Body volume changes during simulated microgravity: Auditory changes,segmental fluid redistribution,and regional hemodynamics

Space adaptation syndrome (SAS), manifested by cephalad fluid shifts, spacial disorientation, nausea, and vomiting, is of varied expression and uncertain etiology. One theory is that fluid shift to the upper body alters the function of the vestibular apparatus to create an entity similar to Meniere's disease. Since clinical vestibular dysfunction syndromes are mirored by altered cochlear function, this experiment was undertaken to study the relation between fluid redistribution and the auditory effects of initial antiorthostatic bed rest. Manual and bone audiometry, impedance tympanometry, and brain-stem evoked potentials were used to monitor auditory changes prior to, during, and following short term exposure to−6° head down tilt. Impedance plethysmography was performed to assess the segmental and intracranial fluid redistribution and hemodynamic changes during short-term head down tilt simulated microgravity. Even though significant cephalad fluid shift produced marked intracranial congestion and the subjects exhibited SAS symptoms, no clinically significant changes in the auditory system could be detected.     

Colloid osmotic pressure of the subcapsular interstitial fluid of rat kidneys during hydropenia and volume expansion

Summary To determine the colloid osmotic pressure of subcapsular interstitial fluid in rat kidneys two different methods were used. Collection of subcapsular fluid with glass pipettes or implanted microcatheters and subsequent protein analysis resulted in a protein concentration of 1.8g%±0.6 and 2.0g%±0.8, respectively. Lymph protein concentration was not significantly different from that of subcapsular fluid samples. During extracellular volume expansion both subcapsular and lymph protein concentration fell to 0.42g%±0.23 and 0.7g%±0.5. Application of anin vivo oncometric method resulted in an effective oncotic pressure about twice that estimated from protein determinations. Using average values for intratubular and intracapillary oncotic and hydrostatic pressures a tubulo-interstitial net driving force of 20 mm Hg and an interstitial-capillary net driving force of 13 mm Hg is estimated in hydropenic animals. During volume expansion net transtubular pressure gradient is reduced to about 60–70% of control while the transcapillary gradient is virtually unchanged.     

Extracellular fluid volume and composition changes during sodium pentobarbitone anaesthesia in the dog

Serial measurements of extracellular fluid (ECF), and plasma volumes were evaluated in dogs before and during general anaesthesia with sodium pentobarbitone and under controlled conditions of arterial pH, pO2, pCO2, and blood pressure. Sodium pentobarbitone anaesthesia caused an early, significant rise in ECF volume with a fall in haematocrit, plasma protein, and plasma potassium concentrations. Plasma osmolality and sodium concentrations were unchanged. The lack of change in ECF sodium concentration suggests that the total ECF sodium content increased in parallel with the expansion of this compartment. Sodium bound to macromolecules in the interstitial space or to bone is suggested as a possible source of sodium ions. It is unlikely that intracellular sodium stores contribute to a significant extent in these changes. During prolonged anaesthesia plasma volume progressively increased while total ECF volume returned towards control values. This work clarifies previous observations and suggests that major fluid movements occur during sodium pentobarbitone anaesthesia primarily associated with altered cell membrane properties and generalised haemodynamic changes.     

Measurement of lung density by photon transmission for monitoring intravascular and extravascular fluid volume changes in the lungs.

Left ventricular (LV) heart failure increases pulmonary blood volume (PBV) and interstitial fluid volume. Continuous measurements of lung density may be a simple non-invasive method for monitoring of the LV function as the lung density should reflect the changes in the PBV and extravascular lung water. The purpose of the study was to optimize transmission measurements of the lung with a gamma camera and a planar source. Another aim was to assess the possibility of transmission monitoring in normal subjects at rest and during exercise and to compare the results with simultaneous measurements of PBV changes. Transmission measurements were made in a water-filled phantom containing lungs of different density. A gamma camera and a planar 57Co source were used. The coefficient of variation in density determination owing to counting statistics in a lung area was calculated for different energy windows, acquisition times and collimation. Dynamic measurements in normal subjects were carried out in a sitting and a supine position at rest and during exercise. Pulmonary blood volume was monitored simultaneously using 99mTc-labelled red blood cells and the registered blood pool activity was corrected for attenuation. Highest precision in relative density determination was obtained with large energy window and uncollimated source. A precision of 1.0% was obtained with 1 min measuring time. About 10% change in transmission corresponding to a 15% change in density was observed during exercise. Changes in blood pool and lung density covariated. We conclude that lung density changes can be monitored with a high degree of statistical precision in a few minutes and with a low radiation dose of radiation using a gamma camera and a planar source.     

The relationship between interstitial fluid pressure and volume in rat trachea

A change of interstitial fluid volume (IFV) will normally change the interstitial fluid pressure (P_if) so as to counteract further fluid movement across the capillaries and changes in IFV. Contrary to this, several acute inflammatory reactions in the trachea are associated with increased negativity of P_if, which will interstitial fluid balance in the trachea, interstitial compliance (ΔIFV/ΔP_if) was measured in pentobarbital anaesthetized rats. IFV was measured as the plasma equivalent extravascular distribution space of [⁵¹Cr]EDTA. P_if was measured in the same animal with sharpened glass pipettes (diameter 3–6 μm) connected to a servocontrolled counterpressure system. In dehydration (30 mL saline i.v., n=10) interstitial compliance was 0.083 mL g dry wt^-1 mmHg^-1. Since control IFV was 1.046 mL g dry wt^-1 (n=10) the interstitial compliance is 8% of IFV per mmHg. In overhydration (30 mL NaCl, n=10) and dextran anaphylaxis (1 mL dextran 70, n=10) compliance remained the same for the first 15% increase in IFV and then increased several-fold since P_if did not increase more than 2 mmHg above control level. The increased negativity of P_if by -10 mmHg associated with acute inflammation will require a reduction of IFV by 80% when interstitial compliance is 8% per mmHg. A more likely explanation is therefore that structural rearrangements are responsible for the events leading to increased negativity of P_if in acute inflammation.     

Dependence of polyethylene glycol-induced dipsogenesis on intravascular fluid volume depletion.

Rats injected with polyethylene glycol did not show changes in serum osmolality, Na⁺, K⁺, Cl^? or extracellular fluid volume when measured 20, 120 or 240 min post injection. Progressive reduction in plasma volume was observed when estimated indirectly from hematocrit or plasma protein values or measured directly with Evans Blue dye. When such hypovolemia was prevented by continuous intravenous infusion, PG-induced drinking was abolished. These results were interpreted as support for the dependence of PG-induced dipsogenesis on intravascular hypovolemia.     

Continuous monitoring of plasma,interstitial, and intracellular fluid volumes in dialyzed patients by bioimpedance and hematocrit measurements

Bioimpedance spectroscopy (BIS) permits evaluation of extra- and intracellular fluid volumes in patients. We wished to examine whether this technique, used in combination with hematocrit measurement, can reliably monitor fluid transfers during dialysis. Ankle to wrist BIS measurements were collected during 21 dialysis runs while hematocrit was continuously monitored in the blood line by an optical device. Extracellular (ECW) and intracellular (ICW) water volumes were calculated using Hanai's electrical model of suspensions. Plasma volume variations were calculated from hematocrit, and changes in interstitial volume were calculated as the difference between ECW and plasma volume changes. Because accuracy of ICW was too low, changes in ICW were calculated as the difference between ultrafiltered volume and ECW changes. Total body water (TBW) volumes calculated pre- and postdialysis were, respectively, 3.25+/-3.2 and 1.95+/-2.5 liters lower on average than TBW given by Watson et al.'s correlation. Average decreases in fluid compartments expressed as percentage of ultrafiltered volume were as follows: plasma, 18%; interstitial, 28%, and ICW, 54%. When the ultrafiltered volume was increased in a patient in successive runs, the relative contributions of ICW and interstitial fluid were augmented so as to reduce the relative drop in plasma volume.     

Central,peripheral, and other blood volume changes during hemodialysis

Volume overload is a factor in development of hypertension in hemodialysis patients. Fluid removal by hemodialysis (HD), however, may cause intradialytic hypotension and associated symptoms. A better understanding of the relationships between blood pressure volume status and the pathophysiology of fluid removal during HD are, therefore, necessary to control blood pressure and to eliminate intradialytic hypotension. The objectives of the study were to determine the amount and direction of change of body fluid compartments after ultrafiltration (UF) and to determine whether any correlations exist between mean arterial pressure (MAP), change in circulating blood volume (deltaBV), total body water (TBW), central blood volume (which constitutes the volume of blood in the lungs, heart, and great vessels [CBV]), and intracellular and extracellular fluid volumes (ICF, ECF). The study population included 20 patients on regular HD. Each individual had their CBV, cardiac output, and peripheral vascular resistance (PVR) measured by means of saline dilution technique and deltaBV monitored by an online hematocrit sensor (Crit Line). MAP was calculated from measured blood pressure and ICF and ECF were measured using bioelectric impedance analysis techniques. Measurements were obtained before and after maximum UF measured by deltaBV (reduction of 6-10% by Crit Line). Ten healthy controls also had ECF and ICF values measured by bioelectric impedance analysis. Before HD, MAP correlated with TBW (r = 0.473, p = 0.035) and CBV (r = 0.419, p = 0.066), suggesting that hypertension here may be due to volume overload. Patients were ECF expanded before HD with an ECF:ICF ratio of 0.96, which was significantly higher than the control ratio of 0.74 (p < 0.0001). During UF, fluid was removed from both ECF and ICF, but more from the ECF volume ratio 0.92 post UF, a significant reduction (p < 0.0001). After UF, MAP no longer correlated with TBW or CBV but correlated with peripheral vascular resistance (r = 0.4575, p = 0.043). After UF, deltaBV correlated inversely with PVR (r = -0.50, p = 0.024). Despite the fall in deltaBV (7.11+/-2.49%) with UF, CBV was maintained. CBV were 0.899 L and 0.967 L pre and post UF, respectively. These data suggest that in hemodialysis patients, predialysis volume status influences predialysis blood pressure. UF causes BV to fall, but CBV is preferentially conserved by increasing PVR, which also maintains blood pressure. Failure of a PVR response likely leads to intradialytic hypotension.     

Influence of splanchnic intravascular volume changes on cardiac output during muscarinic receptor stimulation in the anaesthetized dog

The direct influence of systemic muscarinic receptor stimulation on total splanchnic intravascular volume and the splanchnic organs responsible for the total splanchnic volume change associated with muscarinic receptor stimulation in the animal with an intact circulation are unknown. Furthermore, the subsequent effect of these volume changes on cardiac output is not known. Thus, acetylcholine was infused at 5 micrograms kg-1 min-1 in 25 anaesthetized dogs in which nicotinic blockade of the ganglia was achieved with mecamylamine, while total and regional splanchnic intravascular volume changes were determined with a radionuclide imaging technique. Total splanchnic volume decreased by 4.9 +/- 1.0% (P less than 0.0001), splenic volume decreased by 10.3 +/- 2.0% (P less than 0.0001), hepatic volume increased by 5.8 +/- 1.4% (P less than 0.01), extrahepatosplenic volume increased by 6.6 +/- 1.6% (P less than 0.01) and cardiac output increased from 1960 +/- 190 to 2290 +/- 230 ml min-1 (P less than 0.001). After splenectomy (n = 13), the hepatic and extrahepatosplenic volume increments were abolished, and the increase in cardiac output was not attenuated (1600 +/- 260 to 2040 +/- 370 ml min-1). After subsequent evisceration (n = 5), the cardiac output increment associated with acetylcholine was still not attenuated. Acetylcholine-associated splanchnic volume changes were abolished after muscarinic receptor blockade with atropine. Thus, muscarinic receptor stimulation causes a decrease in total splanchnic volume due entirely to a decrease in splenic volume. The splanchnic volume changes do not influence cardiac output.     

Cardiovascular,hormonal and body fluid changes during prolonged exercise

Summary During prolonged heavy exercise a gradual upward drift in heart rate (HR) is seen after the first 10 min of exercise. This secondary rise might be caused by a reduction in stroke volume due to reduced filling of the heart, which is dependent upon both hemodynamic pressure and blood volume. Swimming and bicycling differ with respect to hydrostatic pressure and to water loss, due to sweating. Five subjects were studied during 90 min of bicycle exercise, and swimming the leg kick of free style. The horizontal position during swimming resulted in a larger cardiac output and stroke volume. After the initial rise in heart rate the secondary rise followed parallel courses in the two situations. The rises were positively related to the measured increments in plasma catecholamine concentrations, which continued to increase as exercise progresssed. The secondary rise in HR could not be explained by changes in plasma volume or in water balance, nor by changes in plasma [K]. The plasma volume decreased 5–6% (225–250 ml) within the first 5 to 10 min of exercise both in bicycling and swimming, but thereafter remained virtually unchanged. The sweat loss during bicycling was four times greater than during swimming; but during swimming the hydrostatic conditions induced a diuresis, so that the total water loss was only 25% less than during bicycling.     

Reversibility of artifacts of fluid volume measurements by bioimpedance caused by position changes during dialysis

The effect of temporary position changes, sitting up from supine, on extracellular (ECW) and intracellular (ICW) resistances and fluid volumes calculated from whole body bioimpedance using a Xitron 4200 impedancemeter was investigated on 8 patients during dialysis for a total of 11 tests. It was found that ECW resistance decreased instantaneously by an average of 2.3% when the patient sits up, due to plasma and interstitial fluid shift into the legs which decreases leg resistance, the major contributor to total resistance. This drop in resistance is incorrectly interpreted by the device as an increase in ECW volume which averages 235 ml. But this effect is completely reversible and both ECW resistance and fluid volume rapidly resume their normal course when the patient returns to his initial position. No significant variation in ICW resistance was observed in any of the patients at the position change. We conclude that segmental impedance, which has been proposed to minimize this artifact, is not advisable in dialysis monitoring and that it is simpler to ignore or switch off measurements during the position change so that later data are not affected by it.