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At least 487 records · Page 27Linked to original sources
PubMed2004

Influence of brain angiotensin on thermoregulation and hydromineral balance during pregnancy in rats.

During mammalian pregnancy, body temperature decreases and there are changes in fluid and electrolyte balance. Angiotensin signaling mechanisms in the brain have been shown to influence thermoregulation and body fluid balance in the nonpregnant state. We hypothesized that brain angiotensin is also implicated in adjusting these physiological systems in the pregnant rat. We compared core temperature and fluid regulation in three groups of pregnant rats: untreated rats, rats receiving continuous infusion of an AT(1) antagonist candesartan (5 microg.kg(-1).day(-1)) into a lateral cerebral ventricle to block brain AT(1) receptors, and rats receiving vehicle [artificial cerebrospinal fluid (aCSF)] vehicle. Untreated and aCSF-treated rats showed a decrease in colonic temperature (-0.5 and -0.8 degrees C respectively) by day 20 of gestation. However, rats treated with candesartan had increased colonic temperature compared with baseline (+0.9 degrees C), and their temperature was significantly higher on days 7 (P < 0.05), 17 (P < 0.05), and 20 (P < 0.001) compared with the other groups (aCSF and untreated). Daily food and water intakes and body weight were not different between the three groups. Similarly, litter sizes and pup weights were equal in all groups. Finally, the expected decreases in plasma Na(+) and osmolality during pregnancy were equivalent in all groups. This study suggests that brain angiotensin mediates the progressive decrease in body temperature that occurs during pregnancy. However, the changes in fluid balance associated with pregnancy are not dependent on brain angiotensin.

Angiotensins↗
PubMed1998

Bioimpedance analysis of fluid compartments in female CAPD patients.

Dry weight is difficult to determine in continuous ambulatory peritoneal dialysis (CAPD) patients. Bioimpedance spectroscopy using a multi-frequency analyzer was used to measure total body water, extracellular water, and intracellular water in 7 female CAPD patients and, for comparison, in 6 normal female controls. One patient was measured a second time after a 10-kg fluid loss. Mean weight in controls and CAPD patients was similar, as was the percent of body weight that was water. However, the ratio of extracellular water to intracellular water was 0.814 in controls but 1.11 in CAPD patients, suggesting either more extracellular water and/or less intracellular water in the CAPD patients compared to the controls. When analyzed, the percent of total body water that was extracellular was significantly greater in the CAPD group. There was also a significant reduction in the percent of intracellular water that contributed to body weight in the CAPD patients. Body cell mass was 38.1% in controls but only 30.2% in CAPD patients. Serum albumin concentration ranged from 2.1 to 4.2 g/dL in CAPD and a linear relationship was present between serum albumin concentration and cell membrane capacitance. We conclude that 60% of body weight as body water may be an overestimate of volume (V) when the formula Kt/V is used to measure adequacy, and that bioimpedance spectroscopy may be a useful technique for assessing both fluid balance and body cell mass or nutritional status in CAPD patients.

Adult↗
PubMed1995

Energy expenditure during antiorthostatic bed rest (simulated microgravity).

Few studies have addressed the interaction between energy balance and lean body mass in healthy subjects during spaceflight or its simulations. We used doubly labeled water to measure total energy expenditure (TEE) in nine healthy adult men during two 7-day periods, once before and once during a 10-day head-down bed-rest period. Mean TEE was 21% less during than before bed rest; however, neither basal (BEE) nor resting (REE) energy expenditures changed, implying that the lesser TEE resulted from a reduction in physical activity. During the bed-rest period, energy intake was 563 +/- 280 kcal/day higher than TEE (P < 0.05) but body weight, fluid balance, BEE, and REE did not change relative to before bed rest. However, the small but statistically significant increase in body fat (0.44 +/- 0.67 kg, P < 0.05) during the bed-rest period suggests that body weight alone does not accurately reflect changes in energy balance during antiorthostatic bed rest.

Adult↗
PubMed1972

Studies on weightlessness in a primate in the Biosatellite 3 experiment.

In June 1969 a male Macaca nemestrina (pigtail macaque) was flown in earth orbit for 8.8 days in NASA Biosatellite 3. The experiment examined in detail central nervous and cardiovascular functions, and included pre- and post-flight whole body metabolic assessment, in-flight urine analysis, and pre-and post-flight bone density measurements. Although the sleep/wake cycle was 24 hr, a phase angle lag of 2 hr from the imposed night/day mode occurred. A definite desynchronosis occurred, with rhythms longer than 24 hr in pCO2, brain and body temperature and heart rate, although arterial blood pressure remained at 24 hr. Sleep states were remarkably fragmented and unusually brief in duration. Vestibular and ocular disturbances were evident. These changes began concurrently with onset of weightlessness and were not secondary to altered fluid balance or body temperature. Sleep patterns lie between those of normal man and man with high cervical cord transection. There was an immediate and sustained increase in central venous pressure in weightlessness and this is considered to have initiated a Henry-Gauer reflex which initially maintained a high urine volume. This, coupled with a high evaporative fluid loss, produced an early dehydration probably associated with electrolyte imbalances. Body weight was 20% lower at recovery than at launch. Ventricular fibrillation supervened 8 hr after recovery.

Adaptation, Physiological↗
PubMed2004

[Analysis and adjustment of acid-base disturbances according to the Stewart-Fencl principle].

In 1983, P. J. Stewart proposed a new approach for evaluation of acid-base balance of body fluids. He defined three independent variables responsible for hydrogen ion concentration in body fluids: 1. the partial pressure of carbon dioxide (pCO2); 2. strong ion difference, SID, i.e. the difference between the sums of all the strong (fully dissociated, chemically nonreacting) cations and sums of the strong anions; 3. the total concentration of all the non-volatile weak acids (mainly albumin) designated as [Atot]. On the basis of this theory, V. Fencl invented a new classification of clinical acid-base disturbances. Respiratory acidosis and alkalosis result from abnormalities of pCO2. The classifications of the respiratory disturbances of ABR is identical as in the conventional viewing which is based on the dissociation equation of carbonic acid. Metabolic acidoses or alkaloses result from derangements of the SID and/or [Atot]. The change of SID value is a consequence of either dehydration (alkalosis) or hyperhydration (acidosis). Other mechanisms of SID deviation are either changes of serum chloride concentration (an increase causes acidosis, a decrease causes alkalosis) or an increase of concentrations of substances not routinely measured (ketones, lactate, exogenous acids). [Atot] value is determined mainly by the serum albumin concentration (alkalosis in hypoalbuminemia, acidosis in hyperproteinemia). The Stewart-Fencl approach to acid-base balance enables to understand and predict what happens to hydrogen ions in body fluids and to control the pH abnormalities quantitatively.

Acid-Base Equilibrium↗