Direct influence of blood viscosity on pulmonary vascular resistance

Tyson, Kenneth R.T.; Fender, H. Roberts

doi:10.1016/0022-3468(75)90384-x

Cited by 5 publications

(2 citation statements)

References 6 publications

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“…This dilution was done to provide sufficient blood to perfuse the system. Because the viscosity of the blood was decreased, its effect on PVR and hysteresis may also have been decreased (22). To date, the relationship of lung inflation to PVR, pulmonary blood flow, and capillary recruitment has not been fully elucidated.…”

Section: Discussionmentioning

confidence: 97%

“…The two-compartment model of alveolar and extra-alveolar vessels attempts to explain this phenomenon (23). Even this model is an oversimplification and fails to accommodate factors such as perfusion conditions (24), rheology (22), or vessel length and diameter (25). Many investigators suggest that surface tension plays a key role in changes of PVR with inflation (2,3,26,27).…”

Section: Discussionmentioning

confidence: 98%

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Ventilation above Closing Volume Reduces Pulmonary Vascular Resistance Hysteresis

Creamer

McCloud

Fisher

et al. 1998

Am J Respir Crit Care Med

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The aim of this study was to determine the relationship of pulmonary vascular resistance (PVR) hysteresis and lung volume, with special attention to the effects of ventilation around closing volume (CV). Isolated, blood-perfused canine left lower lung lobes (LLL) were incrementally inflated and deflated. Airway and pulmonary artery pressures (PAP) were recorded after each stepwise volume change. Constant blood flow was provided (600 ml/min) and the pulmonary vein pressure (PVP) was held constant at 5 cm H2O. PAP changes, therefore, were a direct index of PVR changes. Group 1 lobes underwent a full inflation from complete collapse to total lobe capacity (TLC) followed by a full deflation. Group 2 lobes underwent two deflation/inflation cycles, after an initial full inflation. These cycles, both beginning at TLC, had deflation end above and below CV, respectively. Significant PVR hysteresis was noted when the first inflation and deflation were compared. The maximum difference in PAP on deflation was 3.3 cm H2O or 11%. The mean decrease was 2.7 cm H2O for 18 lobes (p < 0.0001). The PAPs on all subsequent inflations or deflations that began above CV remained 9% lower than the initial inflation (n = 9, p < 0.0001), but were not different from each other. However, the final inflation which began from below CV resulted in a 30% return of PVR hysteresis (mean increase in PAP of 0.8 cm H2O, n = 7, p < 0.004). We conclude that there is hysteresis in the PVR response during ventilation, with decreased PVR during deflation relative to the initial inflation, that this hysteresis is absent when lung volume is maintained greater than CV, and that hysteresis returns when inflation occurs after deflation below CV.

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 98%

Ventilation above Closing Volume Reduces Pulmonary Vascular Resistance Hysteresis

Creamer

McCloud

Fisher

et al. 1998

Am J Respir Crit Care Med

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Heart and lung hypertrophy, changes in blood volume, hematocrit and plasma renin activity in rats chronically exposed to increasing carbon monoxide concentrations

Penney

Davidson

Gargulinski

et al. 1988

J of Applied Toxicology

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Changes in blood volume, heart and lung mass and composition and plasma renin activity were examined in two strains of male albino rats inhaling incrementally-increasing concentrations of CO: 250 ppm for 17 days, 500 ppm for 13-14 days, 750 ppm for 10 days, and 1300 ppm for 10 days. Blood volume increased 86% and erythrocyte mass increased 212% at 1300 ppm, while plasma volume was unchanged or decreased slightly. 'Real' hematocrit (hematocrit corrected for plasma trapping) increased from 50% in controls to a peak of 75% at 1300 ppm CO. Wet weight of right ventricle (RV) and combined right and left atria (2A) increased linearly with CO concentration, paralleling changes in blood volume; while real hematocrit increased non-linearly. Left ventricle + interventricular septum (LV + S) wet weight increased less than RV, but more in Sprague-Dawley than in Wistar rats. Plots of RV, LV + S and 2A weight vs real hematocrit showed sharp upward inflections at real hematocrit 65%, suggesting a possible role of increased viscosity in CO cardiomegaly at the higher hematocrit. Assymetric septal hypertrophy was not present. Lung weight increased with CO concentration, but was not due to increased lung blood volume or edema. Hydroxyproline measurements on heart and lung failed to show increased collagen content. Plasma renin activity measured by radioimmunoassay was depressed at 500 ppm, but was normal at 750 and 1300 ppm CO. Neither heart, lung, liver nor plasma renin measurements suggest congestive heart failure, supporting previous studies in the rat with chronic carboxyhemoglobinemia, in spite of enormously increased blood volume, hematocrit and heart weight.

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Cardiac output and pulmonary vascular resistance in hypertension

Tyson

1978

The American Journal of Cardiology

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Direct influence of blood viscosity on pulmonary vascular resistance

Cited by 5 publications

References 6 publications

Ventilation above Closing Volume Reduces Pulmonary Vascular Resistance Hysteresis

Ventilation above Closing Volume Reduces Pulmonary Vascular Resistance Hysteresis

Heart and lung hypertrophy, changes in blood volume, hematocrit and plasma renin activity in rats chronically exposed to increasing carbon monoxide concentrations

Cardiac output and pulmonary vascular resistance in hypertension

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