scholarly journals Do alterations in pulmonary vascular tone result in changes in central blood volumes? An experimental study

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Jaap Jan Vos ◽  
J. K. Götz Wietasch ◽  
Andreas Hoeft ◽  
Thomas W. L. Scheeren
Keyword(s):  
Cardiac Output ◽  
Right Ventricular ◽  
Blood Volume ◽  
Vascular Tone ◽  
Left Ventricular ◽  
Cardiac Preload ◽  
Circulating Blood Volume ◽  
Ventricular Afterload ◽  
Spontaneously Breathing ◽  
Blood Volumes

Abstract Background The effects of selective pulmonary vascular tone alterations on cardiac preload have not been previously examined. Therefore, we evaluated whether changing pulmonary vascular tone either by hypoxia or the inhalation of aerosolized prostacyclin (PGI2) altered intrathoracic or pulmonary blood volume (ITBV, PBV, respectively), both as surrogate for left ventricular preload. Additionally, the mean systemic filling pressure analogue (Pmsa) and pressure for venous return (Pvr) were calculated as surrogate of right ventricular preload. Methods In a randomized controlled animal study in 6 spontaneously breathing dogs, pulmonary vascular tone was increased by controlled moderate hypoxia (FiO2 about 0.10) and decreased by aerosolized PGI2. Also, inhalation of PGI2 was instituted to induce pulmonary vasodilation during normoxia and hypoxia. PBV, ITBV and circulating blood volume (Vdcirc) were measured using transpulmonary thermo-dye dilution. Pmsa and Pvr were calculated post hoc. Either the Wilcoxon-signed rank test or Friedman ANOVA test was performed. Results During hypoxia, mean pulmonary artery pressure (PAP) increased from median [IQR] 12 [8–15] to 19 [17–25] mmHg (p < 0.05). ITBV, PBV and their ratio with Vdcirc remained unaltered, which was also true for Pmsa, Pvr and cardiac output. PGI2 co-inhalation during hypoxia normalized mean PAP to 13 (12–16) mmHg (p < 0.05), but left cardiac preload surrogates unaltered. PGI2 inhalation during normoxia further decreased mean PAP to 10 (9–13) mmHg (p < 0.05) without changing any of the other investigated hemodynamic variables. Conclusions In spontaneously breathing dogs, changes in pulmonary vascular tone altered PAP but had no effect on cardiac output, central blood volumes or their relation to circulating blood volume, nor on Pmsa and Pvr. These observations suggest that cardiac preload is preserved despite substantial alterations in right ventricular afterload.

Effect of Nembutal on circulating and tissue blood volumes and hematocrits of intact and splenectomized mice

1959 ◽  
Vol 197 (2) ◽  
pp. 399-402 ◽  
Author(s):  
Julius J. Friedman
Keyword(s):  
Blood Volume ◽  
Vascular Tone ◽  
Red Cell ◽  
Circulating Blood Volume ◽  
Relationship Of ◽  
The Relationship ◽  
Cell Volumes ◽  
Blood Volumes

The effect of Nembutal on the circulating and tissue blood volumes and hematocrits was calculated by means of independent determinations of plasma and red cell volumes. Nembutal produced an increase in circulating blood volume accompanied by a reduction in the venous hematocrit. The blood volumes of liver, kidney, spleen and intestine rose following the administration of Nembutal, while the hematocrits of liver, lung, intestine and muscle declined, and that of kidney rose. The administration of Nembutal to splenectomized mice produces similar changes. The relationship of these alterations to changes in periphero-vascular tone are discussed.

scholarly journals Comparison of Doppler Flow Tei-Indexes With Pulmonary Artery Thermodilution Measurement of Cardiac Output in an Experimental Porcine Model

2011 ◽  
pp. 483-492 ◽  
Author(s):  
J. KOBR ◽  
V. TŘEŠKA ◽  
J. MOLÁČEK ◽  
V. KUNTSCHER ◽  
V. LIŠKA ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Pulmonary Artery ◽  
Right Ventricular ◽  
Left Ventricular ◽  
Average Weight ◽  
Ventricular Afterload ◽  
Echocardiographic Examination ◽  
The Right ◽  
Right Ventricular Preload ◽  
Thermodilution Measurement

The objective of our study was to compare Doppler echocardiography imaging with pulmonary artery thermodilution measurement during mechanical ventilation. Total 78 piglets (6 weeks old, average weight 24 kg, under general anesthesia) were divided into 4 groups under different cardiac loading conditions (at rest, with increased left ventricular afterload, with increased right ventricular preload, and with increased afterload of both heart ventricles). At 60 and 120 min the animals were examined by echocardiography and simultaneously pulmonary artery thermodilution was used to measure cardiac output. Tei-indexes data were compared with invasively monitored hemodynamic data and cardiac output values together with calculated vascular resistance indices. A total of 224 parallel measurements were obtained. Correlation was found between values of right Tei-index of myocardial performance and changes in right ventricular preload (p<0.05) and afterload (p<0.01). Significant correlation was also found between left index values and changes of left ventricular preload (p<0.001), afterload (p<0.001), stroke volume (p<0.01), and cardiac output (p<0.01). In conclusion, echocardiographic examination and determination of the global performance selectively for the right and left ventricle can be recommended as a suitable non-invasive supplement to the whole set of methods used for monitoring of circulation and cardiac performance.

Cardiac output, GFR, and renal excretion rates during maintained volume load in rats

1978 ◽  
Vol 235 (6) ◽  
pp. H670-H676 ◽  
Author(s):  
U. Ackermann
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Renal Excretion ◽  
Venous Pressure ◽  
Circulating Blood Volume ◽  
Reservoir Volume ◽  
Volume Load ◽  
Blood Volume Expansion ◽  
Highly Correlated ◽  
Excretion Rates

The correlation among cardiac output (CO), glomerular filtration rate (GFR), fractional tubular sodium rejection (TFRNa), and renal excretion rates of water and salt was investigated during ischemic blood volume expansion in rats. Initially circulating blood volume was equilibrated isovolemically with a reservoir volume of 6% albumin solution equal to one-third the estimated blood volume. Later the equilibrated reservoir contents were infused intravenously. CO was measured by thermodilution, GFR by inulin clearance. Significant linear correlations existed between GFR and the rates of urine flow (r = 0.90), sodium excretion (r = 0.75) and potassium excretion (r = 0.76) that prevailed 5--10 min after a given GFR change. The increased GFR was highly correlated with CO (r = 0.94), probably correlated with mean central venous pressure (r = 0.45), but not correlated with mean abdominal aortic blood pressure. The correlation between CO and time-delayed (5--10 min) TRFNa was also highly significant (r = 0.98). The saluresis appears to have been caused initially by increased tubular load and subsequently by decreased absolute tubular reabsorption.

Cardiac adjustments to left-side inotropic stimulation of in situ pig hearts

1987 ◽  
Vol 252 (6) ◽  
pp. H1164-H1174
Author(s):  
O. A. Vengen ◽  
K. Lande ◽  
O. Ellingsen ◽  
A. Ilebekk
Keyword(s):  
Right Ventricular ◽  
Systemic Circulation ◽  
Left Ventricular ◽  
Segment Length ◽  
Ventricular Afterload ◽  
Computer Based ◽  
The Right ◽  
Isoproterenol Infusion ◽  
Inotropic Stimulation ◽  
Stimulation Of

Cardiac adjustments to inotropic stimulation of the left side of the heart by continuous infusions of isoproterenol (0.6-0.8 microgram/min) and calcium chloride (240 mumol/min) into the left coronary artery were examined in open-chest pigs (17-36 kg) anesthetized with pentobarbital sodium. Both agents caused a reduction in the left ventricular (LV) preload and preejection segment length (PESL). Stroke volume (SV) rose by only 1.2 ml from 15.9 ml (P less than 0.01) during isoproterenol infusion, but when the reduction in LV PESL of 3.2% (P less than 0.01) was restored by saline infusion, SV increased by 27%. The LV PESL reduction was less at hypervolemia than at normovolemia. A computer-based model of the circulation predicted most of these changes and suggested redistribution of blood from the pulmonary to the systemic circulation. During isoproterenol infusion, the pulmonary arterial pressure fell, and the right ventricular end-ejection segment length declined. Reduced right ventricular afterload thus appears to be an important mechanism by which right ventricular output is increased during a selective increase in LV inotropy.

Atrial natriuretic peptide reverses angiotensin-induced venoconstriction in dogs

1989 ◽  
Vol 257 (4) ◽  
pp. H1062-H1067 ◽  
Author(s):  
R. W. Lee ◽  
R. G. Gay ◽  
S. Goldman
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Blood Volume ◽  
Left Ventricular ◽  
Ang Ii ◽  
Central Blood Volume ◽  
Venous Compliance ◽  
Induced Hypertension

To determine whether atrial natriuretic peptide (ANP) can reverse angiotensin (ANG II)-induced venoconstriction, ANP was infused (0.3 micrograms.kg-1.min-1) in the presence of ANG II-induced hypertension in six ganglion-blocked dogs. ANG II was initially administered to increase mean arterial blood pressure (MAP) 50% above control. ANG II did not change heart rate or left ventricular rate of pressure development (LV dP/dt) but increased total peripheral vascular resistance (TPVR) and left ventricular end-diastolic pressure (LVEDP). Mean circulatory filling pressure (MCFP) increased, whereas cardiac output and venous compliance decreased. Unstressed vascular volume did not change, but central blood volume increased. ANP infusion during ANG II-induced hypertension resulted in a decrease in MAP, but TPVR did not change. There were no changes in heart rate or LV dP/dt. ANP decreased cardiac output further. LVEDP returned to base line with ANP. ANP also decreased MCFP and normalized venous compliance. There was no significant change in total blood volume, but central blood volume decreased. In summary, ANP can reverse the venoconstriction but not the arterial vasoconstriction produced by ANG II. The decrease in MAP was due to a decrease in cardiac output that resulted from venodilatation and aggravation of the preload-afterload mismatch produced by ANG II alone. Because TPVR did not change when MAP fell, we conclude that the interaction between ANG II and ANP occurs primarily in the venous circulation.

Effects of pneumatic antishock garment inflation in normovolemic subjects

1989 ◽  
Vol 67 (1) ◽  
pp. 339-345 ◽  
Author(s):  
B. J. Rubal ◽  
M. R. Geer ◽  
W. H. Bickell
Keyword(s):  
Cardiac Output ◽  
Pulmonary Capillary Wedge Pressure ◽  
Vascular Resistance ◽  
Heart Function ◽  
Normal Subjects ◽  
Left Ventricular ◽  
Ventricular Afterload ◽  
Pulmonary Capillary ◽  
Pulmonary Arterial ◽  
Wedge Pressure

This study examines the effects of inflation of pneumatic antishock garments (PASG) in 10 normovolemic men (mean age 44 +/- 6 yr) undergoing diagnostic catheterization. Seven subjects had normal heart function and no evidence of coronary artery disease (CAD); three patients had CAD. High-fidelity multisensor catheters were employed to simultaneously record right and left heart pressures before PASG inflation and after inflation to 40, 70, and 100 mmHg. A thermal dilution catheter was used to obtain pulmonary capillary wedge pressure and cardiac output. Counterpressure increases greater than or equal to 40 mmHg were associated with significant changes in left and right heart pressures. Right and left ventricular end-diastolic pressures increased 100% (P less than 0.01); mean pulmonary arterial and aortic pressures increased 77 and 25%, respectively (P less than 0.01); systemic vascular resistance increased 22% (P less than 0.05) and pulmonary vascular resistance did not change in normal subjects at maximum PASG inflation. Heart rate, cardiac output, and aortic and pulmonary arterial pulse pressures did not change during inflation in either group. Right and left ventricular end-diastolic pressures and pulmonary capillary wedge pressure were greater (P less than 0.05) in the CAD group compared with the normal subjects during PASG inflation. The data suggest that the primary mechanism whereby PASG inflation induces changes in central hemodynamics in normovolemic subjects is through an acute increase in left ventricular afterload. PASG changes in afterload and pulmonary capillary wedge pressure imply that these devices should be used with caution in patients with compromised cardiac function.

Effects of isoproterenol on the cardiovascular system of fetal sheep exposed to long-term high-altitude hypoxemia

1995 ◽  
Vol 78 (5) ◽  
pp. 1793-1799 ◽  
Author(s):  
M. Kamitomo ◽  
T. Ohtsuka ◽  
R. D. Gilbert
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Right Ventricular ◽  
High Altitude ◽  
Arterial Blood Pressure ◽  
Left Ventricular ◽  
Arterial Blood ◽  
Isoproterenol Infusion

We exposed fetuses to high-altitude (3,820 m) hypoxemia from 30 to 130 days gestation, when we measured fetal heart rate, right and left ventricular outputs with electromagnetic flow probes, and arterial blood pressure during an isoproterenol dose-response infusion. We also measured the distribution of cardiac output with radiolabeled microspheres during the maximal isoproterenol dose. Baseline fetal arterial blood pressure was higher in long-term hypoxemic fetuses (50.1 +/- 1.3 vs. 43.4 +/- 1.0 mmHg) but fell during the isoproterenol infusion to 41.3 +/- 1.4 and 37.5 +/- 1.4 mmHg, respectively, at the highest dose. Heart rate was the same in both groups and did not differ during isoproterenol infusion. Baseline fetal cardiac output was lower in the hypoxemic group (339 +/- 18 vs. 436 +/- 19 ml.min-1.kg-1) due mainly to a reduction in right ventricular output. During the isoproterenol infusion, right ventricular output increased to the same extent in both hypoxemic and normoxic fetuses (approximately 35%); however, left ventricular output increased only approximately 15% in the hypoxemic group compared with approximately 40% in the normoxic group. The percent change in individual organ blood flows during isoproterenol infusion in the hypoxemic groups was not significantly different from the normoxic group. All of the mechanisms that might be responsible for the differential response of the fetal left and right ventricles to long-term hypoxia are not understood and need further exploration.

Testosterone receptor blockade after trauma-hemorrhage improves cardiac and hepatic functions in males

1997 ◽  
Vol 273 (6) ◽  
pp. H2919-H2925 ◽  
Author(s):  
Dierk E. Remmers ◽  
Ping Wang ◽  
William G. Cioffi ◽  
Kirby I. Bland ◽  
Irshad H. Chaudry
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Maximum Velocity ◽  
Left Ventricular ◽  
Male Rats ◽  
Microvascular Blood Flow ◽  
Receptor Blockade ◽  
Ringer Lactate ◽  
Ventricular Performance ◽  
Shed Blood

Although studies have shown that testosterone receptor blockade with flutamide after hemorrhage restores the depressed immune function, it remains unknown whether administration of flutamide following trauma and hemorrhage and resuscitation has any salutary effects on the depressed cardiovascular and hepatocellular functions. To study this, male rats underwent a laparotomy (representing trauma) and were then bled and maintained at a mean arterial pressure (MAP) of 40 mmHg until the animals could not maintain this pressure. Ringer lactate was given to maintain a MAP of 40 mmHg until 40% of the maximal shed blood volume was returned in the form of Ringer lactate. The rats were then resuscitated with four times the shed blood volume in the form of Ringer lactate over 60 min. Flutamide (25 mg/kg) or an equal volume of the vehicle propanediol was injected subcutaneously 15 min before the end of resuscitation. Various in vivo heart performance parameters (e.g., maximal rate of the pressure increase or decrease), cardiac output, and hepatocellular function (i.e., the maximum velocity and the overall efficiency of indocyanine green clearance) were determined at 20 h after resuscitation. Additionally, hepatic microvascular blood flow (HMBF) was determined using a laser Doppler flowmeter. The results indicate that left ventricular performance, cardiac output, HMBF, and hepatocellular function decreased significantly at 20 h after the completion of trauma, hemorrhage, and resuscitation. Administration of the testosterone receptor blocker flutamide, however, significantly improved cardiac performance, HMBF, and hepatocellular function. Thus flutamide appears to be a novel and useful adjunct for improving cardiovascular and hepatocellular functions in males following trauma and hemorrhagic shock.

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