Potentially fatal interaction between erythromycin and disopyramide.
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Aged↗
Biomedical subjects
A C Weihl
Publications and source records attributed to A C Weihl.
Metabolic responses of resting man immersed in 25.5 degrees C and 33 degrees C water.
This study was undertaken to determine the hormonal responses to disabling hypothermia as a result of cold water immersion. Thermally unprotected male divers trained by the U.S. Navy were subjected to total body immersion in water at 25.5 degrees C and 33 degrees C. Plasma epinephrine, norepinephrine, growth hormone, and cortisol were measured. Other variables monitored included oxygen consumption, carbon dioxide production, minute ventilation, and rectal temperature. Immersion without cold stress caused suppression of plasma epinephrine without affecting plasma norepinephrine. Cold stress combined with immersion caused a significant increase in plasma norepinephrine in the absence of other indicators of a generalized stress reaction. The degree of chilling seen in this study will produce disabling hypothermia within 1-2 h and may be shown initially only by an increase in plasma norepinephrine.
Body Temperature↗
The relationship between endogenous hyperprolactinaemia and plasma aldosterone.
It has been suggested that prolactin is a regulator of aldosterone secretion. In order to test this hypothesis, we measured prolactin, thyrotrophin and aldosterone by radioimmunoassay and plasma renin activity by the radioimmunoassay of angiotensin I in eight normal women before and after the intravenous injection of 200 microgram of thyrotrophin releasing hormone (TRH). Prolactin increased from 4.1 +/- 1.1 ng/ml (mean +/- SE) to a peak of 27.4 +/- 3.8 (P less than 0.005) at 15 min following TRH. Plasma renin activity was not different from control levels (1.0 +/- 0.2 ng/ml/h) during the first hour following the administration of TRH, nor did the plasma aldosterone concentration differ significantly from the control levels (39 +/- 7 pg/ml) during this period. However, with upright posture, an increase in aldosterone (from 31 +/- 3 pg/ml at 1 h to 68 +/- 9 at 2 h, P less than 0.005) and in plasma renin activity (from 0.9 +/- 0.2 ng/ml/h at 1 h to 2.0 +/- 0.5 at 2 h, P less than 0.05) was noted, demonstrating a normal capacity to secrete aldosterone in these subjects. Similarly, no change in aldosterone was seen in nine patients with primary hypothyroidism given TRH, despite the fact that the increase in prolactin was greater than normal. Chronic hyperprolactinaemia was not associated with hyperaldosteronism in six patients with pituitary tumour. These data demonstrate that acutely or chronically elevated serum prolactin levels do not result in increased plasma aldosterone levels in humans.
Adrenal Cortex↗
Thyroid function tests during the early phase of subacute thyroiditis.
Six patients with subacute thyroditis were followed with serial measurements of T4, FT4, TSH and RAI uptake. Five of the six underwent TRH stimulation early in the course of their illness. All six patients had elevated or high normal values for T4 and FT4 at the time of their clinical presentation (mean = 13.8 microgram per 100 ml and 3.9 ng per 100 ml, respectively). RAI uptakes were 1% or less in all six. TRH testing revealed a suppressed TSH response (mean deltaTSH less than0.1 muU/ml) in all five patients tested, suggesting hyperthyroidism. After initial studies were performed, five patients were treated with L-triiodothyronine (L-T3) and one with aspirin. All patients improved over a two to four week period of time, no relapses being noted.
Adult↗