive of subsequent CHD mortality. These findings are relevant to discussions on the criteria for diabetes which include the definition of an IGT category with increased risk of large-vessel disease, but without the high risk of small-vessel disease as occurs in diabetes mellitus.

Adult↗
PubMed1980

Blockade of chlorpropamide alcohol flush by aspirin.

The blocking effects of aspirin, chlorpheniramine, and cimetidine were tested against the flush provoked by alcohol in twenty-four chlorpropamide-treated patients with non-insulin-dependent diabetes mellitus. Active preparations were compared in a double-blind manner with an indistinguishable placebo. Aspirin significantly decreased the number of patients who flushed. Five patients studied in detail all showed suppression of chlorpropamide/alcohol flush by aspirin, with a mean facial temperature increase during the flush of 2.4 degrees C after pretreatment with placebo and an increase of 0.4 degrees C after pretreatment with aspirin.

Aspirin↗
PubMed1980

The effect of acute hyperglycaemia on the retinal circulation of the normal cat.

The retinal microcirculation of anaesthetised normal cats was studied during hyperglycaemia (15 to 55 mmol/l) induced by intravenous infusion of glucose, using high speed cine fluorescence angiography. Saline (0.150 mmol/l) was infused as a control for the volume effect of glucose solution and equiosmolar mannitol was infused as a control for the osmotic effect. The mean retinal arteriolar inflow rate increased from 34 +/- 1 mm/sec to 41 +/- 4 mm/sec during glucose infusion, and from 46 +/- 1 mm/sec to 56 +/- 3 mm/sec during mannitol infusion. The blood pressure similarly increased from 105 +/- 5 mmHg to 125 +/- 2 mmHg during glucose infusion and from 110 +/- 7 mmHg to 129 +/- 1 mmHg during mannitol infusion. During mannitol infusion the increased inflow was accompanied by a reduction in the arteriolar width so that the volume flow remained unchanged. During glucose infusion this constriction did not occur, resulting in a significantly increased volume of retinal blood flow (9 +/- 1 microliter/min to 12 +/- 1 microliter/min).

Animals↗
PubMed1980

Beta blockade and diabetes mellitus: effect of oxprenolol and metoprolol on the metabolic, cardiovascular, and hormonal response to insulin-induced hypoglycemia in normal subjects.

In a double-blind randomized study, the effect of the acute administration of a single oral dose of oxprenolol, a nonselective beta-blocker, and of metoprolol, a beta 1 selective blocker, on insulin-induced hypoglycemia was tested in seven normal subjects. Neither of the drugs potentiated the hypoglycemic effect of insulin. The recovery from hypoglycemia was delayed by both blocking agents only in the late phases of the experimental observation. This effect could not be accounted for by suppression of release of the counterregulatory hormones glucagon or cortisol, but may be mediated by the inhibition of NEFA and gluconeogenic-substrate release in response to hypoglycemia. Both drugs blocked the hypoglycemia-induced tachycardia. Only oxprenolol raised diastolic blood pressure during hypoglycemia. Symptoms of hypoglycemia were not masked by either blocking agent, and sweating was enhanced and prolonged by both drugs. Thus, no clear-cut differences in the glycemic response to insulin-induced hypoglycemia were found between metoprolol and oxprenolol, but the drugs differed in their influence upon the blood pressure response to insulin-induced hypoglycemia.

Adrenergic beta-Antagonists↗
PubMed1980

Beta blockade and diabetes mellitus: effect of oxprenolol and metoprolol on the metabolic, cardiovascular, and hormonal response to insulin-induced hypoglycemia in insulin-dependent diabetics.

The effect of the administration of a single oral dose of placebo, oxprenolol and metoprolol on insulin-induced hypoglycemia was investigated in seven insulin-dependent diabetics in a double-blind randomized study. Neither of the beta-blocking agents accelerated the plasma glucose lowering effect of insulin. Plasma glucose recovery from hypoglycemia was grossly impaired in diabetics whether blocked or not, and all investigations had to be terminated by i.v. glucose injection after 1 hr of sustained hypoglycemia. During the period of observation, no further delaying effect by either beta-blocker was observed. The lack of plasma glucose recovery seems to be at least in part related to a retarded and reduced glucagon response to hypoglycemia. Both drugs blocked the hypoglycemia-induced pulse rate increase, but neither caused bradycardia. A significant increase in diastolic pressure was recorded with oxprenolol, whereas a drop in systolic pressure was noted with metoprolol. Oxprenolol suppressed the NEFA rise after insulin-infusion termination to a greater extent than did metoprolol. Hypoglycemic symptoms were not affected by beta-blockade. The results suggest that neither drug further worsens the already grossly impaired plasma glucose recovery, but that oxprenolol and metoprolol may differ in their effects on hemodynamic response to hypoglycemia. This aspect of the problem requires further study under careful control in hypertensive diabetics.

Adrenergic beta-Antagonists↗