OSMOREGULATORY INHIBITION OF THERMALLY-INDUCED CUTANEOUS VASODILATIONIN PASSIVELY HEATED HUMANS

We examined the effect of increased plasma osmolality (P-osm) on cutan eous vasodilatory response to increased esophageal temperature (T-es) in passively heated human subjects (n = 6). To modify P-osm, subjects were infused with 0.9, 2, or 3% NaCl infusions (Inf) for 90 min on sep arate days. Infusion rates were 0.2, 0.15, and 0.125 ml . min(-1). kg body wt(-1) for 0.9, 2, and 3% Inf, respectively, which produced relat ively similar plasma volume expansion. Thirty minutes after the end of infusion, subjects immersed their lower legs in a water bath at 42 de grees C (room temperature 28 degrees C) for 60 min after 10 min of pre heating control measurements. Passive heating without infusion (NI) se rved as time control to account for the effect of volume expansion. P- osm (mosmol/kgH(2)O) values at the onset of passive heating were 289.9 +/- 1.4, 292.1 +/- 0.6, 298.7 +/- 0.7, and 305.6 +/- 0.6 after NI, 0. 9% Inf, 2% Inf, and 3% Inf, respectively. The increases in T-es (Delta T-es) at equilibrium during passive heating (mean Delta T-es during 5 5-60 min) were 0.47 +/- 0.08, 0.59 +/- 0.08, 0.85 +/- 0.13, and 1.09 /- 0.12 degrees C after NI, 0.9% Inf, 2% Inf, and 3% Inf, respectively , which indicates that T-es at equilibrium increased linearly as P-osm increased. Delta T-es required to elicit cutaneous vasodilation (Delt a T-es threshold for cutaneous vasodilation) also increased linearly a s P-osm increased as well as the Delta T-es threshold for sweating. Th e calculated increases in these thresholds per unit rise in P-osm from regression analysis were 0.044 degrees C for the cutaneous vasodilati on and 0.034 degrees C for sweating. Thus the Delta T-es thresholds fo r cutaneous vasodilation and sweating are shifted to higher Delta T-es along with the increase in P-osm, and these shifts resulted in the hi gher increase in T-es during passive heating.