To investigate the role of fluid shifts during the short-term adjustment to acute hypobaric hypoxia (AHH), the changes in lower limb (LV) and forearm volumes (FV) were measured using a strain-gauge plethysmograph technique in ten healthy volunteers exposed to different altitudes (450 m, 2500 m, 3500 m, 4500 m) in a hypobaric chamber. Arterial blood pressure, heart rate, arterial oxygen saturation (SaO2), endtidal gases, minute ventilation and urine flow were also determined. A control experiment was performed with an analogous protocol under normobaric normoxic conditions. The results showed mean decreases both in LV and FV of 0.52 (SD 0.39) ml x 100 ml(-1) and -0.65 (SD 0.32) ml x 100 ml(-1), respectively, in the hypoxia experiments [controls: LV 0.28 (SD 0.37), FV 0.41 (SD 0.47) ml x 100 ml(-1)]. Descent to normoxia resulted in further small but not significant decreases in mean LV [-0.02 (SD 0.11) ml x 100 ml(-1)], whereas mean FV tended to increase slightly [ + 0.02 (SD 0.14) ml x 100 ml(-1)]; in the control experiments mean LV and FV decreased continuously during the corresponding times [-0.19 (SD 0.31), -0.18 (SD 0.10) ml x 100 ml(-1) , respectively]. During the whole AHH, mean urine flow increased significantly from 0.84 (SD 0.41) ml x min(-1) to 3.29 (SD 1.43) ml x min(-1) in contrast to the control conditions. We concluded that peripheral fluid volume shifts form a part of the hypoxia-induced acute cardiovascular changes at high altitude. In contrast to the often reported formation of peripheral oedema after prolonged exposure to hypobaric hypoxia, the results provided no evidence for the development of peripheral oedema during acute induction to high altitude. However, the marked increase in interindividual variance in SaO2 and urine flow points to the appearance of the first differences in the short-term adjustment even after 2 h of acute hypobaric hypoxia.
The purpose of this study was to investigate the possible participation of atrial natriuretic factor (ANF) in the natriuretic and diuretic response occurring after stimulation of the peripheral arterial chemoreceptors by almitrine bismesylate in normoxic humans. The experiments were performed in 14 healthy male volunteers undergoing water diuresis. Each subject participated in two experiments. In one of them they ingested 100-mg almitrine at 12 p.m. The other study served as a control. Surprisingly, our subjects responded to almitrine with an elevation of urine flow only, whereas sodium excretion remained almost unchanged over the whole period of the experiments. As regards ANF plasma concentrations, no statistically significant differences between the control and the almitrine group could be observed. Moreover, no direct connection between ANF plasma concentrations and renal volume excretion was detectable. We conclude that a specific stimulation of peripheral arterial chemoreceptors by almitrine in humans undergoing water diuresis did not seem to raise ANF plasma concentrations as is the case at high altitude. Therefore we would suggest that there exists no specific reflex influence of these receptors on ANF release.
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