Alterations In Plasma Volume Research Articles

Acute Effects of a Single Bout of Strength and Endurance Exercise on Vitamin D Metabolites in Young Adults.

The effect of exercise on serum concentration of vitamin D metabolites remains inconclusive, with studies reporting deviating results. This study evaluated the acute effect of a single session of two specific exercise forms; strength training (ST) and high-intensity interval training (HIIT), on circulating 25-hydroxyvitamin D (25(OH)D), free25(OH)D and 1,25-dihydroxyvitamin D (1,25(OH)2D), and skeletal muscle vitamin D receptor (VDR) gene expression, in healthy adults. Thirty-nine participants (19 women and 20 men, age 21-30 years) completed a single bout of ST and HIIT exercise, separated by two weeks. Serum concentration of total 25(OH)D, free25(OH)D and 1,25(OH)2D were assessed before exercise, immediately after, and 3 hours and 24 hours after each session. Muscle biopsies were obtained at rest (1st visit), and at 3 hours and 24 hours post ST and HIIT, and analyzed for VDR gene expression. Repeated measures ANOVA was used to assess serum concentration across time, while paired samples t-test was used for muscle VDR gene expression analyses. Serum concentration of 25(OH)D or free 25(OH)D did not change after either exercise mode when correcting for plasma volume alterations. 1,25(OH)2D was reduced by 13.1 ± 18.3 pmol/L and 7.1 ± 9.6 pmol/L immediately after ST and HIIT, respectively (P < 0.001). Muscle VDR mRNA expression increased after ST by 3.1 ± 1.8 (3 hr) and 2.2 ± 1.7 (24 hr) fold change (P < 0.05). One single session of ST or HIIT did not alter serum concentration of 25(OH)D and free 25(OH)D when correcting for plasma volume changes. Both exercise modes caused a transient reduction in 1,25(OH)2D suggesting utilization of 1,25(OH)2D by muscle cells following exercise. Elevated VDR gene expression following ST suggests a functional role of VDR in fast-twitch muscle fibers.

Unveiling the AyurvedicApproach to Water Balance and Hypertension: Insights and Connections.

Background: Hypertension (HTN) is a non-communicable disease that contributes to heart disease, stroke, kidney failure, and premature mortality and disability. The majority of cardiovascular disease deaths, approximately 80%, occur in low and middle-income countries such as India. Therefore, it is crucial to explore the Ayurvedic perspective on HTN to enable Ayurvedic healthcare providers to effectively manage HTN and its complications. Objective: The aim of this article is to review the Ayurvedic concept of water balance, blood, and blood pressure, and investigate their potential involvement in the development of HTN. Materials and Methods: We conducted a critical review of scattered references in Ayurvedic literature pertaining to water balance and the role of Doshas in maintaining it. Results: Water constitutes a major component of blood, and alterations in plasma volume can impact blood pressure levels. The literature review highlighted the similarity between the properties of Kapha and Pitta and the water-dominant attributes, suggesting their potential to disrupt water balance. Conclusion: Ayurveda emphasizes the greater involvement of Kapha and Pitta in maintaining water balance in the body, while Vata is responsible for its circulation. Factors leading to the imbalance of Kapha and Pitta may initiate and contribute to the pathogenesis of hypertension, which necessitates thorough consideration for effective Ayurvedic management.

Can Variable Plasma Volume Alterations Affect the Efficiency of the First Trimester Screening Test?

The aim of this study was to assess the effect of plasma volume alteration determined by hematocrit on biochemical parameters of the first trimester screening test. Enrolled in this study were 1,424 pregnant women in their first trimester who underwent a first trimester screening test. Fetal Nuchal Trancluciency measurement was obtained by ultrasonographic evaluation. Blood samples were taken for complete blood count, serum free β-HCG, and PAPP-A between 11 and 14 weeks of gestation. The effect of plasma volume alteration on the screening test was evaluated. Mean corpuscular volume was used to rule out possible iron deficiency anemia. There were 59 women with combined risk > 1/270. Of these 59 women, there were 21 false positive results (1.5%). Serum Htc significantly predicted the false positive cases (AUC: 0.839, p < 0.001). The optimal cutoff value was obtained at a value of 30.2% with 85% sensitivity and 75% specificity. Our study suggests that the degree of plasma alterations may affect the serum levels of the biochemical components of the first trimester screening test for aneuploidy, thereby leading to false positive test results.

Alterations in hematologic indices during long-duration spaceflight

BackgroundAlthough a state of anemia is perceived to be associated with spaceflight, to date a peripheral blood hematologic assessment of red blood cell (RBC) indices has not been performed during long-duration space missions.MethodsThis investigation collected whole blood samples from astronauts participating in up to 6-months orbital spaceflight, and returned those samples (ambient storage) to Earth for analysis. As samples were always collected near undock of a returning vehicle, the delay from collection to analysis never exceeded 48 h. As a subset of a larger immunologic investigation, a complete blood count was performed. A parallel stability study of the effect of a 48 h delay on these parameters assisted interpretation of the in-flight data.ResultsWe report that the RBC and hemoglobin were significantly elevated during flight, both parameters deemed stable through the delay of sample return. Although the stability data showed hematocrit to be mildly elevated at +48 h, there was an in-flight increase in hematocrit that was ~3-fold higher in magnitude than the anticipated increase due to the delay in processing.ConclusionsWhile susceptible to the possible influence of dehydration or plasma volume alterations, these results suggest astronauts do not develop persistent anemia during spaceflight.

Effects of vasoactive drugs on crystalloid fluid kinetics in septic sheep

PurposeCrystalloid fluid and vasoactive drugs are used in the early treatment of sepsis. The purpose of the present study was to examine how these drugs alter plasma volume expansion, peripheral edema, and urinary excretion.MethodsTwenty-five anesthetized sheep were made septic by cecal puncture and a short infusion of lipopolysaccharide. After 50 min, a slow infusion of isotonic saline was initiated: the saline either contained no drug, norepinephrine (1 μg/kg/min), phenylephrine (3 μg/kg/min), dopamine (50 μg/kg/min), or esmolol (50 μg/kg/min). Ten min later, 20 mL/kg Ringer´s lactate solution was given over 30 min. Central hemodynamics, acid-base balance, and the urinary excretion were monitored. Frequent measurements of the blood hemoglobin concentration were used as input in a kinetic analysis, using a mixed effects modeling software.ResultsThe fluid kinetic analysis showed slow distribution and elimination of Ringer´s lactate, although phenylephrine and dopamine accelerated the distribution. Once distributed, the fluid remained in the peripheral tissues and did not equilibrate adequately with the plasma. Overall, stimulation of adrenergic alpha1-receptors accelerated, while beta1-receptors retarded, the distribution and elimination of fluid. A pharmacodynamic Emax model showed that Ringer´s lactate increased stroke volume by 13 ml/beat. Alpha1-receptors, but not beta1-receptors, further increased stroke volume, while both raised the mean arterial pressure. Modulation of the beta1-receptors limited the acidosis.ConclusionsStimulation of adrenergic alpha1-receptors with vasoactive drugs accelerated, while beta1-receptors retarded, the distribution and elimination of fluid. The tendency for peripheral accumulation of fluid was pronounced, in particular when phenylephrine was given.

Effectiveness of Commercial versus Homemade Sports Drinks on Fluid Balance and Exercise Capacity during High-intensity Intermittent Exercise

Commercial sports drinks are used widely by athletes involved in high-intensity intermittent (HII) exercise. However, little has been reported on their relative effectiveness compared to simple homemade drink formulations. The purpose of this study was to investigate the effects of different sports drink formulations (commercial v homemade), water and no drink on fluid balance and exercise capacity during HII exercise. Twelve trained men (age: 27 ± 2.1 y) performed a 90-min HII running protocol designed to simulate activity experienced during a football match. The protocol was arranged in six 15-min stages where running speeds ranged between 55% and 120% of VO2max. The HII protocol included half-time and a run to fatigue post 90 min. Using a single-blind, randomized, cross-over design, participants ingested a preload of 5 ml⋅kg-1 10 min before HII exercise and 3 ml⋅kg-1 every 15 min of either Isostar® (ISO), a homemade sports drink (CHO), placebo (P) or no drink (ND). Blood lactate (Hla), blood glucose (Bgluc), heart rate (HR) and ratings of perceived exertion (RPE) were measured before, during (every 15 min) and after the 90-min HII protocol. Changes in plasma volume were measured at half-time and post 90 min. Sweat rate and fluid balance were calculated post each trial. Time to fatigue (TTF) was recorded at exhaustion. In the ND trial, TTF decreased by approximately 17%, 28% and 43% compared to P, CHO and ISO, respectively (p 0.05). No differences were noted in HLa, RPE, PV or SR between the trials (p>0.05) but there were significant effects of time (p<0.05). Bgluc peaked at 30 minutes in ISO and CHO, but dropped by ~27% in ISO and by ~30% in CHO after half time. Absence of fluid ingestion surprisingly had no significant effect on altering plasma volume or decreasing sweat rate despite causing noticeable decreases in exercise capacity. The homemade drink improved exercise capacity in a similar manner to that of the commercial drink, but neither sports drink achieved superior hydration compared to water. Ingestion of exogenous carbohydrate through sports drink consumption caused an exercise-induced glycemic response when exercise was restarted after half-time. This decline in blood glucose after half-time appears to be marginally attenuated in P trial. A possible suggestion for team sports could be to drink water rather than sports drink prior to half-time period.

Impact of skin temperature and hydration on plasma volume responses during exercise.

Heat stress and hydration may both alter plasma volume (PV) responses during acute exercise; potential interactions have not been fully studied. The purpose of this study was to determine the effect of graded elevations in skin temperature (Tsk) on PV changes during steady-state exercise under conditions of euhydration (EU) and hypohydration (HYPO, -4% of body mass). Thirty-two men (22 ± 4 yr) were divided into four cohorts (n = 8 each) and completed EU and HYPO trials in one environment [ambient temperature (Ta) 10, 20, 30, and 40°C]. Thirty minutes of cycle ergometry (50% V̇o2peak) was performed. Core (Tre) and mean skin (Tsk) temperatures were measured; changes in PV, total circulating protein (TCP), and mean arterial pressure (MAP) were calculated; and skin blood flow (SkBF) was estimated. Hypohydration decreased (P < 0.05) PV by 200 ml (-5.7%) but did not alter TCP. Plasma loss was not different between EU and HYPO during exercise at any Ta. Plasma losses were greater (P < 0.05) with elevated Ta with an average -130, -174, -294, and -445 ml losses during the 10, 20, 30, and 40°C trials, respectively. Significant (P < 0.05) correlations (r = 0.50 to 0.84) were found between ΔTCP and ΔPV during exercise when Tsk was cool/warm (<33°C; Ta 10, 20, and 30°C), but not at 40°C (high Tsk). We conclude that 1) graded skin warming proportionally accentuated plasma loss; 2) plasma loss was associated with plasma protein efflux at lower Tsk and SkBF; 3) at high Tsk, additional plasma loss likely results from increased net filtration at the capillaries; and 4) HYPO did not alter vascular fluid loss during exercise in any environment.

Fluid shifts during running with body weight unloading by LBPP

At any given running speed, weight support with a lower body positive pressure (LBPP) device (i.e. Alter‐G treadmill) reduces VO2. We tested the hypothesis that mild LBPP would alter plasma volume (PV) shifts during exercise. Maximal aerobic capacity (VO2max) was determined in 8 male subjects at 100% and 80% (13.5 ± 0.1 mmHg LBPP) body weight loading at 0% grade. VO2, heart rate (HR), mean arterial blood pressure (MAP) and changes in Hct, [Hb], and total protein ([TP]) were determined on separate days in a randomized crossover design. Venous blood samples (5 cc) were taken at rest and at 5, 6, 7, 7.5, 8.0, and 8.5, 9.0 mph (0% grade) during each 3 min stage. Changes in plasma volume were calculated from changes in Hct and [Hb]. VO2max was similar for both BW loading trials and averaged about 52.5 ± 0.9 ml O2•min−1•kg−1 BW. The energy cost of running at 9 mph (42.3 ± 1.7 ml O2•min−1•kg−1 BW ) was reduced by 12% at 80% body weight (p&lt;0.05). During running at 80% BW HR was reduced compared to 100% BW running (p&lt;0.05) however the MAP response was similar. During exercise the reduction in PV, at any given VO2 was larger at 80% BW compared to 100% BW running (p&lt;0.001). At any give energy expenditure exercise with mild LBPP produced a greater shift of fluid out of the vascular space. It is interesting that 80% BW running resulted in a lower HR despite the larger reduction in PV. The impact of mild LBPP on venous return must counteract the role of reduced PV on stroke volume, thereby supporting a lower exercise HR.

Effects of Glycerol and Creatine Hyperhydration on Doping-Relevant Blood Parameters

Glycerol is prohibited as an ergogenic aid by the World Anti-Doping Agency (WADA) due to the potential for its plasma expansion properties to have masking effects. However, the scientific basis of the inclusion of Gly as a “masking agent” remains inconclusive. The purpose of this study was to determine the effects of a hyperhydrating supplement containing Gly on doping-relevant blood parameters. Nine trained males ingested a hyperhydrating mixture twice per day for 7 days containing 1.0 g·kg−1 body mass (BM) of Gly, 10.0 g of creatine and 75.0 g of glucose. Blood samples were collected and total hemoglobin (Hb) mass determined using the optimized carbon monoxide (CO) rebreathing method pre- and post-supplementation. BM and total body water (TBW) increased significantly following supplementation by 1.1 ± 1.2 and 1.0 ± 1.2 L (BM, P < 0.01; TBW, P <0.01), respectively. This hyperhydration did not significantly alter plasma volume or any of the doping-relevant blood parameters (e.g., hematocrit, Hb, reticulocytes and total Hb-mass) even when Gly was clearly detectable in urine samples. In conclusion, this study shows that supplementation with hyperhydrating solution containing Gly for 7 days does not significantly alter doping-relevant blood parameters.

Hypoproteinemia does not alter plasma volume expansion in response to a 0.9% saline bolus in awake sheep

To test the hypothesis that hypoproteinemia reduces plasma volume expansion produced by a bolus of crystalloid solution given to awake sheep. Prospective and observational. Laboratory. Five female merino sheep (n = 5) weighing 37 ± 3 kg were anesthetized. Each animal was subjected to a 5-day test period: day 1: 50 mL/min 0.9% saline infusion over 20 mins. Days 2-4: daily plasmapheresis and replacement of the shed plasma with 6 L of 0.9% saline were performed in increments. Fractional plasma volume expansion after rapid infusion of saline on days 1 and 5 was calculated from changes in hemoglobin concentration. There was a significant reduction in total plasma protein concentration after plasmapheresis (p < .05). Colloid osmotic pressures were also significantly lowered (p < .05). A crystalloid infusion of 0.9% saline did not alter any of these values compared with baseline. The hemodynamic measurements did not show significant differences between the experiments. The plasma volume expansion reached approximately 20% at the end of infusion and stayed at 10-15% during the experiments. No difference was found in plasma volume expansion produced by a bolus of 50 mL/min of 0.9% in the hypoproteinemic state when compared with the euproteinemic state (p = .61). No difference in cumulative urinary output was found between the two states. In contrast to our hypothesis, severe acute hypoproteinemia does not reduce plasma volume expansion in response to 50 mL/min 0.9% saline infusion in nonspleenectomized sheep when compared with the resultant plasma volume expansion after a 50 mL/min of 0.9% infusion in the euproteinemic state.

EPO and doping

It is with great interest that we read exchanges on intermittent hypoxic (Boning 2009; Ferretti 2009) exposure as a potential doping procedure. Erythropoietin (EPO) does introduce potential concerns in terms of doping, both due to its eVects and side eVects. An earlier publication on exogenous EPO (Noakes 2008) clearly showed an increase of sub-maximal performance with a signiWcant increase of time to exhaustion after prolonged rHuEPO administration. It is clear that in healthy subjects, at sub-maximal eVort levels, cardiac output is suYcient to maintain adequate oxygen delivery to active muscles. Accordingly, it appears that EPO achieves more than increasing blood oxygen carrying capacity alone. Being both a hormone and a cytokine, the actual actions of EPO are complex: EPO is neuroprotective and even neuroregenerative in both the peripheral and central nervous system. Moreover, EPO also has antiapoptotic eVects that may be coupled to antioxidant activity. Exercise-induced plasma volume contraction is linked to EPO production (Roberts et al. 2000), whereas the hormone itself appears to alter plasma volume as well. Any of these known actions of EPO could explain a possible increase in exercise capacity. The traditional view of EPO as a haemopoietic agent, therefore, needs to be expanded to incorporate these additional eVects and studies on the eVects of EPO should be designed in such a way that these may be considered more carefully. Urine testing for exogenous EPO has been available for several years. It has been used in international cycling events. However, this does not exclude the possibility of endogenous EPO induction. Intermittent hypoxia (SanchisGomar et al. 2009) is the natural trigger for EPO production, and is widely used by (endurance) athletes since many years. We have recently described the use of intermittent hyperoxia to stimulate EPO production (Balestra et al. 2006). This has subsequently been shown to be capable of increasing haemoglobin levels in a chronically anaemic patient (Burk 2007). The mechanism proposed to explain this “normobaric oxygen paradox” involves a complex play of oxygen-free radicals (OFRs) presence and their “scavenging” enzymes in the cell. In the presence of OFR, the continuously produced hypoxia-inducible factor alpha (HIF-1 ) is instantly linked to the (tumour suppressing) Von Hippel Lindau Protein (VHLp). This complex is subsequently ubiquitinized in the prolyl-oxidase pathway and Wnally recycled in the proteasome. In a hypoxic state, the absence of OFR prevents HIF-1 from linking to VHLp, and allows it to be dimerized with the HIF-1 dimer. This hybrid HIF complex can then start a cascade of EPO gene expression and subsequently, de novo EPO synthesis. In a hyperoxic situation, the presence of OFR will trigger an upregulation of OFR scavenging systems; notably, the activity of the glutathione synthetase enzyme is increased, resulting in an increased availability of glutathione. When now the cell resumes its “normoxic” state, the increased glutathione will scavenge all OFRs present, “mimicking” a hypoxic situation, and allowing the HIF dimers to bind and start the EPO gene expression. In our experience, this mechanism has allowed a clinically valuable increase in haemoglobin in patients with anaemia due to a variety of causes, including bone marrow Communicated by Susan Ward.

Altering plasma volume, plasma osmolality, and the renin‐angiotensin system reduces the vascular responses to a pharmacological stress in conscious rats

Altering plasma volume, plasma osmolality, and the renin‐angiotensin system reduces the vascular responses to a pharmacological stress in conscious rats

Sepsis Produced by Pseudomonas Bacteremia Does Not Alter Plasma Volume Expansion After 0.9% Saline Infusion in Sheep

Clinicians generally consider sepsis to be a state in which fluid is poorly retained within the vasculature and accumulates within the interstitium. We hypothesized that infusion of 0.9% saline in conscious, chronically instrumented sheep with hyperdynamic bacteremic sepsis would be associated with less plasma volume expansion (PVE) and greater interstitial fluid volume expansion than in conscious, nonseptic sheep. Six conscious adult sheep received an IV infusion of 25 mL/kg of 0.9% saline over 20 min (1.25 mL.kg(-1).min(-1)) in a control nonseptic state and during early and late sepsis (4 and 24 h, respectively, after initiation of a standard infusion of live Pseudomonas aeruginosa). The distribution and elimination of infused fluid were studied by mass balance (after measurement of plasma volume using Evans blue dye) and volume kinetic analysis. Mass balance demonstrated no significant differences in the time-course of PVE between control, early sepsis, and late sepsis. At the end of the infusions, which averaged 1050 +/- 125 mL in sheep weighing an average of 42 +/- 5 kg, calculated PVE was 312 +/- 50 mL, 386 +/- 34 mL, and 400 +/- 51, respectively. Volume kinetic analysis was similar in all three protocols. In both nonseptic and septic sheep, infusion of 0.9% saline resulted in similar peak PVE and resolution of PVE over a 3-h interval and similar kinetic parameters. Contrary to clinical impressions and to our hypothesis, the distribution of 0.9% saline in this animal model was not changed by bacteremia produced by infusion of Pseudomonas aeruginosa.

Modulation of body fluids and angiotensin II receptors in a rat model of intra‐uterine growth restriction

We previously reported that sodium restriction during pregnancy reduces plasma volume expansion and promotes intra-uterine growth restriction (IUGR) in rats while it activates the renin-angiotensin-aldosterone system (RAAS). In the present study, we proceeded to determine whether expression of the two angiotensin II (ANGII) receptor subtypes (AT(1) and AT(2)) change in relation to maternal water-electrolyte homeostasis and fetal growth. To this end, pregnant (gestation day 15) and non-pregnant Sprague-Dawley rats were randomly assigned to two groups fed either normal, or Na(+)-restricted diets for 7 days. At the end of the treatment period, plasma aldosterone and renin activity as well as plasma and urine electrolytes were measured. Determinations for AT(1) and AT(2) mRNA and protein were made by RNase protection assay and photoaffinity labelling, respectively, using a number of tissues implicated in volume regulation and fetal growth. In non-pregnant rats, Na(+) restriction decreases Na(+) excretion without altering plasma volume, plasma Na(+) concentration or the expression of AT(1) and AT(2) mRNA or protein in the tissues examined. In normally fed pregnant rats when compared to non-pregnant controls, AT(1) mRNA increases in the hypothalamus as well as pituitary and declines in uterine arteries, while AT(1) protein decreases in the kidney and AT(2) mRNA declines in the adrenal cortex. In pregnant rats, Na(+) restriction induces a decrease in plasma Na(+), an increase in plasma urea, as well as a decline in renal urea and creatinine clearance rates. Protein levels for both AT(1) and AT(2) in the pituitary and AT(2) mRNA in the adrenal cortex are lower in the Na(+)-restricted pregnant group when compared to normally fed pregnant animals. Na(+) restriction also induces a decrease in AT(1) protein in the placenta. In conclusion, these results suggest that pregnancy may increase sensitivity to Na(+) depletion by the tissue-specific modulation of ANGII receptors. Finally, these receptors may be implicated in the IUGR response to low Na(+).

Relationships between fluid and electrolyte hormones and plasma volume during exercise with training and detraining.

The purpose of this study was to investigate the relationship between training-induced alterations in plasma volume (PV) and changes in fluid and electrolyte regulatory hormones during prolonged exercise. Seven male subjects (VO2peak 49.2 +/- 2.4 mL.kg-1.min-1, X +/- SE) performed a cycling test before (C) and after (T) 6 d of training and after 6 d of detraining (DT). Training was conducted for 2 h.d-1 at 68% VO2peak at a room temperature between 26-28 degrees C. The 60-min exercise challenge included 20 min at 50%, 65%, and 75% VO2peak workloads. Training resulted in a calculated 13.8 +/- 1.6% PV expansion (P < 0.05) which recovered to C levels with DT (1.8 +/- 2.3%, P > 0.05). Compared with that at C, training resulted in a reduction of aldosterone (ALDO) concentration at all exercise intensities (P < 0.05) which normalized to C levels with DT. With T, epinephrine (EPI) concentrations were reduced at the highest power output only (365 +/- 51 vs 113 +/- 22 pg.mL-1; P < 0.05) and returned to C levels with DT. Arginine vasopressin (AVP) concentrations were also reduced at the highest workload only (20.2 +/- 3.2 pg.mL-1 vs 10.4 +/- 0.7 pg.mL-1; P < 0.05) and remained depressed after DT (11.8 +/- 1.3 pg.mL-1; P < 0.05). Atrial natriuretic factor (ANF) and norepinephrine (NOREPI) were not affected by T or DT. The results suggest that concentrations of ALDO, and to a lesser extent EPI, during exercise are related to PV levels, whereas ANF and NOREPI concentrations are not. AVP concentrations are related to other adaptive factors, the effects of which persist for a longer time course than do PV changes.

Central c-Fos expression in neonatal and adult rats after subcutaneous injection of hypertonic saline

Centrally-mediated responses to plasma hyperosmolality include compensatory drinking and pituitary secretion of vasopressin and oxytocin in both adult and neonatal rats. However, the anorexia that is produced by plasma hyperosmolality in adult rats is not evident in neonates, perhaps due to functional immaturity of osmoresponsive hindbrain circuits. To examine this possibility, the present study compared treatment-induced brain expression of the immediate-early gene product c-Fos as a marker of neural activation in adult and two-day-old rats after subcutaneous injection of 2 M NaCl (0.1 ml/10 g body weight). This treatment produced marked hypernatremia in adult and two-day-old rats without altering plasma volume. Several brain regions (including components of the lamina terminalis, the paraventricular and supraoptic nuclei of the hypothalamus, and the area postrema) were activated to express c-Fos similarly in adult and two-day-old rats after 2 M NaCl injection, consistent with previous reports implicating a subset of these regions in osmotically-stimulated drinking and neurohypophyseal secretion. In contrast, other areas of the brain that were activated to express c-Fos in adult rats after 2 M NaCl injection were not activated in neonates; these areas included the central nucleus of the amygdala, the parabrachial nucleus and catecholamine cell groups within the caudal medulla. This study demonstrates that certain brain regions that are osmoresponsive in adult rats (as defined by induced c-Fos expression) are not osmoresponsive in two-day-old rats. When considered in the context of known differences between the osmoregulatory capacities of adult and neonatal rats, our results are consistent with the idea that osmoresponsive forebrain centres are primarily involved in osmotically-stimulated compensatory drinking and neurohypophyseal secretion, whereas osmoresponsive regions of the hindbrain are important for concomitant inhibition of feeding and gastric emptying.

Water balance during and after marathon running.

To describe the time course of plasma volume alterations and the changes in the plasma concentrations of hormones regulating water balance in relation to a marathon race, six experienced marathon runners (five men, one women) aged 28 (SD 6) years were studied during and for the 3 days following a treadmill marathon run at 68 (SD 5) percent of maximal oxygen consumption. Haematocrit, haemoglobin, plasma protein (Prot) and electrolyte (Na+, K+) concentration, osmolality (osm), plasma concentrations of renin (Ren), aldosterone (Ald) and atrial natriuretic peptide (ANP) were determined at rest in a sitting position (T(-30)), and then after 30 min in an upright posture (R(0)), while running a marathon at 10 km (R(10)), 30 km (R(30)) and 42.2 km (R end), and after the marathon at 30 min (T(30)), 60 min (T(60)), 120 min (T(120)) and 24 h (TD(+1)), 48 h (TD(+2)) and 72 h (TD(+3)). The changes in plasma volume (PV), Prot, osm and Na+ observed during the race were nonsignificant. Significant increases in plasma concentration of K+ [4.8 (SD 0.6) vs 5.5 (SD 0.6) mmol*1(-1); P <0.01], Ren [38(SD 57) vs 197 (SD 145) pmol*1(-1); P <0.02] and Ald [175 (SD 142) vs 1632 (SD 490) pmol*1(-1); P <0.01] were observed at R(end). A significant increase of ANP (P <0.05) was only found after R(10). Body mass significantly decreased by 2.0 kg (P <0.01) during the race in spite of the ingestion of 1.46 (SD 0.34)1 of a 5 percent glucose solution. Urinary volume and Na+ excretion dropped significantly after the completion of the marathon in comparison with the day before [2600 vs 1452 ml*day(-1)(P <0.02) and 161.3 vs 97.1 mmol*1(-1) (P <0.05)]. At TD(+1) and TD(+2) a significant increase in PV was noted, compared to T(-30). The lack of a decrease in PV during the marathon may have been due to the production of 402 g of metabolic water and by the release of 1280 g of water stored in glycogen complexes in muscle and liver. Thus, the hormone response during the marathon may have been due to the effects of the exercise itself and not to the effects of dehydration. The postmarathon PV expansion may be explained by a protein shift to the intravascular space and by renal sodium retention.

Variations in plasma volume affect total and low-density lipoprotein cholesterol concentrations during the menstrual cycle

Serum lipids are known to vary during the menstrual cycle. To determine if changes in plasma volume contribute to this effect, we determined serum lipids, lipoproteins, and estimated changes in plasma volume in 18 premenopausal women at the start of and at 5-day intervals after menstruation. Eleven men served as a comparison group. Changes in plasma volume were estimated from changes in hemoglobin and hematocrit. Total and low-density lipoprotein (LDL) cholesterol (mean ± SD) increased 15 ± 14 mg/dL (9% ± 10%) and 11 ± 13 (11% ± 14%) within 10 days after the start of menstruation ( P < .05) and then decreased toward baseline during the rest of the cycle. High-density lipoprotein (HDL) cholesterol increased 3 mg/dL, or 5%, ( P < .05) on days 10 and 15 after menstruation. Plasma volume decreased 4% ± 9% ( P < .06) 10 days after the start of menstruation, and this maximum decrease in plasma volume coincided with peak increases in total, LDL, and HDL cholesterol. Except for an 8-mg/dL increase in LDL cholesterol at day 5, lipid changes were no longer significant after adjusting for changes in plasma volume. We conclude that alterations in plasma volume account for approximately half of the increase in total and LDL cholesterol during the menstrual cycle.

Effect of hypertonic and isotonic saline solutions on plasma constituents of conscious horses

SUMMARY Blood constituents and vascular volume indices were determined in 5 standing horses by use of 2-period crossover experimental design. Horses were either administered hypertonic (2,400 mosm/kg of body weight, iv) or isotonic (300 mosm/kg, iv) saline solution. Each solution was administered at a dosage of 5 ml/kg (infusion rate, 80 ml/min). Samples for determination of pcv, plasma volume, blood volume, plasma osmolality, total amount of plasma protein and plasma concentrations of protein, Na, K, and Cl were collected at 0 hour (baseline, before fluid infusion) and 0.5 hour (at the end of fluid infusion), and subsequently, at 0.25- or 0.5-hour intervals for 4.5 hours. All horses were given the predetermined dose of fluids by 0.5 hour after beginning the saline infusion. Values of P ≤ 0.05 were considered significant. Administration of hypertonic saline solution was associated with decreased mean body weight by 4.5 hours, but weight change after isotonic saline administration was not significant. Other than body weight and plasma protein concentration, between-trial difference (treatment effect) was not observed for any measured variable or index. The F values indicated that increasing the number of horses would have not changed these results. A time effect was evident across both trials, so that mean (±sd) plasma volume increased (12.3 ± 1.07%) and mean plasma protein concentration (−12.1 ± 1.03%) and pcv (−11.9 + 0.67%) decreased proportionately and transiently in association with administration of either fluid at that volume. Other time effects included increased plasma osmolality and Na and Cl concentrations. Blood volume estimates and total amount of plasma protein remained unchanged. These data indicate that in conscious clinically normal horses, changes in plasma protein concentration reflect changes in plasma volume and that blood volume may be regulated by alterations in plasma volume and red cell mass. These data also indicate that changes in plasma volume and constituent concentrations may be similar in response to administration of either 0.9% (300 mosm/kg) or 7.2% (2,400 mosm/kg) NaCl solutions (5 ml/kg) and that clinically normal horses can rapidly regulate variable Na loads.

Food deprivation and refeeding in the camel (Camelus dromedarius).

Camels thrive in arid and semiarid areas, although food and water frequently are scarce. However, the mechanisms enabling camels to withstand food deprivation are poorly understood. In this study four female camels were totally deprived of food for 4 days. Their body weight decreased by 6%. Food deprivation caused no change in total plasma protein concentration in the camel, indicating that no alterations in plasma volume occurred. When the first meal was withheld water intake was unchanged. Next day the camels showed signs of hydration with a decreased plasma Na+ concentration and an increased excretion of diluted urine. In the afternoon water intake decreased. Urine K+ excretion fell the first day and urine volume and Na+ excretion from the third day. No activation of the renin-angiotensin-aldosterone system (RAAS) was observed. Plasma and urine urea concentration increased during food deprivation. Plasma glucose concentration and plasma cortisol and thyroxine levels did not change. Body temperature decreased during food deprivation. After refeeding, total plasma proteins increased temporarily by 12%, and a threefold increase in RAAS was seen, implying that both plasma volume and RAAs changed rapidly. Our results show that fluid balance was only slightly affected in the food-deprived camel. We suggest that strategies for the camel to endure food deprivation include maintenance of plasma volume and glucose concentration and a lowering of the body temperature.