Restoration Of Plasma Volume Research Articles

Plasma volume expansion reveals hidden metabolic acidosis in patients with diabetic ketoacidosis

BackgroundHyperchloremic metabolic acidosis that develops during the treatment of diabetic ketoacidosis is usually attributed to the chloride content of resuscitation fluids. We explored an alternative explanation, namely that fluid-induced plasma volume expansion alters the absolute differences in the concentrations of sodium and chloride (the Na–Cl gap) enough to affect the acid–base balance. We analyzed data from a prospective single-center cohort study of 14 patients treated for diabetic ketoacidosis. All patients received 1 L of 0.9% saline over 30 min on two consecutive days. Blood gases were sampled before and after the infusions.ResultsThe initial plasma volume was estimated to be 25 ± 13% (mean ± SD) below normal on admission to the intensive care unit. At that time, most patients had an increased actual Na–Cl gap, which counteracts acidosis. However, the correction of the plasma volume deficit revealed that these patients would have had a decreased Na–Cl gap upon admission if they had been normovolemic at that time; the estimated “virtual Na–Cl gap” of 29 ± 5 mmol/L was significantly lower than the uncorrected value, which was 39 ± 5 mmol/L (P < 0.001). On Day 2, most patients had a decreased actual Na–Cl gap (33 ± 5 mmol/L), approaching the corrected value on Day 1.ConclusionsThe hyperchloremic acidosis commonly seen in diabetic ketoacidosis may not be primarily caused by the chloride content of resuscitation fluids but, rather, by the restoration of plasma volume, which reveals the hidden metabolic acidosis caused by a decreased Na–Cl gap.Trial registration Clinical Trials Identifier NCT02172092, registered June 24, 2014, https://www.clinicaltrials.gov/NCT02172092

Hot water immersion; potential to improve intermittent running performance and perception of in-game running ability in semi-professional Australian Rules Footballers?

This study investigated whether hot water immersion (HWI) could heat acclimate athletes and improve intermittent running performance and perception of in-game running ability, during a competitive Australian Rules Football (ARF) season. Fifteen male semi-professional ARF athletes (Mean (SD); age: 22 (3) years, height: 182.3 (6.5) cm, mass: 80.5 (5.1) kg) completed either HWI (HEAT, N = 8, 13 (2) sessions, 322 (69) min exposure, 39.5 (0.3) °C) or acted as a control (CON, N = 7, no water immersion) over 6-weeks. Athletes completed a 30–15 Intermittent Fitness Test pre and post-intervention to assess intermittent running performance (VIFT), with perception of in-game running ability measured. Heat acclimation was determined via change in resting plasma volume, as well as physiological and perceptual responses during HWI. HEAT elicited large PV expansion (mean ± 90% CI: d = 1.03 ± 0.73), large decreases in heart rate (d = -0.89 ± 0.70), thermal sensation (d = -2.30 ± 1.15) and tympanic temperature (d = -1.18 ± 0.77). Large improvements in VIFT were seen in HEAT (d = 1.67 ± 0.93), with HEAT showing a greater improvement in VIFT when compared to CON (d = 0.81 ± 0.88). HEAT also showed greater belief that in-game running ability improved post-intervention (d = 2.15 ± 1.09) compared to CON. A 6-week HWI intervention can elicit heat acclimation, improve perception of in-game running ability, and potentially improve VIFT in semi-professional ARF athletes.

Expert consensus on the use of human serum albumin in critically ill patients.

Expert consensus on the use of human serum albumin in critically ill patients.

The Effect of Medium-Term Sauna-Based Heat Acclimation (MPHA) on Thermophysiological and Plasma Volume Responses to Exercise Performed under Temperate Conditions in Elite Cross-Country Skiers.

The influence of a series of ten sauna baths (MPHA) on thermophysiological and selected hematological responses in 14 elite cross-country skiers to a submaximal endurance exercise test performed under thermoneutral environmental conditions was studied. Thermal and physiological variables were measured before and after the exercise test, whereas selected hematological indices were studied before, immediately after, and during recovery after a run, before (T1) and after sauna baths (T2). MPHA did not influence the baseline internal, body, and skin temperatures. There was a decrease in the resting heart rate (HR: p = 0.001) and physiological strain (PSI: p = 0.052) after MPHA and a significant effect of MPHA on systolic blood pressure (p = 0.03), hematological indices, and an exercise effect but no combined effect of treatments and exercise on the tested variables. A positive correlation was reported between PSI and total protein (%ΔTP) in T2 and a negative between plasma volume (%ΔPV) and mean red cellular volume (%ΔMCV) in T1 and T2 in response to exercise and a positive one during recovery. This may suggest that MPHA has a weak influence on body temperatures but causes a moderate decrease in PSI and modifications of plasma volume restoration in response to exercise under temperate conditions in elite athletes.

Effects of Ramadan intermittent fasting on inflammatory and biochemical biomarkers in males with obesity

BackgroundTo determine the effects of Ramadan intermittent fasting (RIF) on inflammatory (C-reactive protein (CRP), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α)) and biochemical markers of liver-renal function (aspartate aminotransferase (AST), alanine amino transferase (ALT), bilirubin, lactate dehydrogenase (LDH), urea and creatinine) in males with obesity. Materials and methodsTwenty-eight males with obesity were randomly allocated to an experimental group (EG, n = 14) or a control group (CG, n = 14). The EG group completed their fasting rituals for the entire month of Ramadan (30 days) whereas the CG group continued with their normal daily habits. Blood samples were collected 24 h before the start of Ramadan (T0), on the 15th day of Ramadan (T1), the day after the end of Ramadan (T2), and 21 days after the end of Ramadan (T3). Resting plasma volume variation between pre and post-RIF (ΔPV) was calculated. ResultsDecreases were noted for interleukin-6 (p = 0.02, d = 1.4) and tumor necrosis factor-alpha (p = 0.01, d = 0.7), with no changes for C-reactive protein (p = 0.3; d = 0.1) in the EG compared to CG group. There were no changes (P > 0.05) in ΔPV recorded after RIF for either EG (-0.035 ± 0.02%) and CG (0.055 ± 0.06%). ConclusionThis study demonstrates that RIF improves systemic inflammation biomarkers in males with obesity. Moreover, RIF did not negatively affect biomarkers of liver and renal function.

Heat Training Improves Cardiovascular Responses And Briefly Blunts Sprint Performance In Elite Sprint Track Cyclists

PURPOSE: To investigate the effects of short-term heat training on sprint performance and cardiovascular function in elite sprint track cyclists. METHODS: Five elite male sprint cyclists (23.8 ± 2.0 years; peak power output = 22.8 ± 1.3 W·kg-1) completed 5 d of training for ~60 min in hot conditions (30-35oC, 40-60% relative humidity (RH)) consisting of sprint-interval training and resistance training. Sprint performance was assessed using an inertial load ergometer in temperate conditions (~20oC, 50% RH) on day 1 and 5 of heat training, and 72 h post. Cardiovascular responses were assessed (~20oC, 50% RH) pre and 24 h post heat training and included a submaximal cycling test and resting plasma volume measurement. During the first (heat training day 1 = HT1) and last (HT5) resistance training session thermoregulatory measurements were recorded. RESULTS: There was a transient decrement in performance as observed by a small very likely decrease in sprint peak power output -4.3% (90% CL -6.1, -2.5)] and small possible decrease [-2.0 rpm (-5.1, 1.2)] at 24 h post heat training. This decrement recovered to baseline within 72 h for both sprint performance (trivial change [0.2% (-3.4, 3.9)]) and optimal cadence (trivial change [-0.8% (-3.5,2.0)]). Core temperature during HT5 was lower (-0.29-0.36oC from 10 to 40 min; small possible decrease) during exercise but there was no effect of heat training on skin temperature or sweat rate compared with baseline values. Following heat training, heart rate during submaximal exercise decreased [-10 bpm (-18, -2); large very likely] and recovery heart rate increased [11 bpm (9, 14); large most likely], compared with baseline values. There was a small likely increase in plasma volume [6.3% (2.7-10.0)] immediate post 5 d HT, compared with baseline values. CONCLUSION: Our findings indicate that markers of cardiovascular stability improved with short-term heat training, and that sprint performance was suppressed at 24 h but rebounded at 72 h post.

The Effects Of Mode Of Rehydration On Stress Hormone Respsonse To Subsequent Maximal Intensity Exercise In The Heat.

PURPOSE: Endocrine response to strenuous exercise in the heat can serve as an indicator of the amount of strain the body is experiencing. Previous intravenous (IV) versus oral rehydration studies found no difference cortisol (CORT) response between modes of rehydration, but mixed norepinephrine (NOR) response with ORAL during an exercise-heat challenge (EHC). The purpose of this study was to examine the effects of mode of rehydration on the stress-hormone response to a subsequent EHC that more closely mimics a real-life athletic situation utilizing three traditional modes of rehydration ad libitum (ADL), IV and ORAL and combined half IV and half ORAL (I+O) fluids of identical volume. METHODS: Ten healthy, non-smoking, active men (age 23.3 ± 1.1 y; height, 177.8 ± 2.8 cm; body mass, 81.4 ± 1.3 kg; body fat, 11.0 ± 1.0%; O2max, 58.8 ± 1.3 ml·kg-1·min-1) completed four trials consisting of dehydration by -4% body mass, rehydration to -2% body mass, and an EHC comprised of 25 min of running at 60% O2max, a maximal effort 0.5 mile run, five minutes of rest and five min of self-paced repetitive box lifting (RBL). Plasma catecholamines [epinephrine (EPI) and NOR] and CORT were analyzed at baseline, post-exercise dehydration, immediately before EHC (EHCPRE), immediately-post 0.5 mile run (EHC30), immediately-post RBL (EHCIP), and 15 minutes post-RBL. Data was analyzed with a two-way repeated measures ANOVA or Student’s t-test, p< 0.05. RESULTS: Catecholamine response was not significantly different between modes of rehydration, but significantly increased during EHC (EHCPRE - EPI 0.52±0.44 pmol·L-1, NOR 2.64±0.89 nmol·L-1; EHC30 - EPI 3.59±1.89 pmol·L-1, NOR 21.66±7.42 nmol·L-1; EHCIP - EPI 1.31±0.84 pmol·L-1, NOR 15.45±6.63 nmol·L-1). CORT response was significantly lower during I+O (EHCPRE: 451.8±118.5 nmol·L-1, EHCIP 505.4±237.9 nmol·L-1) compared to all other trials (EHCPRE 567.1±240.5 nmol·L-1, EHCIP - 603.6±270.1 nmol·L-1). CONCLUSIONS: These results suggest a synergistic effect of I+O on plasma CORT concentration resulting in reduced adreno-cortical response. It is possible the I+O treatment resulted in reduced hormonal response or increased removal rate due to a combination of oropharyngeal response and rapid plasma volume restoration since stress was controlled across conditions.

Hypovolemic Shock Complicating Nephrotic Syndrome in a Child

The fundamental abnormality in nephrotic syndrome is the structural and electrochemical changes that have been documented to occur in the glomerular basement membrane lead to proteinuria. It is the proteinuria itself which most likely causes hypoalbuminemia and associated complications such as infections, hypercoagulability and hypovolemia. Hypovolemia may cause postural hypotension, acute renal failure, circulatory collaps or sudden death.&#x0D; An eleven-year-old boy was referred to the Child Health Department of Dr. Kariadi Hospital Semarang with a diagnosis of corticosteroid resistant nephrotic syndrome and acute renal failure. Physical examination showed a severely ill boy with general edema, shock, hemoconcentration, hypoalbuminemia, hypercholesterolemia, massive proteinuria and disturbed renal function.&#x0D; The treatment consisted of infusion of dextrose 10% followed by human plasma and furosemide to restore plasma volume and enhance urine production. Two days later he was in better condition, normovolemia, slight edema, good diuresis, but his blood pressure increased, and ophtalmologic examination supported the diagnosis of grade I hypertensive retinopathy. Intravenous clonidine and furosemide were given and were very effective. Kidney biopsy revealed minimal lesion with slight proliferation.

Short term heat acclimation reduces heat stress, but is not augmented by dehydration

Heat acclimation lowers physiological strain when exercising in the heat, and may be enhanced by promoting dehydration during acclimation. The purpose was to compare fluid intake during heat acclimation by promoting dehydration (DEH=0.5 mL kg−1 15 min−1, ~2.4% dehydration per acclimation session) compared to euhydration (EUH=2.0 mL kg−1 15 min−1, ~1.4% dehydration per acclimation session) following four heat acclimation bouts on thermal strain, and exercise performance.Thirteen males completed 90 min heat stress tests (HST) at 50% VO2max (40 °C, 30%RH) before and after three 90 min heat acclimation trials, involving consecutive bouts with 4-fold less fluid (DEH) or EUH. DEH and EUH trials were separated by 48 h and assigned in a random crossover design separated by a 5 week washout. Wildland firefighter (WLFF) Nomex: shirt, pants, and a cotton T-shirt baselayer were worn.Peak core temperature (Tc) from the HST significantly decreased following both DEH (39.5 ± 0.1–39.0 ± 0.1 °C: P < 0.001) and EUH acclimation (39.5 ± 0.1–38.9 ± 0.1 °C: P < 0.001). HR, RPE, physiological strain index (PSI), and total work (J) completed in a graded exercise test to exhaustion were improved (P < 0.001) in effect for acclimation, but not different when comparing DEH or EUH fluid delivery. SBF was unchanged (P = 0.313). Sweat rate increased greater following DEH (1.52 ± 0.06–1.89 ± 0.09 L h−1) compared to EUH acclimation (1.57 ± 0.06–1.79 ± 0.08 L h−1: P = 0.015). Resting plasma volume increased in effect for acclimation (P = 0.002). Aldosterone decreased in effect for acclimation (P < 0.001) at rest and following exercise, and total protein was unaffected (P = 0.83).In conclusion, short-term heat acclimation (~360 min) attenuates heat stress, and improves exercise capacity in the heat, and was not impaired nor improved by promoting DEH during acclimation.

Effect of alterations in blood volume with bed rest on glucose tolerance.

Bed rest leads to rapid impairments in glucose tolerance. Plasma volume and thus dilution space for glucose are also reduced with bed rest, but the potential influence on glucose tolerance has not been investigated. Accordingly, the aim was to investigate whether bed rest-induced impairments in glucose tolerance are related to a concomitant reduction in plasma volume. This hypothesis was tested mechanistically by restoring plasma volume with albumin infusion after bed rest and parallel determination of glucose tolerance. Fifteen healthy volunteers (age 24 ± 3 yr, body mass index 23 ± 2 kg/m2, maximal oxygen uptake 44 ± 8 ml·min-1·kg-1; means ± SD) completed 4 days of strict bed rest. Glucose tolerance [oral glucose tolerance test (OGTT)] and plasma and blood volumes (carbon monoxide rebreathing) were assessed before and after 3 days of bed rest. On the fourth day of bed rest, plasma volume was restored by means of an albumin infusion prior to an OGTT. Plasma volume was reduced by 9.9 ± 3.0% on bed rest day 3 and area under the curve for OGTT was augmented by 55 ± 67%. However, no association (R2 = 0.09, P = 0.33) between these simultaneously occurring responses was found. While normalization of plasma volume by matched albumin administration (408 ± 104 ml) transiently decreased (P < 0.05) resting plasma glucose concentration (5.0 ± 0.4 to 4.8 ± 0.3 mmol/l), this did not restore glucose tolerance. Bed rest-induced alterations in dilution space may influence resting glucose values but do not affect area under the curve for OGTT.

Preliminary Characterization of Enterade® Rehydration Kinetics Following Intra- and Extracellular Dehydration

Two distinct types of dehydration occur when body water loss is accompanied by small or large solute losses. Small solute losses result in shared water losses between the intra- (ICF) and extracellular (ECF) fluid spaces (intracellular dehydration, ID) while large solute losses primarily reduce volume of the ECF (extracellular dehydration, ED). The distinction between the two has therapeutic implications for rehydration. Enterade® is a commercial beverage blend of amino acids and electrolytes designed to improve gut function and enhance body water restoration. PURPOSE: To compare the rehydration kinetics of Enterade® following two types of dehydration. METHODS: Nine healthy, non-heat acclimatized volunteers participated in this study [mean ± SD; 20 ± 2 yr, 73.3 ± 11.9 kg, 1.8 ± 0.1 m, total body water (TBW), 39.5 ± 7.2 L]. A euhydration baseline was established over three days using standardized fluid intakes (≥3 L/d). On day four volunteers were acutely dehydrated using 80 mg furosemide (ED; n = 6) or exercise-heat stress (ID; n = 3). Volunteers were then rehydrated by replacing 100% of TBW losses with Enterade® over 90 minutes. Blood, urine, and sweat were sampled throughout. Rehydration kinetics were assessed over 4 hours, including plasma volume (PV) restoration, compartmental fluid shifts (Cl- method) and drink volume retention. RESULTS: ID (- 3.8 ± 0.1% body mass) produced a hyper-osmotic (8 ± 1 mmol/kg) hypovolemia (-11 ± 3% PV). Losses in TBW (-2.9 ± 0.7 L) and solute (-535 ± 117 mmol) were shared between the ICF (33%) and ECF (67%). ED (-3.0 ± 0.2% body mass) produced an iso-osmotic (0 ± 2 mmol/kg) hypovolemia (-11 ± 4% PV). TBW (-2.2 ± 0.2 L) and solute losses (-719 ± 98 mmol) came primarily from the ECF (90%). PV was restored to baseline by 30 min in ID and by 60 min in ED, but after 4 hours ID was 5% above baseline while ED was 3.5% below. Enterade® retention was 73 ± 7% in ID and 63 ± 13% in ED. The ICF and ECF were restored by 47% and 88% in ID, while in ED restoration was 113% and 59% for ICF and ECF, respectively. CONCLUSION: Enterade® rehydrated volunteers to within 1% of euhydrated TBW baseline after 4 hours in both ID and ED. However, PV was restored more rapidly and recovery of the ECF volume was more complete in ID. Opinions herein are the private views of the authors; citations of commercial products are not an endorsement by the DOA.

Thirst responses following high intensity intermittent exercise when access to ad libitum water intake was permitted, not permitted or delayed

An increase in subjective feelings of thirst and ad libitum drinking caused by an increase in serum osmolality have been observed following high intensity intermittent exercise (HIIE) compared to continuous exercise. The increase in serum osmolality is closely linked to the rise in blood lactate and serum sodium concentrations. However, during an ensuing recovery period after HIIE when serum osmolality will decrease, the resultant effect on sensations of thirst and subsequent water intake is unclear. Therefore the aim of the study was to assess the sensations of thirst and subsequent effect on ad libitum water consumption when water intake was immediately allowed, delayed or prevented following a period of HIIE. MethodsTwelve males (26±4years, 80.1±9.3kg, 1.81±0.05m, V̇O2peak 60.1±8.9ml·kg−1·min−1) participated in three randomised trials undertaken 7–14days apart. Participants rested for 30min then completed a 60min HIIE exercise period (20×1min at 100% V̇O2peak with 2min rest) followed by 60min of recovery, during which ad libitum water intake was provided immediately (W), delayed until the final 30min (W30) or not permitted (NW). Body mass was measured at the start and end of the trial. Blood lactate and serum sodium concentrations serum osmolality and sensation of thirst were measured at baseline, immediately post-exercise and during the recovery. ResultsBody mass loss was different between all trials (W: 0.25±0.45, W30: 0.49±0.37, NW: 1.29±0.37%; p<0.05). Sensations of thirst peaked post-exercise and decreased in W and W30 following water ingestion (p<0.05). Total voluntary water intake was greater in W trial (0.846±0.417 vs. 0.630±0.277l; p<0.05) but was similar during the first 30min period of allowed drinking (0.618±0.297 vs. 0.630±0.277l; p>0.05). Serum osmolality (299±6 vs. 298±5 vs. 298±3mOsmol·kg−1), blood lactate (7.1±1.1 vs. 7.2±1.1 vs. 7.1±1.2mmol·l−1) and serum sodium concentrations (142±2 vs. 145±2 vs. 145±2 mmol·l−1) peaked post-exercise (W vs. W30 vs. NW; p<0.05) but were not different between trials (p>0.05). ConclusionsSensations of thirst were increased following HIIE and remained until satiated by water intake. This was despite the likely primary stimulus, serum osmolality, decreasing during the recovery period following a post-exercise peak. A combined effect of reduction in blood lactate and serum sodium concentrations, restoration of plasma volume and water intake contributed to the similar decrease in serum osmolality observed throughout the trials.

Compartmental changes in the body-fluid contributions to the plasma volume restoration during recovery from dehydration following heat acclimation

Since water moves freely among fluid compartments, it was of interest to track whole-body fluid movements during a resting recovery from extended exercise in the heat, but without rehydration. This mechanism was investigated before, during and following an extended heat-acclimation experiment.

Swimming in warm water is ineffective in heat acclimation and is non-ergogenic for swimmers.

Heat acclimation (HA) in air confers adaptations that improve exercise capabilities in hot and possibly temperate air. Swimmers may benefit from HA, yet immersion may constrain adaptation. Therefore, we examined whether warm-water swimming constitutes effective HA. In a randomized-crossover study, eight male swimmers swam 60 min/day on 7 days in 33 °C (HA) or 28 °C (CON) water. They performed 20-min distance trials before and after each regime: in 33 °C water (Warm); 28 °C water (Temperate); and cycling in 29 °C air (Terrestrial) following standardized exercise. Rectal temperature (Tre ) rose ∼ 1 °C in HA sessions, and sweat loss averaged 1.4 L/h. After accounting for CON, HA did not confer any clear expansion of plasma volume [1.9% (95% CI: 7.7)], reduction in heart rate during standardized cycling exercise [1 b/min (9)], reduction in Tre during rest [+0.1 °C (0.1)] or exercise, or change in sudomotor function. Only perceived temperature and discomfort tended to improve. Performance was clearly not improved for Warm [+0.3% (1.8)] or Temperate [+0.3% (1.9)], was unclear for Terrestrial [+0.4% (17.7)], and was unrelated to changes in resting plasma volume (r < 0.3). In conclusion, short-term HA using swimming in 33 °C water confers little adaptation and is not ergogenic for warm or temperate conditions.

Hydration and endocrine responses to intravenous fluid and oral glycerol.

Athletes use intravenous (IV) saline in an attempt to maximize rehydration. The diuresis from IV rehydration may be circumvented through the concomitant use of oral glycerol. We examined the effects of rehydrating with differing regimes of oral and IV fluid, with or without oral glycerol, on hydration, urine, and endocrine indices. Nine endurance-trained men were dehydrated by 4% bodyweight, then rehydrated with 150% of the fluid lost via four protocols: (a) oral = oral fluid only; (b) oral glycerol = oral fluid with added glycerol (1.5 g/kg); (c) IV = 50% IV fluid, 50% oral fluid; and (d) IV with oral glycerol = 50% IV fluid, 50% oral fluid with added glycerol (1.5 g/kg), using a randomized, crossover design. They then completed a cycling performance test. Plasma volume restoration was highest in IV with oral glycerol > IV > oral glycerol > oral. Urine volume was reduced in both IV trials compared with oral. IV and IV with oral glycerol resulted in lower aldosterone levels during rehydration and performance, and lower cortisol levels during rehydration. IV with oral glycerol resulted in the greatest fluid retention. In summary, the IV conditions resulted in greater fluid retention compared with oral and lower levels of fluid regulatory and stress hormones compared with both oral conditions.

A decrease in aquaporin 2 excretion is associated with bed rest induced high calciuria

BackgroundExposure to microgravity or immobilization results in alterations of renal function, fluid redistribution and bone loss, which couples to a rise of urinary calcium excretion. We recently demonstrated that high calcium delivery to the collecting duct reduces local Aquaporin-2 (AQP2) mediated water reabsorption under vasopressin action, thus limiting the maximal urinary concentration and reducing calcium saturation. To investigate renal water balance adaptation during bed rest, a model to mimic the effects of microgravity on earth, the effect of changes in urinary calcium on urinary AQP2 excretion were assessed.MethodsTen healthy men (aged 21-28 years) participated in the experiment. Study design included 7 days of adaptation and 35 days of continuous bed rest (days -6 to 0 and 1 to 35, respectively) under controlled diet. Food records and 24-hour urine samples were collected daily from day -3 to 35. Changes in blood hematocrit were used as an indirect index of plasma volume changes. AQP2 excretion was measured by ELISA.ResultsBed rest induced bone demineralization and a transient increase in urinary calcium followed by transient decrease in AQP2 excretion, which can reduce the urine concentrating ability causing plasma volume reduction. The return of calciuria to baseline was followed by a recovery of AQP2 excretion, which allows for a partial restoration of plasma volume.ConclusionsThese results further support the view that urinary calcium can modulate the vasopressin-dependent urine concentration through a down-regulation of AQP2 expression/trafficking. This mechanism could have a key role in the prevention of urine super-saturation due to hypercalciuria.

Whole-body fluid distribution in humans during dehydration and recovery, before and after humid-heat acclimation induced using controlled hyperthermia

This experiment was designed to test the hypothesis that the plasma volume is not selectively defended during exercise- and heat-induced dehydration following humid-heat acclimation. Eight physically active males were heat acclimated (39.8 °C, relative humidity 59.2%) using 17 days of controlled hyperthermia (core temperature: 38.5 °C). Inter-compartmental fluid losses and movements were tracked (radioisotopes and Evans blue dye) during progressive dehydration (cycling) in these same conditions and also during a resting recovery without fluid replacement (28 °C), before (day 1), during (day 8) and after heat acclimation (day 22). On days 8 and 22, there were significant increases in total body water, interstitial fluid and plasma volume (P < 0.05), but the intracellular compartments did not change (P > 0.05). The baseline plasma volume remained expanded throughout: 43.4 [±2.6 (day 1)], 49.1 [±2.4 (day 8); P < 0.05] and 48.9 mL kg(-1) [±3.0 (day 22); P < 0.05]. During progressive dehydration, plasma reductions of 9.0% (±0.9: day 1), 12.4% (±1.6: day 8) and 13.6% (±1.2: day 22) were observed, with day 8 and 22 losses significantly exceeding day 1 (P < 0.05). During recovery, plasma volume restoration commenced, with the intracellular fluid contribution becoming more pronounced as acclimation progressed. It is concluded that the plasma volume was not defended more vigorously following humid-heat acclimation. Indeed, a greater fluid loss may well underlie the mechanisms for enhancing plasma volume recovery when heat acclimation is induced using the controlled-hyperthermia technique.

Ad libitum fluid intake and plasma responses after pickle juice, hypertonic saline, or deionized water ingestion.

Adding sodium (Na(+)) to drinks improves rehydration and ad libitum fluid consumption. Clinicians (∼25%) use pickle juice (PJ) to treat cramping. Scientists warn against PJ ingestion, fearing it will cause rapid plasma volume restoration and thereby decrease thirst and delay rehydration. Advice about drinking PJ has been developed but never tested. To determine if drinking small volumes of PJ, hypertonic saline (HS), or deionized water (DIW) affects ad libitum DIW ingestion, plasma variables, or perceptual indicators. Crossover study. Laboratory. Fifteen, euhydrated (urine specific gravity ≤ 1.01) men (age = 22 ± 2 years, height = 178 ± 6 cm, mass = 82.9 ± 8.4 kg). Participants completed 3 testing days (≥ 72 hours between days). After a 30-minute rest, a blood sample was collected. Participants completed 60 minutes of hard exercise (temperature = 36 ± 2°C, relative humidity = 16 ± 1%). Postexercise, they rested for 30 minutes; had a blood sample collected; rated thirst, fullness, and nausea; and ingested 83 ± 8 mL of PJ, HS, or DIW. They rated drink palatability (100-mm visual analog scale) and were allowed to drink DIW ad libitum for 60 minutes. Blood samples and thirst, fullness, and nausea ratings (100-mm visual analog scales) were collected at 15, 30, 45, and 60 minutes posttreatment drink ingestion. Ad libitum DIW volume, percentage change in plasma volume, plasma osmolality (OSMp,) plasma sodium concentration ([Na(+)]p), and thirst, fullness, nausea, and palatability ratings. Participants consumed more DIW ad libitum after HS (708.03 ± 371.03 mL) than after DIW (532.99 ± 337.14 mL, P < .05). Ad libitum DIW ingested after PJ (700.35 ± 366.15 mL) was similar to that after HS and DIW (P > .05). Plasma sodium concentration, OSMp, percentage change in plasma volume, thirst, fullness, and nausea did not differ among treatment drinks over time (P > .05). Deionized water (73 ± 14 mm) was more palatable than HS (17 ± 13 mm) or PJ (26 ± 16 mm, P < .05). The rationale behind advice about drinking PJ is questionable. Participants drank more, not less, after PJ ingestion, and plasma variables and perceptual indicators were similar after PJ and DIW ingestion. Pickle juice did not inhibit short-term rehydration.

Nitric oxide synthase inhibition reduces albumin induced lung damage in acute pancreatitis

Background/objectivesColloid resuscitation in acute pancreatitis (AP) is a matter of controversy due to the possible deleterious effect on lung function. A previous study demonstrates that albumin administration increases lung damage in burns and this effect can be reversed by inducible nitric oxide synthase (iNOS) inhibition. This study evaluates the effects of S-methylisothiourea (SMT), a specific iNOS inhibitor, on lungs and pancreas of rats with AP receiving intravenous albumin. MethodsAP was induced in Wistar rats by intraductal 5% taurocholate injection. To evaluate the effect of albumin on lung damage, animals received IV saline or human albumin immediately after AP (Groups: Saline and Albumin). To evaluate the effect of iNOS inhibition on lung damage, SMT was given immediately after AP (Group Saline+SMT, and Group Albumin+SMT). At 12 h after AP induction, serum amylase activity, lung vascular permeability and myeloperoxidase (MPO) activity were evaluated. Lung and pancreas histological analysis were performed. ResultsSerum amylase activity, pancreatic edema, lung vascular permeability, MPO activity, and inflammatory infiltration were significantly increased after AP. Albumin administration increased lung vascular permeability, inflammatory infiltration, and pancreatic edema compared to saline administration (p < 0.05). Albumin administration with SMT reduced lung vascular permeability, MPO activity, and inflammatory infiltration compared to albumin administration alone (p < 0.05). ConclusionLung and pancreatic damage induced by albumin administration for restoration of plasma volume in AP are reduced by iNOS inhibition. Awareness of this fact may be useful in high-risk patients who need to receive albumin for volume replacement.

Rapid plasma volume restoration increased skin sympathetic nerve activity component synchronized with cardiac cycle and cutaneous vasodilation in hypovolemic and passively warmed men

We have suggested in passively warmed men that skin sympathetic nerve activity (SSNA) involved a component synchronized with cardiac cycle, the component increased as esophageal temperature (Tes) increased, but the increase was suppressed by hypovolemia with reduced cutaneous vasodilation. However, it remained unknown if rapid plasma volume (PV) restoration increased/recovered the component and cutaneous vasodilation. Fourteen young men with ~13% hypovolemia with a diuretic, were divided into 2 groups; time control (n=7, TC) and rapid infusion (n=7, RI). Subjects were warmed for 80min by infusing 47‐°C water into a perfused suit, while Tes, SSNA (microneurography; the peroneal nerve), skin blood flow (SkBF; laser‐Doppler flowmetry; the dorsal foot), and mean arterial pressure (MAP) were measured. After 50‐min warming, the component and cutaneous vascular conductance (CVC=SkBF/MAP) increased (all P&lt;0.0001) as Tes rose by ~0.5°C. Then, when 37‐°C saline was infused at 0.7ml/min/kg for 30min in RI so that PV was restored to the baseline, the component and CVC rose by 17% and 10%, respectively, compared with before infusion in RI (all P&lt;0.03) and the increases were higher than those in TC where saline was infused at 0.1ml/min/kg (all P&lt;0.01). Thus, rapid PV restoration in hypovolemic hyperthermia recovered the component and cutaneous vasodilation.