Lung inflation and longitudinal distribution of pulmonary vascular resistance during hypoxia

1979 ◽  
Vol 47 (3) ◽  
pp. 532-536 ◽  
Author(s):  
C. A. Dawson ◽  
D. J. Grimm ◽  
J. H. Linehan
Keyword(s):  
Vascular Resistance ◽  
Pressor Response ◽  
Transpulmonary Pressure ◽  
Longitudinal Distribution ◽  
Local Resistance ◽  
Lung Inflation ◽  
Hypoxic Conditions ◽  
Low Viscosity ◽  
Major Increase ◽  
Vessel Resistance

Using the low-viscosity bolus method, we examined the influence of lung inflation on the longitudinal distribution of vascular resistance during hypoxia in isolated cat lungs. During hypoxia, increasing transpulmonary pressure decreased vascular resistance but did not change the volume into the lung at which the maximum local resistance was located. This was in contrast to the normoxic situation in which inflation caused an increase in resistance over much of the transpulmonary pressure range studied and moved the maximum local resistance downstream. These results indicate that during hypoxia the major increase in resistance was in extra-alveolar vessels and that distension of these vessels by lung inflation decreased the magnitude of the pressor response. The increase in resistance in alveolar vessels, which occurred on inflation, was similar during control and hypoxic conditions but was a smaller part of the total resistance during hypoxia because of the much larger extra-alveolar vessel resistance.

Effects of lung inflation on longitudinal distribution of pulmonary vascular resistance

1977 ◽  
Vol 43 (6) ◽  
pp. 1089-1092 ◽  
Author(s):  
C. A. Dawson ◽  
D. J. Grimm ◽  
J. H. Linehan
Keyword(s):  
Pulmonary Vascular Resistance ◽  
Blood Volume ◽  
Vascular Resistance ◽  
Transpulmonary Pressure ◽  
Longitudinal Distribution ◽  
Total Blood Volume ◽  
Total Blood ◽  
Lung Inflation ◽  
Low Viscosity ◽  
Vascular Bed

A low-viscosity bolus technique was employed to determine the influence of lung inflation on the distribution of pulmonary vascular resistance in isolated cat lungs. When the lungs were collapsed, the longitudinal distribution of resistance was concentrated near the proximal (arterial) part of the vascular bed. As the lungs were inflated, the resistance became more evenly distributed with the maximum located close to the midpoint of the total blood volume. The fraction of total pressure drop across the lung which occurred proximal to the midpoint of the total lung blood volume decreased from 0.69 in the collapsed lung to 0.43 at a transpulmonary pressure of 16 cmH2O.

Influence of hypoxia on the longitudinal distribution of pulmonary vascular resistance

1978 ◽  
Vol 44 (4) ◽  
pp. 493-498 ◽  
Author(s):  
C. A. Dawson ◽  
D. J. Grimm ◽  
J. H. Linehan
Keyword(s):  
Pulmonary Artery ◽  
Vascular Resistance ◽  
Main Pulmonary Artery ◽  
Pulmonary Arteries ◽  
Longitudinal Distribution ◽  
Local Resistance ◽  
Lung Water ◽  
Low Viscosity ◽  
Double Indicator Dilution ◽  
Intravascular Pressure

We have examined the influence of hypoxia on the longitudinal distribution of vascular resistance and intravascular pressure in isolated cat lungs using the low-viscosity bolus technique. Hypoxia increased total vascular resistance, decreased total lung blood volume, and moved the maximum local resistance downstream away from the main pulmonary artery. The circumference of the main pulmonary artery was increased and the extravascular lung water (double indicator dilution technique) was decreased by hypoxia. Thus, it would appear that distension of the large pulmonary arteries and a decrease in the amount of lung tissue perfused contributed to the change in resistance distribution brought about by hypoxia.

Effect of lung inflation and hypoxia on pulmonary arterial blood volume

1977 ◽  
Vol 43 (1) ◽  
pp. 8-13 ◽  
Author(s):  
E. J. Quebbeman ◽  
C. A. Dawson
Keyword(s):  
Blood Flow ◽  
Pulmonary Artery ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Transpulmonary Pressure ◽  
The Other ◽  
Lung Inflation ◽  
Arterial Blood ◽  
Pulmonary Arterial ◽  
Arterial Blood Volume

Isolated cat lungs were perfused with constant blood flow. During control conditions (Pa02, 100 Torr), pulmonary artery pressure increased as the lungs were inflated. Hypoxia (Pa02, 22 Torr) increased arterial pressure. However, as the lungs were inflated arterial pressure fell. Thus, the magnitude of the hypoxic pressor response was reduced by inflation. During control conditions, arterial volume (ether bolus method) increased with increasing transpulmonary pressure. Hypoxia decreased arterial volume, and the increase in arterial volume with inflation was somewhat less than that during control conditions. When the influences of vascular and transpulmonary pressures were examined independently by changing one while holding the other constant, increasing transpulmonary pressure increased arterial volume beyond that which could be accounted for by changes in the differences between arterial and pleural pressure. However, this influence of transpulmonary pressure did not appear to be altered by hypoxia. Thus, while hypoxia decreased arterial volume at all levels of lung inflation, it had relatively little effect on the influence of interdependence between the pulmonary arterial bed and the surrounding lung tissue.

Pulmonary vasomotion and the distribution of vascular resistance in a dog lung lobe

1978 ◽  
Vol 45 (4) ◽  
pp. 545-550 ◽  
Author(s):  
D. J. Grimm ◽  
C. A. Dawson ◽  
T. S. Hakim ◽  
J. H. Linehan
Keyword(s):  
Vascular Resistance ◽  
Stellate Ganglion ◽  
Lower Lobe ◽  
Longitudinal Distribution ◽  
Sympathetic Stimulation ◽  
Lung Lobe ◽  
Maximum Resistance ◽  
Upstream Side ◽  
Low Viscosity ◽  
Infusion Of Norepinephrine

We examined the influence of stellate ganglion stimulation, hypoxia, and the infusion of norepinephrine, PGF2alpha, serotonin, and histamine on the longitudinal distribution of vascular resistance and intravascular pressures in an isolated left lower lobe of the dog lung using the low-viscosity bolus technique. Sympathetic stimulation, norepinephrine, serotonin, PGF2alpha, and hypoxia increased total pulmonary vascular resistance by increasing the resistance, primarily on the arterial or upstream side of the volume midpoint, whereas histamine increased the resistance near the venous end of the lobar vascular bed. Hypoxia increased the volume upstream from the site of maximum resistance, suggesting that the larger lobar arteries were distended by the elevated lobar artery pressure. Sympathetic stimulation, norepinephrine, PGF2alpha, and serotonin, on the other hand, had little effect on the volume upstream from the maximum resistance, suggesting that these vasomotor stimuli prevented distension of the larger arteries.

Longitudinal distribution of vascular resistance in the lung

1977 ◽  
Vol 43 (6) ◽  
pp. 1093-1101 ◽  
Author(s):  
D. J. Grimm ◽  
J. H. Linehan ◽  
C. A. Dawson
Keyword(s):  
Pulmonary Artery ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Pattern Search ◽  
Geometric Factor ◽  
Longitudinal Distribution ◽  
Pressure Curve ◽  
Search Technique ◽  
Small Segment ◽  
Low Viscosity

We have modified the low-viscosity bolus technique for determining the longitudinal distribution of pulmonary vascular resistance. A bolus of saline was introduced into the pulmonary artery of an isolated cat lung. As this low-viscosity bolus passed through the lung, a fall in inflow pressure was recorded which had a characteristic shape depending on the changing shape and position of the low-viscosity bolus and the longitudinal distribution of resistance. The shape and position of the bolus within the lung at a given time were calculated using the change in viscosity of the blood measured as the bolus entered the pulmonary artery and as it emerged from the left atrium. Assuming that the hemodynamic resistance of a small segment of the vasculature is proportional to the product of the viscosity and its geometric factor, we employed a sequential-pattern search technique to calculate the “best” longitudinal distribution of the geometric factor, compatible with the position and dispersion of the bolus at any time and the arterial pressure curve.

Influence of state of inflation of the lung on pulmonary vascular resistance

1960 ◽  
Vol 15 (5) ◽  
pp. 878-882 ◽  
Author(s):  
James L. Whittenberger ◽  
Maurice McGregor ◽  
Erik Berglund ◽  
Hans G. Borst
Keyword(s):  
Blood Flow ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Flow Resistance ◽  
Transpulmonary Pressure ◽  
Lung Inflation ◽  
Pulmonary Arterial ◽  
Low Levels ◽  
The Relationship ◽  
Complete Collapse

The relationship between the degree of pulmonary inflation and the pulmonary vascular resistance was studied in an open-chested dog preparation. It was possible to control the state of inflation and the blood flow to the lung under study. Vascular resistance could then be observed under controlled conditions. In most cases the resistance at complete collapse was very slightly higher than at moderate levels of inflation. In a few instances collapse was associated with a more marked elevation of resistance. Higher levels of inflation resulted in elevation of vascular resistance. At high levels of pulmonary blood flow and pulmonary arterial pressure, the flow resistance curve is lower than at low levels of blood flow. The resistance values obtained during deflation of the lung were consistently different at equal transpulmonary pressures from those obtained during inflation. The possible reasons for this hysteresis are discussed. Evidence is presented that the increased resistance at high levels of lung inflation is due to the effect of transpulmonary pressure on the vessels surrounding the alveoli. Submitted on January 11, 1960

Effect of chronic cigarette smoke exposure on pulmonary vasomotion in beagle dogs

1985 ◽  
Vol 59 (6) ◽  
pp. 1815-1822 ◽  
Author(s):  
T. S. Hakim ◽  
M. King ◽  
C. G. Wang ◽  
M. Cosio
Keyword(s):  
Cigarette Smoke ◽  
Vascular Resistance ◽  
Pressor Response ◽  
Venous Occlusion ◽  
Smoke Exposure ◽  
Longitudinal Distribution ◽  
Cigarette Smoke Exposure ◽  
Pulmonary Vasculature ◽  
Control Group ◽  
Prostaglandin F2 Alpha

To study the effect of chronic cigarette smoke exposure on the resistive properties of the pulmonary vasculature, left lower lobes from 12 control beagles and 6 beagles who had smoked cigarettes (50 cigarettes/wk for 40 wk) were perfused in situ to measure the vascular pressure-flow relationship and the resistance of the three vascular segments with the arterial and venous occlusion technique. In control subjects the vascular resistance in the arterial, middle, and venous segments was 23, 36, and 41% of the total, respectively. The segmental distribution of vascular resistance was not significantly different in the cigarette smoke-exposed dogs, despite the fact that the absolute values were 30–40% less than that of the control group. The longitudinal distribution of resistance among the three vascular segments and their response to drugs were different in beagles than was previously found in mongrels. In all beagles the veins were considerably more reactive than arteries. Vasoconstriction with serotonin (5-HT) prostaglandin F2 alpha (PGF2 alpha), norepinephrine, histamine, and methacholine (M) infusion occurred predominantly in the veins. The effect of PGF2 alpha and 5-HT was totally different than that previously observed in mongrels in which the constriction was predominantly in the arteries. Chronic cigarette smoking reduced the basal pulmonary vascular resistance and attenuated the venoconstrictor response to 5-HT and M but potentiated the hypoxic pressor response of the microvessels.

Effect of inflation on microvascular pressures in lungs of young rabbits

1987 ◽  
Vol 252 (1) ◽  
pp. H80-H84 ◽  
Author(s):  
J. U. Raj ◽  
P. Chen ◽  
L. Navazo
Keyword(s):  
Vascular Resistance ◽  
Lung Volume ◽  
Total Lung Capacity ◽  
Important Variable ◽  
Longitudinal Distribution ◽  
Positive Pressure ◽  
Lung Inflation ◽  
Lung Capacity ◽  
Pulmonary Arterial ◽  
Lung Blood Flow

We have examined the effect of positive pressure inflation on the longitudinal distribution of vascular resistance and intravascular pressures in isolated blood-perfused lungs of 3- to 4-wk-old rabbits. Lungs were perfused in zone 3 at airway inflation pressures (P airway) of 6, 14, and 19 cmH2O (pleural pressure, atmospheric) corresponding to 60, 80, and 90% of total lung capacity. We measured microvascular pressures by the micropipette servo-nulling technique in 20- to 50-microns diameter subpleural arterioles and venules. Pulmonary arterial and left atrial pressures were also measured. Lung blood flow was kept constant at 145 +/- 18 ml X kg body wt-1 X min-1. We found that at P airway of 6 cmH2O, approximately 55% of the total pressure drop was in arteries, approximately 23% in microvessels, and approximately 22% in veins. With increasing P airway and lung volume, there was a significant decrease in arterial and venous resistance, but an increase in resistance in microvessels. We conclude that lung inflation significantly alters the distribution of segmental vascular resistance, and therefore lung volume is an important variable that should be considered during estimation of capillary filtration pressure.

Sexual dimorphism in regional blood flow responses to vasopressin in conscious rats

1997 ◽  
Vol 273 (3) ◽  
pp. R1126-R1131 ◽  
Author(s):  
Y. X. Wang ◽  
J. T. Crofton ◽  
S. L. Bealer ◽  
L. Share
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Regional Blood Flow ◽  
Pressor Response ◽  
Peripheral Resistance ◽  
Female Rats ◽  
Sexually Dimorphic ◽  
Arterial Blood ◽  
Vasoconstrictor Response ◽  
Renal Vascular

The greater pressor response to vasopressin in male than in nonestrous female rats results from a greater increase in total peripheral resistance in males. The present study was performed to identify the vascular beds that contribute to this difference. Mean arterial blood pressure (MABP) and changes in blood flow in the mesenteric and renal arteries and terminal aorta were measured in conscious male and nonestrous female rats 3 h after surgery. Graded intravenous infusions of vasopressin induced greater increases in MABP and mesenteric vascular resistance and a greater decrease in mesenteric blood flow in males. Vasopressin also increased renal vascular resistance to a greater extent in males. Because renal blood flow remained unchanged, this difference may be due to autoregulation. The vasopressin-induced reduction in blood flow and increased resistance in the hindquarters were moderate and did not differ between sexes. Thus the greater vasoconstrictor response to vasopressin in the mesenteric vascular bed of male than nonestrous females contributed importantly to the sexually dimorphic pressor response to vasopressin in these experiments.

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