Abstract. Head-out water immersion at thermoneutral temperature (34-35 C) increases cardiac output for a given O2 consumption, leading to a relative hyperperfusion of peripheral tissues. To determine if subjects immersed in water at a colder temperature show similar responses and to explore the significance of the hyperperfusion, cardiovascular functions were investigated (impedance cardiography) on 10 men at rest and while performing exercise on a leg cycle ergometer (DM = ~95 W·m -2 ) in air and in water at 34.5 C and 30 C, respectively. In subjects resting in water, the cardiac output increased by ~50% compared to that in air, mainly due to a rise in stroke volume. The stroke volume change tended to be greater in 30 C water than in 34.5 C water, and this was due to a greater increase in cardiac preload, as indicated by a significantly greater left ventricular end-diastolic volume. Arterial systolic pressure rose slightly during water immersion. Arterial diastolic pressure remained unchanged in 34.5 C water, but it rose in 30 C water. The total peripheral resistance fell 37% in 34.5 C water and 32% in 30 C water. Both in air and in water, mild exercise increased the cardiac output, and this was mainly due to an increase in heart rate. Since, however, the stroke volume increased with water immersion, cardiac output at a given work load appeared to be significantly higher in water than in air. The arterial pressures did not decrease with water immersion, despite a marked reduction in total peripheral resistance. These results suggest that 1) during cold water immersion, peripheral vasoconstriction provides an additional increase in cardiac preload, leading to a further increase in the stroke volume compared to that of the thermoneutral water immersion, 2) the mechanism of cardiovascular adjustment during dynamic exercise is not changed by the persistent increase in cardiac preload in water immersion, and 3) a relatively high cardiac output during water immersion is to maintain a proper arterial pressure in the face of reduced vascular resistance.(Appl Human Sci,

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Effects of cadmium intoxication on renal transport systems for various organic compounds were studied. Subcutaneous injections of CdCl2 (2 mg Cd/kg.day) for two to three weeks induced marked polyuria, glycosuria, and proteinuria without altering glomerular filtration rate. In renal cortical brush border membrane vesicles (BBMV) isolated from cadmium treated rats, Na(+)-dependent D-glucose uptake was markedly attenuated, and this was due to reduction in Vmax and not Km. Likewise, Na(+)-driven L-glutamate transport and H(+)-driven tetraethylammonium transport were significantly reduced. In renal cortical basolateral membrane vesicles (BLMV) of cadmium intoxicated rats, Na(+)-dependent succinate transport was drastically reduced. These results indicate that cadmium intoxication impairs various transport systems for organic compounds in the brush border and basolateral membranes of proximal renal tubules.