[Improved insulin action by ACE inhibition in type-2 diabetics]. / Verbesserte Insulinwirkung durch ACE-Hemmung beim Typ-II-Diabetiker.

The effect of the angiotensin converting enzyme inhibitor captopril (25 mg by mouth) on glucose metabolism of skeletal muscle and the whole organism was studied in nine normotensive type II (non-insulin dependent) diabetics using a combination of euglycaemic-hyperinsulinaemic glucose-clamp and forearm catheter techniques. The administration of captopril resulted in a significant rise of both the whole-body glucose elimination and utilization rate in the forearm musculature. At the same time the arterial kinin level rose, while the concentrations of insulin, free fatty acids and gluconeogenesis precursors, as well as the number and activity of insulin receptors (measured in an erythrocyte-binding study) remained unchanged. The data support the view that, in type II diabetics, ACE inhibition raises the insulin-stimulated glucose uptake of the whole organism, predominantly due to an increased glucose uptake by the skeletal musculature. The demonstration of an increased kinin level points to this effect possibly being caused by the reduced breakdown of locally liberated kinins.

Brachial plexus anesthesia and axillary sheath elastance.

Large volumes of an anesthetic solution used during regional axillary anesthesia may produce elevated pressures within the axillary sheath that lead to arterial compression and diminished blood flow. We measured axillary sheath pressure as a function of injected volume in 20 patients scheduled for hand surgery. Bupivacaine without epinephrine was injected into the axillary sheath in 10-ml increments until a cumulative volume of 50 ml was attained. Elastance (delta P/delta V), where delta P equals change in pressure (mm Hg) and delta V equals change in volume (ml), was 0.8 +/- 0.1 (+/- SEM) mm Hg/ml in successful block and 0.09 +/- 0.1 mm Hg/ml in unsuccessful blocks. Axillary sheath pressure did not exceed mean arterial pressure for periods longer than 60 s. We conclude that vascular insufficiency resulting from arterial compression following axillary block anesthesia is unlikely.

Axillary 5 alpha-androst-16-en-3-one, cholesterol and squalene in men; preliminary evidence for 5 alpha-androst-16-en-3-one being a product of bacterial action.

Twenty-four hour axillary levels of the odorous steroid 5 alpha-androst-16-en-3-one, have been measured in six men by radioimmunoassay. Initially, no control of bacterial activity was made and conditions attempting a normal axillary environment were maintained. The level of 5 alpha-androst-16-en-3-one was significantly higher (P = 0.028) in one axilla ("superior") than the other ("inferior") and levels showed considerable variation both between and within individuals. This difference between axillae was also observed for cholesterol (P = 0.0013) but not for squalene (P = 0.18). This suggests that the presence of 5 alpha-androst-16-en-3-one in the axilla does not correlate with sebum secretion. The effect of a general germicidal agent was tested by shaving and applying Povidone-iodine to the "superior" axilla whilst treating the "inferior" axilla as a control. A highly significant drop in the level of 5 alpha-androst-16-en-one in the "superior" axilla below that in the control axilla was obtained (P = 0.000014, double tailed, as calculated using the Fisher Exact test). Squalene and cholesterol were measured in an attempt to monitor glandular activity and their levels were not significantly affected by Povidone-iodine. It is likely, therefore, that the production of 5 alpha-androst-16-en-3-one is from metabolism of a percursor in the axillae by skin micro-organisms.