SUIMMARY1. Plasma cortisol and corticosterone concentrations increased significantly in eleven resting, unacclimatized subjects after 2 hr exposure to an ambient temperature of 460 C dry bulb, 36°C wet bulb and in two subjects investigated by controlled elevation of body temperature in a hyperthermia test-bed.2. In the same experiments the urinary excretion of 17-hydroxycorticosteroids (17-OHCS) estimated as the 1l-oxy and il-deoxy fractions did not differ significantly in hot and in control conditions. 3. Following an initial fall in plasma cortisol concentration during the first hour of heat exposure, cortisol levels increased in the second hour when body temperatures exceeded a 'critical' level of 38-3°C. Two acclimatized subjects did not attain this body temperature even after 2 hr heating and showed no increase in plasma glucocorticoid levels.4. Sweat collected in arm bags, or by suction, in controlled hyperthermia experiments contained negligible amounts of cortisol (0*34-1*70 jtg/100 ml. sweat).5. Changes in plasma cortisol specific activity after intravenous injection of 1,2P3H]cortisol indicated that the raised plasma concentration was brought about by increased adrenal secretion, though this was accompanied by more rapid removal of cortisol from the circulation in hot conditions. Excretion of tritium by the kidney was not significantly altered. It was not possible to determine whether changes in liver function contributed to the elevation of the plasma cortisol level but it was found that a larger proportion of cortisol was oxidized to cortisone, or to a metabolite closely resembling cortisone, in the heat.
Abnormal dispersion of the QT interval (QTd), measured as interlead variability of QT, may reflect a regional variation in duration of ventricular action potential and, hence, of cardiac electrical instability. In this retrospective study, we analyzed the effect of QTd on survival and its relation to other known predictors of subsequent cardiac death (CD) and sudden cardiac death (SCD) in 162 patients with coronary heart disease (CHD). QTd was calculated as the difference between the highest and lowest values measured in each of the 12 ECG leads (Qtmax - QTmin). Seventeen CDs occurred, including nine SCDs, during a 25 +/- 11 month follow-up. There were significant differences in CD (P < 0.001 in log-rank test) and in SCD (P < 0.01). The 1- and 3-year survivals were 87.5% and 76.5% in patients with QTd > 0.060 seconds versus 98% and 93.5% in patients with QTd < 0.060 seconds, respectively. Additionally, a stepwise Cox regression analysis revealed that increased QTd was an independent risk factor of CD and SCD. A cut-off value of 60 ms for QTd had a 53% sensitivity and 79% specificity in discriminating patients who are at risk of CD. The positive and negative prognostic values were 23% and 93%, respectively. Our findings support the hypothesis that increased QTd has a prognostic value in the stratification of patients with CHD independent of other known risk factors.
Heart rate variability (HRV) assesses the electrical stability of the heart and can identify patients at risk of sudden cardiac death (SCD). The value of 10 HRV parameters from 24 hour ECG (in both time and frequency domain) to predict serious arrhythmic events (SAE) in a group of 56 patients with ventricular tachycardia and/or ventricular fibrillation of different etiologies not due to acute myocardial infarction was explored. Eighteen patients had low left ventricular ejection fractions (LVEF). During follow-up (6-46 months, mean = 24) 8 SCD and 12 recurrences of malignant ventricular arrhythmias or ICD discharges were recorded. Proportional hazard analysis (Cox model) for SAE revealed that the mean of all 5 minute standard deviation of RR intervals (SD) and the amplitude of low frequency spectrum (L) were independent risk factors of SAE (P < 0.05). The best models were: SD+EF and L+EF where predictive values were high (sensitivity approximately 60%, specificity over 95%, positive predictive value over 90% and negative predictive value approximately 80%). Event-free survival curves revealed a significantly shorter survival in patients with EF < 40%: 47% vs. 92%, SD < 43 ms; 56% vs. 92% and L < 16 ms; 56% vs. 89% (all P < 0.001) after 2 years. The subgroup with low EF and SD < 43 ms revealed a significantly shortened survival (27% vs 83% at 2 years, P < 0.01). Some HRV parameters, SD from the time and L from the frequency domain, were predictive of a fatal outcome in VT/VF patients. Combined SD+EF and L+EF values are powerful predictors of serious arrhythmic events.
Sweating responses to heat exposure were compared in healthy subjects pretreated with pitressin or alcohol and in the control group. Between the three groups, there were no consistent differences in the rate of sweating expressed both as a total body weight loss during 2-h heat exposure and in mg of sweat per skin area covered by a paper disc. Likewise, there were no differences in the sweat osmolality or electrolyte concentration. There was also no evidence of inverse correlation between plasma ADH level and rate of sweat secretion or its concentration when pooled data of all subjects were analyzed. It was concluded that ADH did not substantially affect thermal sweating in men.
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