Rise In Blood Volume Research Articles

Improved cardiac filling facilitates the postprandial elevation of stroke volume in Python regius.

To accommodate the pronounced metabolic response to digestion, pythons increase heart rate and elevate stroke volume, where the latter has been ascribed to a massive and fast cardiac hypertrophy. However, numerous recent studies show that heart mass rarely increases, even upon ingestion of large meals, and we therefore explored the possibility that a rise in mean circulatory filling pressure (MCFP) serves to elevate venous pressure and cardiac filling during digestion. To this end, we measured blood flows and pressures in anaesthetized Python regius The anaesthetized snakes exhibited the archetypal tachycardia as well as a rise in both venous pressure and MCFP that fully account for the approximate doubling of stroke volume. There was no rise in blood volume and the elevated MCFP must therefore stem from increased vascular tone, possibly by means of increased sympathetic tone on the veins. Furthermore, although both venous pressure and MCFP increased during volume loading, there was no evidence that postprandial hearts were endowed with an additional capacity to elevate stroke volume. In vitro measurements of force development of paced ventricular strips also failed to reveal signs of increased contractility, but the postprandial hearts had higher activities of cytochrome oxidase and pyruvate kinase, which probably serves to sustain the rise in cardiac work during digestion.

Assessment of changes in blood volume in response to resuscitative fluid administration in dogs

AbstractObjective: To determine the continuous changes in blood volume in response to fluid administration using an in‐line hematocrit monitor.Design: Prospective study.Setting: Research laboratory.Animals: Four healthy dogs.Interventions: Each dog received intravenous boluses of 80 mL/kg of 0.9% saline (S), 4 mL/kg of 7.5% saline (HS), 20 mL/kg of dextran 70 (D), 20 mL/kg of hetastarch (HES), or no fluids (control, C) on separate occasions. Fluids were administered at 150 mL/min in the S, D, and HES groups, and at 1 mL/kg/min in the HS group.Measurements and main results: Blood volume changes were measured every 20 seconds for 240 minutes using an in‐line hematocrit monitor. There was a rapid rise in blood volume during all infusions. Immediately after the administration of crystalloid fluids, the rapid rise in blood volume ceased. Subsequently, there was a steep decline in blood volume for 10 minutes, and a slower decline thereafter. In contrast, the rise in blood volume continued for at least 10 minutes after the infusion of the colloids was complete, and a plateau was observed for the remainder of the experiment. The blood volume effect, as measured by area under the curve, was significantly greater in the saline group than the other groups during the infusion time and for the 0–240 minutes time period. The areas under the curve for the two colloid solutions were not significantly different from each other during any time periods. The percent increase in blood volume immediately following the infusions was 76.4±10.0 in the S group, 17.1±3.2 in the HS group, 23.0±10.5 in the D group, and 27.2±6.4 in the HES group. At 30 minutes from the start of the infusion, the mean percent increases in blood volumes were 35.2±9.3 in the S group, 12.3±0.9 in the HS group, 35.9±7.3 in the D group, and 36.8±6.5 in the HES group. At 240 h post‐infusion, the mean percent increases in blood volume were 18.0±9.7 in the S group, 2.9±6.1 in the HS group, 25.6±16.1 in the D group, and 26.6±8.6 in the HES group. The C group had a mean percent change in blood volume of −3.7±3.4 at the end of the experiment.Conclusions: This study indicates that the rapid administration of saline at clinically relevant doses leads to the largest immediate increase in blood volume, although this change is transient because of rapid redistribution of the fluid. Despite a brief increase in blood volume that was almost 3 times the volume administered, hypertonic saline led to the smallest increase in blood volume post‐infusion. The synthetic colloid solutions increased the blood volume by an amount greater than that infused and the effect was sustained for a longer period of time than seen following crystalloid administration, but the maximum increase in blood volume was significantly less than saline. The measurement of continuous changes in blood volume, using an in‐line hematocrit monitor, was a useful means of assessing the dynamic effects of fluid administration in dogs in a research setting.

ROLE OF ALLOPURINOL IN REDUCING CEREBRAL HVPOXIC-ISCHEMIC INJURY DURING REOXYGENATION-REPERFUSION

Oxidation of hypoxanthine (HX) by xanthine oxidase (XO) has been hypothesized to be a potential source of oxygen-derived free radicles (O2−) during reoxygenation-perfusion of hypoxic-ischemic organs. Allopurinol (Al), a XO inhibitor, can reduce reperfusion injury. During hypoxia-ischemia, components of the mitochondrial electron-transport chain become reduced. With reoxygenation-reperfusion O2− are generated. A Near Infrared Spectroscope (Niroscope) was used to continuously monitor changes in cytochrome aa3 (Cytaa3), blood volume (BV), saturated Hb (HbO) and desaturated (HB-) in 24 rats. The rats were divided into 2 groups (Gp). Gp1 (12). Wt=286±38 g (m±SD) received Al (dose 200 mg/kg IP) and was subjected to 1/2 hr period of 9.7%O2 followed by 100%O2 GP2 (12). Wt=282±4lg (m±SD) was subjected to the same 2 periods of FiO2 but without prior Al Results: Gp1 With administration of 9.7% O2, Cytaa3 became more reduced, by as much as 100% of total labile signal (TLS), with concomitant fall in BV and HbO and rise in Hb. With administration of 100% O2, Cytaa3 became more oxidized with concomitant rise in BV and HbO and fall in Hb. Gp2. During the hypoxic period (9.7%O2) the changes in Cytaa3, BV, HbO and Hb- were similar to those obtained in Gp1. However on reoxygenation with 100% O2 the Cytaa3 remained reduced despite increases in BV and HbO and fall in Hb-. To evaluate the role of HX and XO in these changes, an additional 6 rats on 100% O2 were infused with I. HX (dose calculated 10 provide a plasma concentration 30 μM/dl). 2.HX with Arabinose (dose 2-4 ml of 1.6 M Sol.) 3. HX + XO (I unit) Infusion of HX, and XO, with or without arabinose, did not result in any change in cytaa3 Our results suggest that allopurinol protect the mitochondrial electron-transport chain from O2− during reoxygenation-reperfusion following cerebral hypoxic-ischemic injury probably by scavenging O2− rather than by inhibition of xanthine oxidase.

Hemodynamic Response to Volume Stress in Awake Late-Pregnant and Nonpregnant Rats

The present study was designed to determine whether the often observed gestational rise in blood volume alters the hemodynamic response to volume stress relative to the nonpregnant state. Late-pregnant and nonpregnant Wistar rats, prepared with an electromagnetic flow probe around the ascending aorta and/or intravascular catheters were used for this study. One of the following sets of measurements were performed either before and after volume loading or before and after volume depletion (24 h thirst): 1) continuous monitoring of cardiac output, blood pressure, heart rate, and fluid balance (only during volume loading); 2) measurement of cardiac output and regional blood flows (microspheres); and 3) measurement of the inferior vena cava diameter (x-ray). Both rapid (bolus) and slow volume loading (infusion) led to a rise in cardiac output. The generated surplus in cardiac output was distributed to the kidneys, skeletal tissues, and intestines (only in nonpregnant rats), and was paralleled in the pregnant rats by a consistent fall in placental blood flow. Slow volume depletion had neither a consistent effect on cardiac output nor on its distribution, with even a preserved maturational rise in placental blood flow during the 24 h of thirst. Slow volume loading and depletion led to an increase and decrease of the caliber of the inferior vena cava, respectively. The nonnuterine hemodynamic response to all forms of volume stress had not changed in pregnancy.(ABSTRACT TRUNCATED AT 250 WORDS)

Increase in the plasma levels of the N-terminal and C-terminal portions of the prohormone of atrial natriuretic factor during normal pregnancy

The influence of pregnancy on the circulating concentrations of atrial natriuretic factor, the 28 amino acid carboxy (C)-terminal end of the 126 amino acid atrial natriuretic factor prohormone, and the amino (N)-terminus of the prohormone was studied with three specific radioimmunoassays recognizing: (1) atrial natriuretic factor (i.e., amino acids 99 through 126), (2) the 98 amino acid N-terminus, and (3) amino acids 31 through 67 from the midportion of the N-terminus of the prohormone. Plasma atrial natriuretic factor in normal pregnant women gradually increased as pregnancy progressed, with the mean -t SEM being 58 ± 4 pg/ml in the first trimester, 74 ± 5 pg/ml in the second trimester, and 89 ± 7 pg/ml in the third trimester. Likewise, proatrial natriuretic factor 31 through 67 increased from 1421 ± 76 pg/ml (first trimester) to 1509 ± 84 pg/ml (second trimester) to 1758 ± 83 pg/ml in the third trimester, whereas the whole N-terminus of the prohormone increased from 1804 ± 98 pg/ml (first trimester) to 1909 ± 111 pg/ml (second trimester) to 2160 ± 79 pg/ml in the third trimester. These results suggest that release of the N-terminus of the prohormone, as well as atrial natriuretic factor, increases with the rise in blood volume associated with a normal pregnancy. The circulating concentrations of both the C-terminus and N-terminus of the atrial natriuretic factor prohormone increased further in the 48 hours after delivery. Because both the C-terminus and N-terminus of the atria[ natriuretic factor prohormone contain diuresis-producing peptides, these results suggest that postpartum diuresis may be mediated by these peptides.

Preservation of blood volume during edema removal in nephrotic subjects

During the gradual removal of edema with diuretics in 21 edematous patients with the nephrotic syndrome (NS) we monitored blood volume. For comparison, nine healthy subjects were studied after equilibration on diets containing 20, 200, and 1138 mEq sodium. The initial extracellular fluid volume (ECFV) in the patients exceeded the final ECFV by 63.4 +/- 8.4%. In 10 patients with a very low plasma oncotic pressure (8.2 +/- 0.4 mm Hg, Group 1), the blood volume changed little. In Group 2 (plasma oncotic pressure 13.4 +/- 1.0 mm Hg), it was 11.0 +/- 2.5% higher at entry than after edema withdrawal. In the normal volunteers, the highest sodium intake raised the ECFV by 21.4 +/- 4.1%. The accompanying rise in blood volume, 11.2 +/- 3.0%, was larger than in the patients of Group 1 (2.4 +/- 1.9%, P less than 0.04), but not of Group 2 (8.1 +/- 1.9%, NS) at similar degrees of expansion. There was no difference in blood volume between the edema-free patients and the normal subjects at low-sodium diet. The course of blood pressure and creatinine clearance during edema removal gave no evidence that functional hypovolemia was induced, but the plasma renin activity was higher than in the normal subjects at similar degrees of expansion. We conclude that the blood volume to ECFV relationship curve is flattened in the presence of hypoalbuminemia. Thus, the increase in blood volume that normally follows ECFV expansion is less in patients with the NS, but a drop below normal upon removal of edema is absent also.

Hydrostatic Pulmonary Edema in the Cat. Effects on Pulmonary Blood and Water Volumes and on Lung Compliance

The effect on lung compliance of changes in intra- and extravascular volumes has been studied. Such changes were induced by inflation and deflation of a balloon placed in the left atrium in open-chest cats. Blood constituents were labeled with isotopes, and tissue water content was found from the wet/dry labeled with isotopes, and tissue water content was found from the wet/dry weight ratio. When left atrial pressure (PLA) was elevated to a value not exceeding 32 mmHg (4.256 kPa), there was only a minute increase in tissue water volume, and we observed a reversible reduction in lung compliance related to the rise in lung blood volume. At higher PLA, a rapid rise occurred in extravascular fluid volume, with evidence of alveolar flooding. Earlier experiemtns have shown that, in isolated perfused lung, a situation of slow, steady increase in interstitial fluid can be created. This does not seem to be the case with lungs in situ: once the lymphatic drainage is unable to cope with transvascular fluid flow, an unstable situation is created. This rapidly leads to alveolar flooding and a fall in compliance in addition to that caused by a rise in blood volume. From our fluid and pressure determinations, we calculated a filtration coefficient (Kf) of 0.45 ml/100 g wet lung X cmH2O X h. This is within the range reported for sheep lungs. Observation of dynamic lung compliance cannot be used for detection of interstitial fluid accumulation. It appears, however, that in contrast to isolated lungs, this phase of edema-formation rapidly leads to alveolar flooding.

THE EFFECT OF INSULIN ON THE GLUCOSE-CHLORIDE RELATIONSHIP AND ANHYDREMIA IN THE BLOOD OF RABBITS

A study of the literature regarding the effect of insulin on blood volume or water content reveals the fact that a considerable controversy exists at present as to whether insulin does or does not influence the water content of the blood, producing a condition of anhydremia. For the acceptance of anhydremia as a distinct insulin effect we have the experimental evidence of Nitzescu and Mangiuca (l), Levine and Kolars (2), Drabkin and Edwards (3), Villa (4). The work of Mazzocco and Morera (5) and that of Olmstead and Taylor (6) indicates that anhydremia is not a specific insulin effect. On the other hand, the evidence presented by Widal, Abrami, Weill, and Laudat (7), and that of Haldane, Kay, and Smith (8) supports the view that a rise in blood volume (hydremia) may be the direct effect of insulin injections. Regardless of the particular direction of this water shift, the explanation offered is based on the assumption that the hypoglycemia induced by the insulin is directly responsible for disturbances in the osmotic pressure equilibrium of the body which involve this water shifting. Herrick (9), studying the simultaneous determinations of blood reducing substance and whole blood chlorides in patients undergoing the glucose tolerance test, discovered an inverse relationship between glucose and chlorides in the blood. When the glucose concentration of the blood rose, the blood chlorides fell in such proportion as to indicate a possible direct reciprocal relationship. Herrick suggests that this shifting of the chlorides is necessary in order to preserve optimal osmotic conditions in