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Effect of meal feeding on plasma volume and urinary electrolyte clearance in ponies.

The effect of meal size and frequency on plasma volume, plasma aldosterone concentration and urinary Na and K clearances was determined in ponies. A daily maintenance ration of hay-grain pellets was provided either as a multiple feeding regimen, ie, 12 equal portions fed at 2-hour intervals, or as single large feedings, ie, half the ration fed every 12 hours at 0800 and 2000 hours. Only the effect of the single morning feeding was studied, using the latter regimen. Serial measurements of plasma volume were made by use of an indicator-dilution technique and indocyanine green (0.15 mg/kg of body weight, IV) that allowed repeated determinations at 2-hour intervals. Ingestion of the single large meal caused a 15% decrease in plasma volume by the end of a 1-hour feeding period. Feeding hypovolemia was confirmed by a coincident increase in plasma protein concentration (12%) and, in separate experiments, by analysis of postfeeding changes in the elimination of Evans blue dye. Plasma aldosterone concentration was significantly (P less than 0.05) increased from 2 to 5 hours after feeding. Urinary Na clearance decreased in response to feeding and remained lower than the prefeeding value until 9 hours after feeding. Urinary K clearance increased from prefeeding and reached a peak value between 5 and 7 hours after feeding. Creatinine clearance was unaffected. In contrast, the aforementioned variables were unchanged during the multiple regimen. Results indicate that ingestion of a large concentrate meal by ponies causes periprandial hypovolemia, activation of the renin-angiotensin-aldosterone system, and a subsequent antinatriuresis-kaliuresis that lasts for several hours.

Aldosterone↗

Effect of catecholamines and insulin on plasma volume and intravascular mass of albumin in man.

1. The effect of intravenous catecholamine infusions and of intravenous insulin on plasma volume and intravascular mass of albumin was investigated in healthy males. 2. Physiological doses of adrenaline (0.5 microgram/min and 3 microgram/min) increased peripheral venous packed cell volume significantly; intravenous noradrenaline at 0.5 microgram/min had no effect on packed cell volume, whereas packed cell volume increased significantly at 3 micrograms of noradrenaline/min. No significant change in packed cell volume was found during saline infusion. 3. During adrenaline infusion at 6 micrograms/min, packed cell volume increased, plasma volume decreased and intravascular mass of albumin decreased significantly. During noradrenaline infusion at 6 micrograms/min, packed cell volume increased and plasma volume decreased, but intravascular mass of albumin did not change. 4. Application of a hyperinsulinaemic, euglycaemic glucose clamp led to an increase in transcapillary escape rate of albumin and a decrease in intravascular mass of albumin. Packed cell volume remained constant, while plasma volume, measured by radiolabelled albumin, decreased. 5. We conclude that the previously reported changes in packed cell volume, plasma volume, intravascular mass of albumin and transcapillary escape rate of albumin during hypoglycaemia may be explained by the combined actions of adrenaline and insulin.

Adult↗

Long-term exposure to intermittent hypoxia results in increased hemoglobin mass, reduced plasma volume, and elevated erythropoietin plasma levels in man.

While it is well established that highlanders have optimized their oxygen transport system, little is known about the acclimatization of those who move between different altitudes. The purpose of this study was to establish whether the acclimatization to long-term intermittent hypoxic exposure in members of the Chilean Army who frequently move from sea level to 3,550 m altitude is correlated with acute acclimatization or chronic adaptation to hypoxia. A group of officers was exposed intermittently to hypoxia for about 22 years (OI, officers at intermittent hypoxia) and a group of soldiers for 6 months (SI, soldiers at intermittent hypoxia). Both groups were compared to residents at altitude (RA) and to soldiers at sea level (SL). When compared to SL, we observed an 11% increase in total hemoglobin mass (tHb) as well as a corresponding increase in red cell volume (RCV), hemoglobin concentration and hematocrit in all three groups at altitude. Plasma volume (PV) and blood volume (BV) decreased at altitude but increased when OI and SI returned to sea level. Moreover, intermittent hypoxic exposure of OI and SI resulted in increased plasma erythropoietin (Epo) levels, which peaked on day 2 at high altitude followed by decreasing levels during the successive days, and reaching pre-altitude values in SI even when staying at altitude. In conclusion, with regard to tHb and RCV, the acclimatization to long-term intermittent hypoxia resembles the adaptation to chronic hypoxia, while PV and BV regulation mimicked acclimatization to acute hypoxia. Remarkably, finely controlled regulation of Epo expression still occurs after up to 22 years of weekly exposure to altitude.

Adaptation, Physiological↗

Hormonal and renal response to plasma volume expansion in the primate Macaca mulatta.

The purpose of this study was to investigate the hormonal and renal response to plasma volume expansion in the ketamine-anesthetized rhesus monkey. The blood volume was determined in nine animals and found to be 6% of the body weight. Six monkeys received isoncotic isotonic fluid amounting to 25% of the blood volume. Plasma volume expansion led to significant decrease in the plasma concentrations of antidiuretic hormone (46.7%) and aldosterone (78.4%) as well as plasma renin activity (50.0%). The mean arterial pressure, plasma osmolality, and plasma concentrations of Na+ and K+ were unaffected by plasma volume expansion. However, renal plasma flow, glomerular filtration rate, the excretion of Na+ and K+, and urine flow increased. It was concluded that, in the ketamine-anesthetized rhesus monkey, circulating hormones contribute to blood volume homeostasis presumably through a neural mechanism similar to that observed in dogs and humans.

Aldosterone↗

The effects of body position and exercise on plasma volume dynamics.

We examined the plasma volume changes associated with a protocol of either exercise or controlled rest under identical positional and ambient conditions. Nine healthy adult males rode (E) and on another occasion sat quietly (C) on a cycle ergometer for 30 min. Ten minutes of cycle exercise immediately followed the resting C protocol. Ambient temperature was 30 degrees C (rh = 35%) and exercise load was equal to 50% of peak VO2. Venous blood samples were obtained with subjects both in the supine and seated positions prior to all experiments. Additional blood was drawn during minutes 1, 5, 10, and 30 in both experimental conditions. A final sample was taken during C after the 10 min exercise. Moving from the supine to a seated position resulted in an average loss of 162 ml of plasma across all experiments. During the E condition a further reduction in plasma volume (76 ml) occurred by one minute of exercise. Plasma volume stabilized by 5 min of exercise under the E protocol. During the C condition, subsequent fluid loss (98 ml) was not apparent until 10 min after the first seated sample and totalled 176 ml at the end of 30 min of rest. Ten minutes of cycling at the end of the C experiment resulted in a further plasma volume reduction of 137 ml. Plasma protein and albumin contents decreased by 5 min of exercise in E and by 30 min of rest in C. [Na+] and [Cl-] did not change in either condition but a rapid increase in [K+] during exercise indicated an addition of potassium to the vascular volume.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Proximal tubule reabsorption after hyperoncotic albumin infusion. Role of parathyroid hormone and dissociation from plasma volume.

Preferential expansion of the plasma volume by infusion of salt-poor hyperoncotic albumin solution decreases sodium reabsorption by the proximal tubule. The present micropuncture studies test the thesis that albumin infusion depresses proximal reabsorption by an effect unrelated to expansion of the plasma volume, perhaps due to an effect of parathyroid hormone (PTH) on proximal sodium reabsorption. Infusion of salt-poor hyperoncotic albumin significantly decreased plasma ionized calcium, increased immunoreactive PTH (iPTH) in plasma, decreased sodium reabsorption by the proximal tubule, and increased phosphate clearance. In contrast, infusions of albumin, in which the ionized calcium was restored to normal plasma levels, had no significant effect on ionized calcium, iPTH, proximal reabsorption, or phosphate clearance in intact dogs. Similarly, in parathyroidectomized animals given a constant replacement infusion of PTH, albumin infusion had no significant effect on proximal reabsorption or phosphate clearance. Plasma volume was markedly expanded following albumin infusion in all groups of dogs. These findings (a) indicate that PTH plays a significant role in the decrease in sodium reabsorption by the renal proximal tubule after salt-poor hyperoncotic albumin infusion, and (b) dissociate preferential expansion of the plasma volume from decreases in sodium reabsorption by the proximal tubule.

Absorption↗

Stimulation of rhesus monkey GH release: arginine vs plasma volume expansion.

Plasma GH and cortisol responses were examined in unanesthetized adult male rhesus monkeys infused with approximately 30 ml (8.3 ml/kg) of arginine monohydrochloride (Arg 0.5 g/kg), 0.9% saline (NS) or Dextran 75 and following 15 ml infusions of acid-saline (AS), or somatostatin (GHRIH 30 mug/kg). None of the infusions were accompanied by GH elevations. Rebound GH elevations occurred after each 30 ml infusion and after GHRIH but not after 15 ml AS. Although the amplitude of GH responses were not significantly different (p greater than 0.05), responses to Arg and dextran were significantly delayed as compared to responses following NS and GHRIH which did not differ from each other. Both of the latter responses occurred within 15 min of infusion completion. The delay following dextran was significantly longer than that following Arg (p less than 0.05). Since the volume of saline and the dosage of Arg were equivalent to those used in the standard intravenous Arg test, results suggest that effects of infusion volume upon GH secretion and upon GH responses to Arg warrant examination in the human. In addition, it is suggested that GH responses to NS and to dextran are mediated via an intravascular volume control mechanism and that GHRIH may be released upon activation of such a mechanism. GH elevations may represent rebound responses upon termination of GHRIH secretion.

Animals↗

Effect of afterload reduction on plasma volume during acute heart failure.

Previous investigations in our unit indicated that acute cardiogenic pulmonary edema is associated not only with an increase in left ventricular end-diastolic pressure and pulmonary arterial wedge pressure but also with a relative increase in colloid osmotic (oncotic) pressure and peripheral hemoglobin concentration. This combination of changes suggested that acute congestive heart failure with pulmonary edema, unlike chronic congestive heart failure, is associated with a contraction of intravascular blood volume. In this study, plasma volume changes were measured before and during the treatment of acute cardiogenic pulmonary edema in 14 patients with arteriosclerotic heart disease. The plasma volume measurement in all 14 patients before the initiation of treatment was either normal or decreased. After treatment with the alpha adrenergic blocking agent phentolamine, the plasma volume increased rather than decreased when measured 4 and 12 hours after the initiation of treatment. During this time colloid osmotic pressure and peripheral hemoglobin concentration progressively decreased. These findings suggest that acute cardiogenic pulmonary edema is associated with the extravasation of large quantities of plasma water from the intravascular compartment into the interstitial compartment and contraction of the intravascular plasma volume. The treatment of acute cardiogenic pulmonary edema is associated with the return of hypo-oncotic fluid from the interstitial compartment back into the intravascular compartment with expansion of plasma volume and reduction of colloid osmotic pressure and hemoglobin concentration.

Acute Disease↗

Plasma volume nomograms for use in therapeutic plasma exchange.

Nomograms have been developed for the convenient estimation of the plasma volumes of patients undergoing therapeutic plasma exchange (TPE), based on equations employing height, body weight, and hematocrit. These nomograms are offered as an aid to prescribing continuous-flow TPE procedure exchange volumes.

Humans↗

Plasma volume shifts during moderate exercise in splenectomized greyhounds.

1. Plasma volume was measured in splenectomized greyhounds, using T-1824, and sequential changes in plasma volume were measured using two independent methods, based on T-1824 plasma decay characteristics and on changes in haematocrit. 2. There were no significant differences between estimates of plasma volume made by the two methods in resting or exercising dogs. Therefore it was concluded that the characteristics of the decay of dye concentration in plasma were not affected by exercise and that sequential determinations of plasma volume from a single dye injection provide a valid determination of plasma volume during exercise in dogs. 3. During submaximal exercise, the plasma volume increased by 0-11.8% of its initial value. In no case did plasma volume decrease significantly. 4. An increase in plasma volume during excercise was also seen in animals previously made acutely hypervolemic or hypovolemic. 5. It is suggested that the increase in plasma volume constitutes part of a mechanism maintaining oxygen delivery to tissues during exercise.

Animals↗

Hypertension produced by chemical renal medullectomy or partial nephrectomy in the rat: comparison of renal function and plasma volume.

Glomerular filtration rate, plasma volume and intra-arterial blood pressure were measured in conscious rats, with hypertension induced by chemical medullectomy or partial nephrectomy and compared with those in sham treated normal rats. Both medullectomy and partial nephrectomy caused a similar rise in blood pressure. Hypertension produced by partial nephrectomy was associated with plasma volume expansion but after chemical medullectomy there was a marked hypovolaemia. These results suggest that volume expansion plays no part in chemical medullectomy hypertension but are in keeping with the hypothesis that the renal medulla releases a vasodepressor substance which plays an important role in the maintenance of normal blood pressure.

Animals↗

Role for endogenous endothelin in the regulation of plasma volume and albumin escape during endotoxin shock in conscious rats.

To explore the role of endogenous endothelin (ET) in the regulation of vascular functions, we studied the effects endothelin receptor blockade on blood pressure, plasma volume and albumin escape during endotoxin shock in conscious, chronically catheterized rats. Red blood cell volume and plasma volume were determined by using chromium-51-tagged erythrocytes and iodine-125-labelled albumin, respectively. Intravenous injection of lipopolysaccharide (LPS, 10 mg kg(-1)) resulted in hypotension, haemoconcentration, and increased total-body albumin escape, which is reflected by a 30% reduction in plasma volume. Plasma ET-1 concentrations increased 2.1 fold and 5.4 fold at 30 and 120 min post-LPS, respectively. LPS-induced losses in plasma volume and albumin escape were significantly attenuated by pretreatment of animals with the dual ET(A)/ET(B) receptor antagonist bosentan (17.4 micromol kg(-1), i.v. 15 min prior to LPS) or the ET(A) receptor antagonist FR 139317 (3.8 micromol kg(-1), i.v.) during both the immediate and delayed phases of endotoxin shock. The inhibitory actions of bosentan and FR 139317 were similar. Both antagonists augmented the hypotensive action of LPS. Administration of bosentan or FR 139317 70 min after injection of LPS also attenuated further losses in plasma volume and increases in total body and organ albumin escape rates with the exception of the lung and kidney. These results indicate a role for endogenous endothelin in mediating losses in plasma volume and albumin escape elicited by LPS predominantly through activation of ET(A) receptors, and suggest that by attenuating these events, ET(A) or dual ET(A)/ET(B) receptor blockers may be useful agents in the therapy of septic shock.

Animals↗

Effect of 5 alpha-pregnan-3 alpha-ol-20-one on nitric oxide biosynthesis and plasma volume in rats.

Plasma 5 alpha-pregnan-3 alpha-ol-20-one (pregnan) levels and nitric oxide (NO) biosynthesis increase during pregnancy. These factors have independently been implicated in the control of blood pressure and volume. We wished to determine whether pregnan might be responsible both for the increase in NO biosynthesis and for the increase in plasma volume observed during pregnancy. Virgin female Long-Evans rats were implanted with indwelling cannulas and maintained on a low nitrate/nitrite diet. After the rats recovered from surgery, 500 microg of pregnan or vehicle were given daily for 2 days. NO biosynthesis and plasma volume were measured in conscious animals before and after treatment. Pregnan caused a significant increase in NO biosynthesis (1.9 +/- 0.8 micromol/24 h, n = 10) compared with the vehicle-treated control group (0.3 +/- 0.4 micromol/24 h, n = 10, P < 0.05). Similarly, there was a significant increase in plasma volume in the pregnan-treated group (0.7 +/- 0.2 ml/100 g, n = 11) compared with the vehicle-treated control group (0.2 +/- 0.1 ml/100 g, n = 11, P < 0.05). These results confirm that pregnan can mimic pregnancy by its ability to increase both NO biosynthesis and plasma volume.

Animals↗

Plasma volume expansion is necessary for edema formation in the rate with Heymann nephritis.

Edema formation in nephrotic syndrome has been attributed to intravascular volume depletion resulting from leakage of plasma water into the interstitial space and activating secondary renal sodium retention. However, clinical studies indicate that edematous patients with nephrotic syndrome may have normal or expanded plasma volumes. We evaluated the relationship between plasma volume and edema formation in control rats and rats with chronic renal failure (CRF) produced by 7/8 nephrectomy. In each group, plasma volume and 22Na space were measured during the control period and after induction of hypoalbuminemia from passive Heymann nephritis. Rats with CRF had expanded plasma volume during the initial period (4.23 +/- 0.46 vs. 3.32 +/- 0.68 ml/100 g body wt) that became significantly more expanded (to 5.44 +/- 1.16 ml/100 g body wt) when they became nephrotic as 22Na space also increased. Plasma volume and 22Na space did not change in the sham-operated rats when nephrosis was produced. Plasma renin activity was lower in the CRF rats during the control period than in the sham-operated rats and fell significantly during the nephrotic period when edema developed. Nonnephrotic rats had a plasma colloid osmotic pressure (COP) of 17.8 +/- 4.3 mmHg compared with 8.5 +/- 2.9 mmHg when nephrotic. Despite this large difference in COP, both nephrotic and nonnephrotic rats exhibited the same relationship between plasma volume and extravascular sodium space, a measure of edema formation. Hypoproteinemia is not sufficient for edema formation in the rat with passive Heymann nephritis; concomitant plasma volume expansion resulting from CRF is a necessary additional component.

Animals↗

Hormonal and plasma volume alterations following endurance exercise. A brief review.

Plasma volume expansion usually occurs with acute endurance exercise and endurance training both in humans and in animals. In most cases, the increase in plasma volume is associated with lower haematocrit without red cell mass change or an actual reduction in red cell mass, causing relative or true anaemia, respectively. The combination of exercise and heat acclimation (which produces also hypervolaemia, but at a lesser degree than exercise) enhances hypervolaemia induced by exercise training alone. The onset of the phenomenon is extremely rapid: hypervolaemia is observed within minutes or hours of the cessation of exercise. However, 2 days are necessary to reach peak plasma volume expansion after a marathon run or longer race. The magnitude of this natural expansion ranges from 9 to 25%, corresponding to an additional 300 to 700 ml of plasma. The magnitude of this alteration depends on preceding exercise: ambient conditions, intensity and duration of exercise, body posture and frequency of the exercise bouts. The larger the reduction in plasma volume during exercise, the greater the subsequent hypervolaemia. The hydration status of the subjects before and during exercise might modify also plasma volume changes: sufficient fluid ingestion can lead to plasma volume expansion even during prolonged exercise. Fluid-regulating hormones (aldosterone, arginine vasopressin and atrial natriuretic factor) in conjunction with an elevation in plasma protein content promote hypervolaemia. However, the role and the mechanism of the increase in protein mass remain unclear and the hormonal role in the induction of chronic hypervolaemia is still an open question. Hypervolaemia can improve performance by inducing better muscle perfusion, and by increasing stroke volume and maximal cardiac output. By increasing skin blood flow, plasma volume expansion also enhances thermoregulatory responses to exercise. This leads to the important concept of optimal plasma volume and haematocrit, and performance.

Adaptation, Physiological↗

The influence of halothane, isoflurane, and pentobarbital on cerebral plasma volume in hypocapnic and normocapnic rats.

Cerebral blood volume (CBV = cerebral plasma volume [CPV] + cerebral red cell volume [CRBCV]) is one determinant of intracranial pressure. In an effort to quantitate the effects of anesthetics and PaCO2 on CBV, the authors measured cerebral plasma volume (CPV) in normocapnic (PaCO2 approximately 42 mmHg) and hypocapnic (PaCO2 approximately 22 mmHg) rats receiving 1 MAC doses of isoflurane or halothane, or given an approximately equivalent dose of pentobarbital. All animals were paralyzed, their lungs mechanically ventilated, and body temperature kept normal throughout the study. CPV was measured using 14C-labeled dextran, a large (70,000 molecular weight [M.W.]), nondiffusible compound that was given intravenously and allowed to circulate for approximately 5 min. The experiments then were terminated by freezing the brains in situ with liquid N2 poured into a funnel affixed to the exposed calvarium. Isotope concentrations in solubilized brain and in plasma were determined by scintillation counting, and CPV was calculated as the ratio between these values. CPV during both hypocapnic and normocapnic pentobarbital anesthesia was less than with either volatile agent. During normocapnia, CPV for pentobarbital = 2.1 +/- 0.26 ml/100 g (mean +/- SD, n = 8), compared with 2.96 +/- 0.44 ml/100 g (n = 9) and 3.06 +/- 0.44 ml/100 g (n = 9) for halothane and isoflurane, respectively. There were no differences in CPV between the two volatile agents during normocapnia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

[Improved the accuracy of 99mTc-MAG3 plasma clearance method: the problem of the calculated plasma volume and its modification].

The 99mTc-MAG3 plasma clearance method (MPC method), reported by Oriuchi et al., is a simple and useful count-based gamma camera method for calculating the 99mTc-MAG3 plasma clearance (CLMAG). However, a discrepancy of CLMAG calculated by MPC method (MPC-CLMAG) from the tubular extraction rate (TER) calculated by Russell's single-sample clearance determination (Russell-TER) was noted. The calculated plasma volume is assumed to be the cause. Since the plasma volume is reported to have a linear correlation with body surface area, Dissmann's formula was applied to calculate the plasma volume. Then Dissmann's formula was replaced by Ogawa's formula in the MPC method, and the procedure was then called the modified MPC method. The CLMAG were obtained using MPC method, modified MPC method and the TER was obtained Russell's method in 95 patients with urological disorders. Then the MPC-CLMAG and modified MPC-CLMAG were compared with Russell-TER. Comparison of the MPC-CLMAG with the Russell-TER demonstrated a coefficient of correlation of 0.82, but dissociation of the slope of regression lines was found between males and females. The modified MPC-CLMAG improved the coefficient of correlation to 0.92, and diminished the dissociation of the slope of regression lines between males and females. We verified that the dissociation was due to the plasma volume calculated by Ogawa's formula. Ogawa's formula included hematocrit, body weight, body height and different coefficients for gender. The plasma volume calculated by Ogawa's formula were lower in males and higher in females than that calculated by Dissmann's formula. And marked discrepancy in the plasma volume in patients with a body surface area below 0.5 m2 was observed. So the MPC method might become more accurate by substituting Dissmann's formula for Ogawa's formula resolting in a method that is applicable to both males and females, children and adults in clinical use.

Adolescent↗