Erythropoietin (EPO) and red blood cells were studied in 15 well-trained men before and several times after a marathon run. Changes in red blood cells reflected changes of plasma volume. Immediately after the run, red blood cells were increased due to haemoconcentration, whereas 31 h later the values were decreased due to haemodilution. The EPO concentration was increased 3 h, and more impressive 31 h, after the run. This long-lasting increase in EPO concentration after the marathon run would seem to be responsible for the increased red blood cell mass in long distance runners.
Aerosolized amiloride normalizes the excessive sodium absorption cystic fibrosis (CF) respiratory epithelium. The aims of this study were to assess the dose-effect relationship and the duration for which amiloride inhibits Na+ transport, to determine acute and chronic pharmacokinetics, and to test the effect of acute aerosolized amiloride on the amount of sputum expectorated. The effect of inhaled amiloride was assessed principally by nasal potential difference (PD) measurements. Amiloride serum levels were measured in 23 patients after inhalation of different doses of aerosolized amiloride. Twenty CF patients inhaled amiloride (10(-3)M) or a placebo in a double-blinded, randomized order, and sputum production was quantitated. The results of this study showed that maximal initial PD inhibition was achieved by 6 x 10(-3)M of amiloride. The duration of inhibition of PD (effective time until return to 50% delta PD [ET50] after nasal administration) was dose dependent (10(-3)M, 39 +/- 0.8 minutes; 10(-2)M; 133 +/- 14 minutes). Amiloride serum levels were below 2.5 ng/ml in 20 of 28 patients; levels were above 5 ng/ml only within 4 hours after high dose inhalation (10(-2)M). In the double-blinded, crossover study, more sputum was expectorated after amiloride inhalation as compared with that after a placebo (P < 0.05). In conclusion, the bioelectric effects of amiloride and serum levels after inhalation are dose dependent, and amiloride is effective at inducing sputum expectoration in CF.
Catecholamines and some of their metabolites were determined in urine and blood plasma of guinea-pigs before, during and after acclimation to a cold or warm environment. During adaptation to 5 degrees C the amounts of noradrenaline in plasma and 24-h urine samples continuously increased up to 600% compared with values obtained at an ambient temperature of 22 degrees C. Higher levels of dihydroxyphenylglycol and 3-methoxy-4-hydroxyphenylglycol further indicated an increased turnover of noradrenaline during cold adaptation. Acclimation to an ambient temperature of 28 degrees C reduced the peripheral release of noradrenaline in comparison to the release observed at 22 degrees C. Cold-induced increases in metabolic rate and electrical muscle activity both occur at a considerably lower mean body temperature in cold-than in warm-adapted guinea-pigs. The shift of thermoregulatory cold defence reactions to a lower mean body temperature could also be observed in warm-adapted animals after intramuscular infusion of noradrenaline in amounts comparable to those released during cold adaptation. It is concluded that high peripheral sympathetic activity directly or indirectly inhibits noradrenergic neurons in the lower brain stem that modulate the thermoregulatory control system by means of their afferents to the hypothalamus. As a consequence of this peripheral influence the thermoregulatory set point is shifted to a lower mean body temperature.
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