Heat acclimatization improves thermoregulatory responses to heat stress and decreases sweat sodium concentration ([Na(+)](sweat)). The reduced [Na(+)](sweat) results in a larger increase in plasma osmolality (P(osmol)) at a given amount of sweat output. The increase in P(osmol) inhibits thermoregulatory responses to increased body core temperature. Therefore, we hypothesized that the inhibitory effect of plasma hyperosmolality on the thermoregulatory responses to heat stress should be attenuated with the reduction of [Na(+)](sweat) due to heat acclimatization. Eleven subjects (9 male and 2 female) were passively heated by immersing their lower legs into water at 42 degrees C (room temperature 28 degrees C and relative humidity 30%) for 50 min following isotonic or hypertonic saline infusion. We determined the increase in the esophageal temperature (T(es)) required to elicit sweating and cutaneous vasodilation (CVD) (DeltaT(es) thresholds for sweating and CVD, respectively) in each condition and calculated the elevation of the T(es) thresholds per unit increase in P(osmol) as the osmotic inhibition of sweating and CVD. The osmotic shift in the DeltaT(es) thresholds for both sweating and CVD correlated linearly with [Na(+)](sweat) (r = 0.858 and r = 0.628, respectively). Thus subjects with a lower [Na(+)](sweat) showed a smaller osmotic elevation of the DeltaT(es) thresholds for sweating and CVD. These results suggest the possibility that heat acclimatization attenuates osmotic inhibition of thermoregulatory responses as well as reducing [Na(+)](sweat).

No abstract

ABSTRACT:The fetal cardiovascular responses to hypoxia include decreased peripheral blood flow and increased cerebral, cardiac, and adrenal blood flow. Prostanoids, metabolites of cyclooxygenase enzyme activity, have potent effects on vascular tone in both the adult and the fetus. To examine the role of prostanoids in the regulation of fetal cerebral blood flow (CBF) during acute hypoxic stress, eight near term fetal sheep were studied after infusing vehicle or diclofenac, a cyclooxygenase inhibitor, followed by a 30-min period of hypoxia (arterial PO 2 12 Torr). In the control experiments, CBF, measured continuously with laser Doppler flowmetry, increased to 148% of baseline values (p Ͻ 0.01) and cerebral vascular resistance decreased to 70% of baseline values after 30 min of hypoxic stress. During diclofenac infusion, hypoxia resulted in a CBF increase to only 129% of baseline, a significant attenuation (p Ͻ 0.05), accompanied by decreased plasma prostanoid concentrations. Increases in mean arterial blood pressure during hypoxia were also attenuated by diclofenac infusion. Flow and pressure responses were not accompanied by changes in cerebral vascular resistance. These results indicate that prostanoids indirectly modulate fetal CBF responses to hypoxia, but that their effects are mediated through modulation of systemic rather than cerebral vascular tone. T he fetus is often subjected to hypoxic insult during gestation and labor. In defense against hypoxic injury, mechanisms come into play that optimize the balance between oxygen delivery and consumption in vital organs such as the brain, heart, and adrenals. In the fetal brain, this is accomplished in part by an increase in CBF (1-3), a regulated reduction in oxidative metabolism (4 -6), and an increase in anaerobic metabolism. This increase in CBF is accomplished in part by redistribution of blood flow during hypoxic stress resulting in increased blood flow to vital organs and decreased blood flow to peripheral organs (1). The redistribution of flow to these organs is the result of increased systemic arterial blood pressure and decreased local cerebral vascular resistance (1,7). Previous work by our group and others has shown that both adenosine and nitric oxide are important mediators of this effect (5,6). However, the changes in CBF and vascular resistance during hypoxia cannot be completely attributed to these systems. The studies presented here focus on the role of prostanoids in mediating these changes in blood flow to the fetal brain during hypoxia.Prostanoids, a subclass of eicosanoids that includes prostaglandins and thromboxanes, are found throughout biologic tissues and are important modulators of vascular tone. Prostanoids are synthesized by oxidation of free arachidonic acid, a reaction catalyzed by cyclooxygenase enzymes cyclooxygenase 1 (COX-1) and cyclooxygenase 2 (COX-2). In adult vascular tissues, COX-1 is a constitutive enzyme, whereas COX-2 is an inducible enzyme, both of which are involved in the production of precursors of the vasoconstr...

: Purpose : To investigate the utility of the Short Nutritional Assessment Questionnaire (SNAQ) in the nutritional evaluation of patients with cancer undergoing outpatient chemotherapy. Methods : We included 229 patients with cancer who were undergoing outpatient chemotherapy between October 2015 and April 2016. The SNAQ and the revised SNAQ (addition of age and body mass index) were implemented, and their relationships with Controlling Nutritional Status (CONUT), an indicator of bionutritional assessment, were examined. Results : The cutoff value of the SNAQ score corresponding to moderate-to -severe undernourishment in CONUT values was 0.5, with a sensitivity of 87.5% % and a specificity of 65.9% %, and the corresponding values for the revised SNAQ score were 2.5, 91.7% %, and 62.9% %, respectively. This cutoff value and the corresponding positive prediction value for the revised SNAQ were superior to those of SNAQ. Binary logistic regression analysis with the revised SNAQ and sex as independent variables and the CONUT value as the dependent variable revealed that the higher the SNAQ score, the more likely it was that CONUT moderate-to-severe undernourishment would be identified (odds ratio, 1.48 ; , 1.34-1.96) . Conclusion : Nutritional evaluation with the revised SNAQ can predict moderateto-severe undernourishment according to CONUT in patients with cancer undergoing outpatient chemotherapy.