The circulatory changes observed seemed to be mediated largely by LLLI-induced reduction of [Ca2+]i in VSMCs, in addition to the involvement of NO in the initial phase.

We examined if an exercise-heat acclimation program improves body fluid regulatory function in older subjects, as has been reported in younger subjects. Nine older (Old; 70 +/- 3 yr) and six younger (Young; 25 +/- 3 yr) male subjects participated in the study. Body fluid regulatory responses to an acute thermal dehydration challenge were examined before and after the 6-day acclimation session. Acute dehydration was produced by intermittent light exercise [4 bouts of 20-min exercise at 40% peak rate of oxygen consumption (VO(2 peak)) separated by 10 min rest] in the heat (36 degrees C; 40% relative humidity) followed by 30 min of recovery without fluid intake at 25 degrees C. During the 2-h rehydration period the subjects drank a carbohydrate-electrolyte solution ad libitum. In the preacclimation test, the Old lost approximately 0.8 kg during dehydration and recovered 31 +/- 4% of that loss during rehydration, whereas the Young lost approximately 1.2 kg and recovered 56 +/- 8% (P < 0.05, Young vs. Old). During the 6-day heat acclimation period all subjects performed the same exercise-heat exposure as in the dehydration period. Exercise-heat acclimation increased plasma volume by approximately 5% (P < 0.05) in Young subjects but not in Old. The body fluid loss during dehydration in the postacclimation test was similar to that in the preacclimation in Young and Old. The fractional recovery of lost fluid volume during rehydration increased in Young (by 80 +/- 9%; P < 0.05) but not in Old (by only 34 +/- 5%; NS). The improved recovery from dehydration in Young was mainly due to increased fluid intake with a small increase in the fluid retention fraction. The greater involuntary dehydration (greater fluid deficit) in Old was accompanied by reduced plasma vasopressin and aldosterone concentrations, renin activity, and subjective thirst rating (P < 0.05, Young vs. Old). Thus older people have reduced ability to facilitate body fluid regulatory function by exercise-heat acclimation, which might be involved in attenuation of the acclimation-induced increase in body fluid volume.

Oxygen transport from the blood to the tissues is a diffusive process driven by the gradient of oxygen tension (PO2). We developed an oxygen-quenching fluorescent membrane that allowed visualization of the PO2 distribution near the microvessels as optical patterns on the membrane by epifluorescence microscopy. This membrane was highly gas permeable to allow PO2 measurement and was transparent enough to also permit observation of the microcirculation. In combination with a newly devised gastight chamber and a micropositioning system, this membrane technique made it possible to visualize the PO2 distribution in the rat mesenteric microvascular network under well-defined conditions. Our preliminary findings indicate that the oxygen distribution in the microvascular network is heterogeneous and suggest that there is considerable release of oxygen from the arterioles. The time lag of the system for tracking rapid PO2 changes in vitro was shown to be negligible, indicating that dynamic PO2 changes occurring in vivo can also be assessed. This technique should provide a novel tool for the study of oxygen transport and metabolism under normal and abnormal conditions.

Increases in age and height and decreases in weight systolic blood pressure and heart rate are major preoperative risk factors of intraoperative hypothermia during major surgery.

Dynamic changes in the distribution of PO2 in the rat mesentery were measured to determine the O2 diffusion coefficient (DO2) and consumption rate (VO2). The distribution of PO2 was obtained in two-dimensional maps by microscopic fluorometry on the basis of oxygen quenching. The corresponding vasculature was also recorded on a video recorder to analyze the PO2 distribution consistent with the arrangement of the microvessels. Anesthetized rats breathing room air were subjected to 100% O2 ventilation to induce dynamic changes in PO2 distribution. We assumed a homogenous and constant VO2 in the tissue, and a one-dimensional diffusion equation was applied to simulate oxygen transport. The PO2 data corresponded very well to the theoretical curves, and calculated DO2 was 1.04 +/- 0.78 X 10(-5) cm2/s (mean +/- SD, n = 38) and VO2 was 8.2 +/- 3.9 x 10(-6) cm3 O2.cm-3 tissue.s-1 (n = 27) at 37 degrees C. However, PO2 values at points remote from the arterioles remained higher than the theoretical prediction.