No abstract

The purpose of this experiment was to explore the complex relationship between fluid consumption and consumption factors (thirst, voluntary dehydration, water alliesthesia, palatability, work-rest cycle) during a simulated 14.5-km desert walk (treadmill, 1.34 m X s-1, 5% grade, 40 degrees C dry bulb/26 degrees C wet bulb, and wind speed of approximately 1.2 m X s-1). Twenty-nine subjects were tested (30 min X h-1, 6 h) on each of two nonconsecutive days. The subjects were randomly assigned to one of three groups: tap water (n = 8), iodine-treated tap water (n = 11), or iodine-treated flavored tap water (n = 10). The temperature of the water was 40 degrees C during one trial and 15 degrees C on the other. Mean sweat losses (6 h) varied between 1.4 kg (warm iodine-treated; 232 +/- 44 g X h-1) and 3.0 kg (cool iodine-treated flavored; 509 +/- 50 g X h-1). Warm drinks were consumed at a lower rate than cool drinks (negative and positive alliesthesia). This decreased consumption resulted in the highest percent body weight losses (2.8 and 3.2%). Cooling and flavoring effects on consumption were additive and increased the rate of intake by 120%. The apparent paradox between reduced consumption concomitant with severe dehydration and hyperthermia is attributed to negative alliesthesia for warm water rather than an apparent inadequacy of the thirst mechanism. The reluctance to drink warm iodine-treated water resulted in significant hyperthermia, dehydration, hypovolemia, and, in two cases, heat illness.

The effect of gram-negative sepsis on the kinetics and oxidation of very low-density lipoprotein (VLDL) fatty acids was assessed in conscious dogs in the normal state and 24 h after infusion of live Escherichia coli. VLDL, labeled with [2-3H]glycerol and [1-14C]palmitic acid, was used to trace VLDL kinetics and oxidation, and [1-13C]palmitic acid bound to albumin was infused simultaneously to quantify kinetics and oxidation of free fatty acid (FFA) in plasma. Sepsis caused a fivefold increase in the rate of VLDL production (RaVLDL). In the control dogs, the direct oxidation of VLDL-fatty acids was not an important contributor to their overall energy metabolism, but in dogs with sepsis, 17% of the total rate of CO2 production could be accounted for by VLDL-fatty acid oxidation. When glucose was infused into dogs with insulin and glucagon levels clamped at basal levels (by means of infusion of somatostatin and replacement of the hormones), RaVLDL increased significantly in the control dogs, but it did not increase further in dogs with sepsis. We conclude that the increase in triglyceride concentration in fasting dogs with gram-negative sepsis is the result of an increase in VLDL production and that the fatty acids in VLDL can serve as an important source of energy in sepsis.