Distribution of blood flow during exercise after blood volume expansion in swine

1990 ◽  
Vol 69 (5) ◽  
pp. 1578-1586 ◽  
Author(s):  
K. I. Norton ◽  
M. D. Delp ◽  
M. T. Jones ◽  
C. Duan ◽  
D. R. Dengel ◽  
...  
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Blood Volume ◽  
Volume Expansion ◽  
O2 Uptake ◽  
Miniature Swine ◽  
Blood Flows ◽  
Blood Volume Expansion

To study the distribution of blood flow after blood volume expansion, seven miniature swine ran at high speed (17.6-20 km/h, estimated to require 115% of maximal O2 uptake) on a motor-driven treadmill on two occasions: once during normovolemia and once after an acute 15% blood volume expansion (homologous whole blood). O2 uptake, cardiac output, heart rate, mean arterial pressure, and distribution of blood flow (with radiolabeled microspheres) were measured at the same time during each of the exercise bouts. Maximal heart rate was identical between conditions (mean 266); mean arterial pressure was elevated during the hypovolemic exercise (149 +/- 5 vs. 137 +/- 6 mmHg). Although cardiac output was higher and arterial O2 saturation was maintained during the hypervolemic condition (10.5 +/- 0.7 vs. 9.3 +/- 0.6 l/min), O2 uptake was not different (1.74 +/- 0.08 vs. 1.74 +/- 0.09 l/min). Mean blood flows to cardiac (+12.9%), locomotory (+9.8%), and respiratory (+7.5%) muscles were all elevated during hypervolemic exercise, while visceral and brain blood flows were unchanged. Calculated resistances to flow in skeletal and cardiac muscle were not different between conditions. Under the experimental conditions of this study, O2 uptake in the miniature swine was limited at the level of the muscles during hypervolemic exercise. The results also indicate that neither intrinsic contractile properties of the heart nor coronary blood flow limits myocardial performance during normovolemic exercise, because both the pumping capacity of the heart and the coronary blood flow were elevated in the hypervolemic condition.

Maternal responses to long-term hypoxemia in sheep

1989 ◽  
Vol 256 (6) ◽  
pp. R1340-R1347 ◽  
Author(s):  
T. Kitanaka ◽  
R. D. Gilbert ◽  
L. D. Longo
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Blood Volume ◽  
Cardiovascular Responses ◽  
Uterine Blood Flow ◽  
O2 Uptake ◽  
Arterial Po2

To determine the maternal cardiovascular responses to long-term hypoxemia, we studied three groups of animals: 1) pregnant ewes (n = 20) at 110-115 days gestation subjected to hypoxia for up to 28 days; 2) pregnant ewes (n = 4) that served as normoxic controls; and 3) nonpregnant ewes (n = 6) subjected to hypoxemia for up to 28 days. We measured mean arterial pressure, heart rate, uterine blood flow, and uterine vascular resistance continuously for 1 h/day while the ewe was exposed to an inspired O2 fraction of 12-13% for at least 17 days. Arterial PO2, O2 saturation, hemoglobin, arteriovenous O2 difference, and uterine O2 uptake were measured daily while blood volume and erythropoietin concentration were measured weekly. In the pregnant hypoxic group arterial PO2 decreased from a control value of 101.5 +/- 5.1 to 59.2 +/- 5.1 Torr within a few minutes, where it remained throughout the study. The hemoglobin concentration increased from 8.9 +/- 0.5 to 10.0 +/- 0.5 g/dl within 24 h where it remained, whereas erythropoietin concentration increased from 16.6 +/- 2.1 to 39.1 +/- 7.8 mU/ml at 24 h but then returned to near-control levels. Arterial glucose concentration, mean arterial pressure, and cardiac output decreased slightly but insignificantly. In contrast, body weight, heart rate, blood volume, uterine blood flow, uterine O2 flow, uteroplacental O2 uptake, and the concentrations of catecholamines and cortisol remained relatively constant. Thus both pregnant and nonpregnant sheep experience relatively minor cardiovascular and hematologic responses in response to long-term hypoxemia of moderate severity.

scholarly journals Hemodilution mediates hemodynamic changes during acute expansion in unanesthetized rats

2000 ◽  
Vol 279 (6) ◽  
pp. R2243-R2251 ◽  
Author(s):  
Rosana Y. Inoue ◽  
José A. R. Gontijo ◽  
Kleber G. Franchini
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Volume Expansion ◽  
Renal Hemodynamics ◽  
Relative Importance ◽  
Hemodynamic Changes ◽  
Isovolemic Hemodilution ◽  
Blood Volume Expansion ◽  
Renal Vascular

Studies were carried out to determine the relative importance of volume and hemodilution on hemodynamic adjustments to acute volume expansion. Systemic and renal hemodynamics were monitored in unanesthetized and unrestrained rats during progressive and equivalent blood volume expansion with saline (Sal; 1, 2, and 4% body wt), 7% BSA solution (0.35, 0.7, and 1.4% body wt), and reconstituted whole blood from donor rats (WBL; 0.35, 0.7, and 1.4% body wt). Mean arterial pressure remained unchanged in Sal and BSA but increased progressively in WBL-expanded rats (from 92 to 106 mmHg after maximal expansion). In Sal and BSA-expanded rats, cardiac output (CO) and renal blood flow (RBF) increased (CO: Sal from 19 to 20, 22, and 25; BSA from 21 to 23, 27, and 31; RBF: Sal from 1.6 to 1.8, 2.2, and 2.5; BSA from 2 to 2.4, 2.7, and 3.1 ml · min−1 · 100 g body wt−1), whereas total peripheral (TPR) and renal vascular (RVR) resistance decreased in parallel with the expansions. After expansion with WBL, CO increased progressively but less extensively than in cell-free expanded rats (21 to 22, 24, and 26 ml · min−1 · 100 g body wt−1), whereas TPR and RVR remained unchanged. Systemic hematocrit (Hct) decreased approximately the same after expansion with Sal or BSA solutions but remained unchanged after expansion with WBL. Isovolemic hemodilution to Hct levels comparable to those seen after maximal expansion with cell-free solutions also reduced SVR and RVR, although less extensively. These findings suggest that in unanesthetized rats hemodilution plays a major role in the systemic and renal hemodynamics during expansion.

Effects of haemorrhage and volume expansion on portal–systemic collateral vascular resistance in conscious portal hypertensive rats

1990 ◽  
Vol 78 (2) ◽  
pp. 193-197 ◽  
Author(s):  
Abraham Koshy ◽  
Tatsuya Sekiyama ◽  
Jean-Michel Cereda ◽  
Antoine Hadengue ◽  
Catherine Girod ◽  
...  
Keyword(s):  
Blood Flow ◽  
Body Weight ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Blood Volume ◽  
Vascular Resistance ◽  
Volume Expansion ◽  
Portal Pressure ◽  
Blood Flows ◽  
Regional Blood Flows

1. In order to study the acute effects of blood volume changes on the vascular resistance of portal-systemic collaterals (collateral vascular resistance), a model of total portal vein occlusion with 100% portal-systemic shunts was developed in the rat. In this model, we determined the haemodynamic effects of haemorrhage (1.8 ml/100 g body weight) or intravenous infusion of a volume expander (1.8 ml/100 g body weight). Cardiac output and regional blood flows were measured by the radioactive microsphere method. 2. Haemorrhage significantly reduced arterial pressure from 108 ± 4 to 92 ± 4 mmHg (mean ± sem), cardiac output from 56 ± 4 to 24 ± 2 ml min−1 100 g−1 body weight, portal pressure from 15.1 ± 1.5 to 10.0 ± 1.4 mmHg and portal tributary blood flow from 19.9 ± 2.3 to 8.3 ± 1.4 ml/min. Consequently, collateral vascular resistance significantly increased from 6.6 ± 0.9 × 103 to 11.1 ± 2.0 × 103 kPal−1 s. 3. Volume expansion reduced arterial pressure from 98 ± 3 to 90 ± 3 mmHg, and significantly increased cardiac output from 43 ± 3 to 55 ± 3 ml min−1 100 g−1 body weight, portal pressure from 13.9 ± 0.7 to 16.5 ± 0.8 mmHg and portal tributary blood flow from 16.4 ± 1.3 to 28.2 ± 3.2 ml/min. Consequently, collateral vascular resistance significantly decreased from 7.0 ± 0. 5 × 103 to 4.9 ± 0.4 × 103 kPa l−1 s. 4. This study shows that in rats with portal hypertension, portal-systemic collateral vascular resistance is modified by alterations in blood volume.

Effects of central venous blood volume shifts on arterial baroreflex control of heart rate

1981 ◽  
Vol 241 (4) ◽  
pp. H571-H575 ◽  
Author(s):  
G. E. Billman ◽  
D. T. Dickey ◽  
K. K. Teoh ◽  
H. L. Stone
Keyword(s):  
Heart Rate ◽  
Blood Volume ◽  
Volume Expansion ◽  
Body Position ◽  
Venous Blood ◽  
Receptor Blockade ◽  
Baroreflex Control ◽  
Beta Receptor ◽  
Blood Volume Expansion ◽  
Beta Receptor Blockade

The purpose of this study was to investigate the effects of anesthesia, body position, and blood volume expansion on baroreflex control of heart rate. Five male rhesus monkeys (7.0-10.5 kg) were given bolus injection of 4.0 micrograms/kg phenylephrine during each of the following situations: awake sitting, anesthetized (AN) (10 mg/kg ketamine-HCl) sitting, AN recumbent, AN 90 degrees head down tilt, and AN 50% blood volume expansion with normal saline. beta-Receptor blockade was also performed on each treatment after anesthesia. Four additional animals were similarly treated after 20% blood volume expansion. R-R interval was plotted against systolic aortic pressure, and the slope was determined by linear regression. Baroreflex slope was significantly (P less than 0.05) reduced by 90 degrees head down tilt and 50% volume expansion both before and after beta-receptor blockade. A similar trend was seen after 20% volume expansion. These data are consistent with the thesis that baroreflex control of heart rate is reduced by central blood volume shifts.

Circulation of sympathectomized dogs under pentobarbital anesthesia

1965 ◽  
Vol 208 (4) ◽  
pp. 790-794
Author(s):  
Shu Chien ◽  
Shunichi Usami
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Blood Volume ◽  
Total Blood Volume ◽  
Central Blood Volume ◽  
Total Blood ◽  
Pentobarbital Anesthesia ◽  
Blood Flows ◽  
The Mean ◽  
Mean Circulation

In sympathectomized-splenectomized dogs under pentobarbital anesthesia, the total blood volume averaged 78 ml/kg, with 20% in the splanchnic circulation and 28% in the central blood volume. These values are almost the same as those found in the splenectomized (control) dogs with the sympathetic system intact. The over-all and the splanchnic Fcells factors are also not significantly different between these two groups. The sympathectomized animals had lower arterial pressure, cardiac output, and splanchnic blood flow, but the resistances calculated for the total and the splanchnic circulations were not significantly different from those of the control dogs. The mean circulation times for the total, the central, and the splanchnic circulations were all longer in the sympathectomized dogs. The data indicate that, under pentobarbital anesthesia, sympathectomized dogs are characterized by slower blood flows without any significant changes in either the blood volume or vascular resistance.

scholarly journals Changes in regional blood volume and blood flow during static handgrip

2007 ◽  
Vol 292 (1) ◽  
pp. H215-H223 ◽  
Author(s):  
Julian M. Stewart ◽  
Leslie D. Montgomery ◽  
June L. Glover ◽  
Marvin S. Medow
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Blood Volume ◽  
Cardiac Contractility ◽  
Peripheral Resistance ◽  
Low Frequencies ◽  
Exercise Pressor Reflex ◽  
Heart Rate Regulation ◽  
Pressor Reflex

Increased blood pressure (BP) and heart rate during exercise characterizes the exercise pressor reflex. When evoked by static handgrip, mechanoreceptors and metaboreceptors produce regional changes in blood volume and blood flow, which are incompletely characterized in humans. We studied 16 healthy subjects aged 20–27 yr using segmental impedance plethysmography validated against dye dilution and venous occlusion plethysmography to noninvasively measure changes in regional blood volumes and blood flows. Static handgrip while in supine position was performed for 2 min without postexercise ischemia. Measurements of heart rate and BP variability and coherence analyses were used to examine baroreflex-mediated autonomic effects. During handgrip exercise, systolic BP increased from 120 ± 10 to 148 ± 14 mmHg, whereas heart rate increased from 60 ± 8 to 82 ± 12 beats/min. Heart rate variability decreased, whereas BP variability increased, and transfer function amplitude was reduced from 18 ± 2 to 8 ± 2 ms/mmHg at low frequencies of ∼0.1 Hz. This was associated with marked reduction of coherence between BP and heart rate (from 0.76 ± 0.10 to 0.26 ± 0.05) indicative of uncoupling of heart rate regulation by the baroreflex. Cardiac output increased by ∼18% with a 4.5% increase in central blood volume and an 8.5% increase in total peripheral resistance, suggesting increased cardiac preload and contractility. Splanchnic blood volume decreased reciprocally with smaller decreases in pelvic and leg volumes, increased splanchnic, pelvic and calf peripheral resistance, and evidence for splanchnic venoconstriction. We conclude that the exercise pressor reflex is associated with reduced baroreflex cardiovagal regulation and driven by increased cardiac output related to enhanced preload, cardiac contractility, and splanchnic blood mobilization.

Loss of cerebral regulation during cardiac output variations in focal cerebral ischemia

1992 ◽  
Vol 77 (2) ◽  
pp. 253-259 ◽  
Author(s):  
Bruce I. Tranmer ◽  
Ted S. Keller ◽  
Glenn W. Kindt ◽  
David Archer
Keyword(s):  
Cardiac Output ◽  
Cerebral Ischemia ◽  
Blood Volume ◽  
Volume Expansion ◽  
Focal Cerebral Ischemia ◽  
Brain Regions ◽  
Ischemic Brain ◽  
Content Type ◽  
Blood Volume Expansion ◽  
Fine Print

✓ Focal cerebral ischemia was induced in anesthetized macaque monkeys by unilateral middle cerebral artery occlusion. The effect of blood volume expansion by a colloid agent and subsequent exsanguination to baseline cardiac output (CO) on local cerebral blood flow (CBF) was measured by the hydrogen clearance technique in both ischemic and nonischemic brain regions. Cardiac output was increased to maximum levels (159% ± 92%, mean ± standard error of the mean) by blood volume expansion with the colloid agent hetastarch, and was then reduced a similar amount (166% ± 82%) by exsanguination during the ischemic period. Local CBF in ischemic brain regions varied directly with CO, with a correlation coefficient of 0.89 (% change CBF/% change CO), while CBF in nonischemic brain was not affected by upward or downward manipulations of CO. The difference in these responses between ischemic and nonischemic brain was highly significant (p < 0.001). The results of this study show a profound loss of regulatory control in ischemic brain in response to alterations in CO, thereby suggesting that blood volume variations may cause significant changes in the intensity of ischemia. It is proposed that CO monitoring and manipulation may be vital for optimum care of patients with acute cerebral ischemia.

Systemic and uterine responses to chronic infusion of estradiol-17 beta

1993 ◽  
Vol 265 (5) ◽  
pp. E690-E698 ◽  
Author(s):  
R. R. Magness ◽  
C. R. Parker ◽  
C. R. Rosenfeld
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Stroke Volume ◽  
Ang Ii ◽  
Uterine Blood Flow ◽  
Pressor Responses ◽  
Chronic Infusion

Human and ovine pregnancies are associated with increases in plasma levels of estrogens and angiotensin II (ANG II), cardiac output (CO), blood volume (BV), and uterine blood flow (UBF), as well as attenuated ANG II pressor responses. We hypothesized that, in nonpregnant animals, prolonged estradiol-17 beta (E2 beta) treatment would reproduce these endocrine and hemodynamic alterations. Nonpregnant ovariectomized ewes (n = 5) received 5 microgram E2 beta/kg iv followed by 220 micrograms/day for 14 days. Plasma E2 beta increased from 36 +/- 6 to 269 +/- 79 (SE) pg/ml (P < 0.05) during E2 beta treatment, returning to control values 4 days posttreatment. By 3 days of E2 beta, mean arterial pressure (MAP) and systemic vascular resistance (SVR) fell 9 +/- 1 and 29 +/- 1%, whereas heart rate (HR) and CO increased 20 +/- 5 and 26 +/- 1% (P < 0.05). Stroke volume (SV), BV, and plasma volume were unchanged until 7 days of E2 beta, with values rising 17 +/- 5, 13 +/- 3, and 14 +/- 4, respectively (P < 0.05). Although MAP remained similarly depressed (-11 +/- 1%) during week 2 of E2 beta, SVR decreased further (-37 +/- 3%) and was associated with additional increases (P < 0.05) in CO to 44 +/- 5%, reflecting rises in SV (21 +/- 2%) but not HR. Increases in BV correlated with rises in CO (r = 0.55) and SV (r = 0.64) but not HR (r = -0.04).(ABSTRACT TRUNCATED AT 250 WORDS)

Blood-Volume Expansion in the Rat: Natriuresis Accompanied by a Fall in Filtration Fraction

1981 ◽  
Vol 60 (3) ◽  
pp. 283-293
Author(s):  
D. Querido ◽  
L. C. Isaacson
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Blood Volume ◽  
Whole Blood ◽  
Volume Expansion ◽  
Fractional Excretion ◽  
Filtration Fraction ◽  
Natriuretic Hormone ◽  
Blood Volume Expansion ◽  
Measured Volume

1. We have attempted to confirm the existence of a natriuretic hormone released in response to acute expansion of blood volume. 2. Isolated kidneys, perfused with whole blood at constant pressure, were incorporated within an extracorporeal circulation in recipient rats. In six control experiments urine flow rate, renal blood flow, glomerular filtration rate, filtration fraction, and the fractional excretion of filtered sodium and water were measured for periods of up to 120–140 min thereafter. The same variables were measured in a further 12 experiments in which, after 63 ± 11 min, the rats were volume expanded with equilibrated whole blood (15, 18 or 28 ml/kg body wt.). 3. On average the controls revealed no change in any of the variables measured; volume expansion was followed by increased renal blood flow and fractional excretion of filtered sodium and water, while the filtration fraction fell. 4. In both the control and volume-expansion experiments, there were 12 instances in which the fractional excretion of filtered sodium increased; in 10 of these, including those experiments in which the natriuresis was most marked, there was a closely correlated fall in filtration fraction. 5. In all the experiments changes in the fractional excretion of filtered sodium and water varied in parallel. 6. We conclude that volume expansion (a) changes the concentration of some circulating vasoactive substance(s) and (b) results in natriuresis and diuresis consequent upon a fall in filtration fraction.

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