Effects of serotonin on pulmonary blood volume in the dog

1962 ◽  
Vol 202 (5) ◽  
pp. 957-960 ◽  
Author(s):  
Charles J. McGaff ◽  
William R. Milnor
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Vascular Resistance ◽  
Transit Time ◽  
Mean Transit Time ◽  
Dilution Method ◽  
Continuous Intravenous Infusion ◽  
Pulmonary Blood Volume ◽  
Control Value ◽  
Vascular Bed

Changes in pulmonary blood volume produced by continuous intravenous infusion of serotonin (5-hydroxytryptamine) were measured in 16 experiments on ten dogs. Pulmonary mean transit time was measured by the dye dilution method, using consecutive injections into pulmonary artery and left atrium; pulmonary blood volume was calculated by multiplying this mean transit time by the cardiac output. Serotonin lowered pulmonary blood volume by an average of 2.9 ml/kg, or 26% of the control value ( P <0.001). Pulmonary vascular resistance increased 94 ru (resistance units) kg, and systemic vascular resistance fell 294 ru kg, effects similar to those reported by other investigators. The magnitude of the decrease in pulmonary blood volume indicates that a relatively large part of the pulmonary vascular bed is constricted by serotonin, and provides an example of shifting of blood from pulmonic to systemic circuits by reciprocal changes in the distensibility of these beds.

Determination of central blood volume. Comparison of Stewart-Hamilton method with direct measurements in dogs

1959 ◽  
Vol 196 (3) ◽  
pp. 499-501 ◽  
Author(s):  
Robert C. Schlant ◽  
Paul Novack ◽  
William L. Kraus ◽  
Charles B. Moore ◽  
Florence W. Haynes ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Transit Time ◽  
Mean Transit Time ◽  
Total Radioactivity ◽  
Indicator Dilution ◽  
Dilution Method ◽  
Central Blood Volume ◽  
Volume Comparison ◽  
Direct Measurements

Central blood volume (cardiac output times mean transit time) from right atrium to ascending aorta was determined by the indicator-dilution method in 22 open-chested dogs which had previously had their red blood cells tagged with Cr51. The actual amount of blood in the heart and lungs was calculated from the total radioactivity in the blended homogenate of these organs. The two measurements of central blood volume correlated well ( r = +.88), the indicator-dilution volumes averaging 12% greater. The discrepancy between measurements is probably related to the pulmonary circuit having a lower hematocrit than the large vessels. The results substantiate the use of the Stewart-Hamilton formula (cardiac output times mean transit time) to measure central blood volume.

Evaluation of slope method for measuring pulmonary blood volume in man

1962 ◽  
Vol 17 (3) ◽  
pp. 497-502 ◽  
Author(s):  
Lockhart B. McGuire ◽  
Donald S. Dock ◽  
John W. Hyland ◽  
Donald C. Harrison ◽  
Florence W. Haynes ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Blood Volume ◽  
Transit Time ◽  
Human Subjects ◽  
Mean Transit Time ◽  
Close Correlation ◽  
Artery Occlusion ◽  
Pulmonary Blood Volume ◽  
Slope Method ◽  
Predominant Effect

Knowledge of the pulmonary blood volume is important in several areas of circulatory physiology. However, adequate methods for measuring this volume have not been established. The slope of an indicator-dilution curve across the central circulation has been used in several studies as an indication of this volume. In the present study the blood volume between pulmonary artery and left atrium was measured in 31 human subjects by an application of the well-established mean transit time principle. Slope volumes were also measured. There was poor agreement between the results of the two techniques. Unilateral pulmonary artery occlusion consistently reduced pulmonary blood volume by the mean transit time method, with only minor and less consistent changes in slope volumes. A close correlation between the slopes of curves from simultaneous pulmonary artery and left atrial injections suggested a predominant effect on both curves of factors at or distal to the left side of the heart. It was concluded that the slope method did not measure the pulmonary blood volume in man. Submitted on June 8, 1961

Effects of lung collapse on pulmonary blood volume, flow and resistance

1959 ◽  
Vol 197 (1) ◽  
pp. 187-189
Author(s):  
Alceo Barrios ◽  
Colin Fell ◽  
W. F. Hamilton
Keyword(s):  
Pulmonary Artery ◽  
Blood Volume ◽  
Vascular Resistance ◽  
Aortic Pressure ◽  
Pulse Contour ◽  
Contour Method ◽  
Dilution Method ◽  
Sodium Pentobarbital ◽  
Pulmonary Blood Volume ◽  
Pulse Contour Method

Pulmonary blood flow, pressures, volume and vascular resistance were measured when the lungs occupied an expiratory position in the closed chest and when they were collapsed by introducing air into the thorax. Circulation and innervation were intact. Variations due to respiratory movements or asphyxia were ruled out. Mongrel dogs were used, anesthetized with morphine and sodium pentobarbital. Pressures were measured from pulmonary artery, left atrium, aortic arch and intrapleural space. Pulmonary flow was evaluated utilizing the dye dilution method and the pulse contour method. Vascular volume was estimated by the product of mean circulation time and flow. When the lungs were collapsed there was an immediate elevation of intraluminal left atrial pressure but not a comparable rise in pulmonary arterial pressure. However, the direct records of arteriovenous pressure drop suggest that there was a delayed rise in pulmonary artery pressure. Flow, aortic pressure, heart rate and pulmonary vascular resistance showed no consistent changes. In 8 of 11 cases the pulmonary blood volume decreased when the lungs were collapsed.

Regional differences in erythrocyte transit in normal lungs

1985 ◽  
Vol 59 (4) ◽  
pp. 1266-1271 ◽  
Author(s):  
J. C. Hogg ◽  
B. A. Martin ◽  
S. Lee ◽  
T. McLean
Keyword(s):  
Blood Volume ◽  
Transit Time ◽  
Regional Differences ◽  
Regional Blood Flow ◽  
Mean Transit Time ◽  
Vascular Bed ◽  
Transit Times ◽  
Regional Blood Volume ◽  
The Relationship ◽  
Normal Lungs

We measured regional blood volume and flow in the lungs of nine mongrel dogs. The time taken for the erythrocytes to transit through individual lung regions was calculated from the relationship t = V/Q, where V is blood volume and Q is flow. The data show that the total pulmonary blood volume was 82 +/- 6 ml and that the average time spent in the pulmonary vascular bed was 2.86 +/- 0.31 s. The frequency distribution of the transit times ranged from 0.41 to 6 s in the experiment with the shortest mean transit (1.62 s) and from 0.9 to greater than 20 s in the experiment with the longest mean transit time (4.6 s). The regional data show that the longer transit times were in the upper lung and that expansion of the blood volume as flow increased down the lung prevented an excessive shortening of the transit time. We conclude that increasing regional blood flow is associated with an expansion of regional blood volumes so that the transit times remain relatively constant.

Systemic and pulmonary hemodynamic responses to intracranial hypertension

1984 ◽  
Vol 247 (5) ◽  
pp. H715-H721 ◽  
Author(s):  
H. I. Chen ◽  
D. J. Wang
Keyword(s):  
Intracranial Hypertension ◽  
Blood Volume ◽  
Vascular Resistance ◽  
Venous Pressure ◽  
Resistance Response ◽  
Pulmonary Blood Volume ◽  
Control Value ◽  
Pulmonary Hemodynamic ◽  
Arterial Inflow ◽  
Capacitance Vessels

Experiments were conducted in anesthetized, vagotomized, and open-chest dogs. Total heart bypass was performed to perfuse the systemic and pulmonary circulations with constant flow. The venous outflows were diverted into reservoirs. We studied the simultaneous changes in systemic vascular resistance (SVR) and capacity (SVC) as well as pulmonary vascular resistance (PVR) and capacity (PVC) during a period of intracranial hypertension (ICH). In 20 dogs with an intracranial pressure of 164 +/- 12 mmHg, SVR increased by 110% and SVC decreased by 8.4 +/- 1.2 ml/kg. The increase in PVR reached 69%, and the decrease in PVC amounted to 1.24 +/- 0.40 ml/kg body wt or 9.7 +/- 3.9 ml/100 g lung wt. The results indicate that ICH exerts profound effects on both systemic and pulmonary resistance and capacitance vessels. An analysis from the pulmonary blood volume change suggested that the pulmonary vascular compliance was significantly reduced by ICH from a control value of 0.33 +/- 0.06 to 0.26 +/- 0.05 ml X mmHg-1 X kg-1. In the pulmonary circulation, an elevation of left atrial pressure with lung volume expansion attenuated the resistance response, while it increased the capacity reduction. When pulmonary blood volume was kept constant by a constant venous outflow equal to the arterial inflow, the response of capacitance vessels to ICH increased both pulmonary arterial and venous pressures associated with a slight change in PVR. These findings suggest that an increase in pulmonary venous pressure with a constant or increased blood volume reduced the ICH-induced change in resistance.

Observations on Cardiac Output and ”Pulmonary Blood Volume” in Normal Man by External Recording of the Intracardiac Flow of 131I Labelled Albumin

1961 ◽  
Vol 1 (04) ◽  
pp. 353-379
Author(s):  
Jacques Lammerant ◽  
Norman Veall ◽  
Michel De Visscher
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Normal Subjects ◽  
Published Data ◽  
Total Blood Volume ◽  
Total Blood ◽  
Pulmonary Blood Volume ◽  
Intracardiac Flow ◽  
Normal Man ◽  
Mean Circulation

Summary1. The technique for the measurement of cardiac output by external recording of the intracardiac flow of 131I labelled human serum albumin has been extended to provide a measure of the mean circulation time from right to left heart and hence a new approach to the estimation of the pulmonary blood volume.2. Values for the basal cardiac output in normal subjects and its variations with age are in good agreement with the previously published data of other workers.3. The pulmonary blood volume in normal man in the basal state was found to be 28.2 ± 0.6% of the total blood volume.4. There was no correlation between cardiac output and pulmonary blood volume in a series of normal subjects in the basal state.5. The increase in cardiac output during digestion was associated with a decrease in pulmonary blood volume equal to 6.3 ± 1.2% of the total blood volume, that is, about 280 ml.6. The increase in cardiac output during exercise was associated with a decrease in pulmonary blood volume equal to 4.5 ± 1.0% of the total blood volume, that is, about 200 ml.7. The increase in cardiac output attributed to alarm is not associated with a decrease in pulmonary blood volume, the latter may in fact be increased.8. The total blood volume is advocated as a standard of reference for studies of this type in normal subjects in preference to body weight or surface area.9. The significance of these results and the validity of the method are discussed.

P4129cMR-Pulmonary transit time and pulmonary blood volume have an additional prognostic value over cMR-right ventricular ejection fraction in predicting mortality in HF-rEF patients

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
L Houard ◽  
H Langet ◽  
S Militaru ◽  
M F Rousseau ◽  
A C Pouleur ◽  
...  
Keyword(s):  
Blood Volume ◽  
Transit Time ◽  
Primary Endpoint ◽  
Prognostic Value ◽  
Beta Blockers ◽  
Class Iii ◽  
Baseline Model ◽  
Pulmonary Blood Volume ◽  
Pulmonary Transit Time ◽  
Overall Mortality

Abstract Background Assessment of congestion and cardiac function has been shown to have both therapeutic and prognostic implication for the management of patient with CHF. Pulmonary transit time (PTT) assessed by cMR is a novel parameter, which reflects not only hemodynamic congestion but also LV and RV function. Purpose We sought to explore the prognostic value of the pulmonary transit time assessed in seconds (PTT) and in beats (PTB) and the pulmonary blood volume indexed (PBVi) above conventional well-known risk factors including cMR-RVEF and estimated pulmonary artery pressure (eSPAP) in predicting outcomes. PBVi is defined by the product of PTB and the stroke volume indexed to body surface area. Methods 401 patients in sinus rhythm with a LVEF <35% (age 61±13 years; 25% female) underwent a cMR and an echocardiography. Patients were followed for a primary endpoint of overall mortality. Results Average cMR-LVEF was 23±7%, cMR-RVEF was 43±15%, average estimated systolic pulmonary pressure (eSPAP) was 33±12mmH, average PTT was 11±6s, PTB 8.9±5.6 bpm and average PBVi 305.5±254.9ml/m2. After a median follow-up of 6 years, 182 reached the primary endpoint. In univariate cox regression, age, ischemic cardiomyopathy, hypertension, diabetes, NYHA class III-IV, eSPAP >40mmHg, E/A ratio, e/e'ratio, cMR-RVEF, LV scar, PTT, PTB, PBVi, GFR, beta blockers and diuretics were associated with overall mortality. For the multivariate analysis, a baseline model was created where age, ischemic etiology, NYHA functional class III-IV, eSPAP >40 mmHg, beta-blockers and cMR-RVEF were found to be significantly and independently associated with the primary endpoint. PTT (X2 to improve = 5.3, HR: 1.03; 95% CI: [1.01; 1.06]; P=0.015), PTB (X2 to improve = 11.8, HR: 1.06; 95% CI: [1.03; 1.09]; P<0.001) and PBVi (X2 to improve = 7.7, HR: 1.08; 95% CI: [1.03; 1.14]; P=0.002) showed a significantly additional prognostic value over the baseline model (p<0.001). Conclusion Pulmonary transit time and pulmonary blood volume provide higher prognostic information over well-known risk factors including cMR-RVEF and eSPAP with high power to stratify prognosis in HF-rEF and might be promising tools to identify patients at higher risk among HF patients. Acknowledgement/Funding Fond National de recherche scientifique (FNRS)

RSR-13, an allosteric effector of hemoglobin, increases systemic and iliac vascular resistance in rats

1996 ◽  
Vol 271 (2) ◽  
pp. H602-H613 ◽  
Author(s):  
M. P. Kunert ◽  
J. F. Liard ◽  
D. J. Abraham
Keyword(s):  
Cardiac Output ◽  
Vascular Resistance ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Experimental Models ◽  
Metabolic Demand ◽  
Flow Probe ◽  
Inositol Hexaphosphate ◽  
Control Value ◽  
Allosteric Effector

Tissue O2 delivery in excess of metabolic demand may be a factor in the development of high vascular resistance in experimental models of volume-expanded hypertension. This hypothesis was previously tested in rats with an exchange transfusion of red blood cells treated with inositol hexaphosphate or an intravenous infusion of RSR-4, allosteric effectors of hemoglobin. The binding of these drugs with hemoglobin effect a conformational change in the molecule, such that the affinity for O2 is reduced. However, in both preparations, the changes in vascular resistance could have been nonspecific. The present studies used intravenous infusions of RSR-13, which did not share some of the problematic characteristics of RSR-4 and inositol hexaphosphate. Conscious instrumented rats (an electromagnetic flow probe on ascending aorta or an iliac, mesenteric, or renal Doppler flow probe) were studied for 6 h after an RSR-13 infusion of 200 mg/kg in 15 min. This dose significantly increased arterial P50 (PO2 at which hemoglobin is 50% saturated) from 38 +/- 0.8 to 58 +/- 1.4 mmHg at 1 h after the start of the infusion. In the 3rd h cardiac output fell significantly from a control value of 358 +/- 33 to 243 +/- 24 ml.kg-1.min-1 and total peripheral resistance significantly increased from 0.31 +/- 0.03 to 0.43 +/- 0.04 mmHg.ml-1.kg.min. Cardiac output and P50 returned toward control over the next few hours. Neither cardiac output nor total peripheral resistance changed in the group of rats receiving vehicle alone. In a separate group of rats, iliac flow decreased significantly to 60% of control and iliac resistance increased to 160% of control. Iliac flow increased significantly in the group of rats that received vehicle only. Although the mechanism of these changes has not been established, these results suggest that a decreased O2 affinity leads to an increased total peripheral resistance and regional vascular resistance and support the hypothesis that O2 plays a role in the metabolic autoregulation of blood flow.

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