Asunto(s)
Insuficiencia Cardíaca/fisiopatología , Trasplante de Corazón/fisiología , Corazón/fisiología , Hemodinámica/fisiología , Consumo de Oxígeno , Función Ventricular Izquierda/fisiología , Adulto , Anaerobiosis , Prueba de Esfuerzo , Corazón/fisiopatología , Frecuencia Cardíaca , Humanos , Cinética , Persona de Mediana Edad , Valores de Referencia , Factores de TiempoRESUMEN
The relationship between plasma cortisol levels, core temperatures, heat storage and the appearance of subjective manifestations of heat intolerance were investigated in two groups of 4 and 3 men, respectively. The first group underwent 4 randomized experimental sessions: a control session and three heat-exposure sessions (A: 48 degrees C, 34 Torr, 80 min; B: 55 degrees, 15 Torr, 120 min; C: 48 degrees C, 15 Torr, 180 min). During control periods, the subjects were maintained in a thermoneutral climate (28 degrees C, 10.5 Torr). The second group of subjects was studied before and after five successive daily exposures to hot and humid conditions (D: 43 degrees C, 32 Torr, 165 min). Signs of subjective discomfort in experiments A and B were accompanied by an increase in cortisol values over control day values, and this increase began at a mean rectal temperature of about 38 degrees C. Condition C was well tolerated, the plasma cortisol remained at basal levels and mean rectal temperature averaged 38 degrees C at the end of the exposure. Repeated exposures in condition D improved heat tolerance with a lesser effect on plasma cortisol levels and a lower body temperature at the end of exposure. Circulating cortisol is shown to be a very sensitive index of heat stress heralding the onset of poor tolerance of severe climates. The relation between concomitant levels of cortisol and rectal temperatures, in fit men, is affected by additional factors (hypotension, uncomfortable posture). These reduce tolerance time and are not reflected by body temperatures, but by rapidly increasing cortisol levels.
Asunto(s)
Regulación de la Temperatura Corporal , Agotamiento por Calor/sangre , Hidrocortisona/sangre , Adulto , Humanos , MasculinoRESUMEN
To assess the role of the renin-angiotensin system in the control of aldosterone reease in response to heat exposure, 6 sodium restricted subjects were studied on three random experimental days: a control day and two heat exposure days (46C, 35 mbar, 90 min) with and without propranolol. Plasma aldosterone, renin activity, ACTH and K+ were determined from plasma samples taken every 20 min from 08:00 to 14:00. After propranolol administration, plasma aldosterone responsiveness to heat exposure increased, though plasma renin activity was depressed. Concurrently, propranolol reduced heat tolerance, leading to an increased ACTH and cortisol release in 3 of the subjects. Plasma levels of K+ were not significantly different during both heat exposure days. The enhanced response of plasma aldosterone may in part be related to the concurrent rises in ACTH, but a similar sustained aldosterone response was observed in subjects without ACTH release. Except for a significantly lower heart rate, propranolol induced no changes in hemodynamic and thermal response to heat. Plasma volume, blood pressure, sodium excretion, mean skin and rectal temperature rises and body weight losses were not modified by prior administration of the drug. The dissociation between aldosterone and renin activity after propranolol administration suggests that the aldosterone response to heat exposure is not primarily mediated by changes in activity of the renin-angiotensin system. Propranolol may lead to a reduced metabolic clearance rate of aldosterone or increase the sensitivity of the adrenal cortex to concomitant changes in the known stimuli, but the involvement of an additional factor in aldosterone regulation during heat exposure cannot be excluded.