Effect of surface tension on circulation in the excised lungs of dogs

1964 ◽  
Vol 19 (4) ◽  
pp. 707-712 ◽  
Author(s):  
I. Bruderman ◽  
K. Somers ◽  
W. K. Hamilton ◽  
W. H. Tooley ◽  
J. Butler
Keyword(s):  
Surface Tension ◽  
Arterial Pressure ◽  
Pulmonary Vascular Resistance ◽  
Lung Volume ◽  
Pulmonary Circulation ◽  
Pulmonary Arterial Pressure ◽  
Alveolar Pressure ◽  
Pulmonary Arterial ◽  
Air Liquid Interface ◽  
Effect Of Surface

The hypothesis that the surface tension of the fluid film which lines the lung alveoli reduces the pericapillary pressure in air-filled lungs was tested by perfusing the excised lungs of dogs with saline, 6% dextran in saline, and blood. After almost maximal inflation with air from low volumes or the degassed state (inflation state) the pulmonary arterial pressure, relative to the base of the lungs, was lower than the alveolar pressure with flows up to 50 ml/min. It was higher than the alveolar pressure at any flow when the air-liquid interface had been abolished by filling the lungs to the same volume with fluid. The pulmonary arterial pressure at the same flow and alveolar pressure was lower in the inflation state than after deflation from higher volumes (the deflation state). However, lung volume was larger in the deflation state. The possibility of some low resistance channels in the inflation state could not be excluded. However, histological examinations showed that the alveolar capillaries were patent and failed to show any airless lung. pulmonary circulation; pericapillary pressure in lungs; surface tension and pulmonary vascular resistance Submitted on July 29, 1963

Pregnancy blunts pulmonary vascular reactivity in dogs

1980 ◽  
Vol 239 (3) ◽  
pp. H297-H301 ◽  
Author(s):  
L. G. Moore ◽  
J. T. Reeves
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Circulation ◽  
Vascular Reactivity ◽  
Pulmonary Arterial Pressure ◽  
Acute Hypoxia ◽  
Limited Data ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Arterial

Pregnancy decreases systemic vascular reactivity but comparatively little is known about the effects of pregnancy on the pulmonary circulation. Pulmonary vascular resistance (PVR) during acute hypoxia was lower (P < 0.01) in eight intact anesthetized pregnant dogs compared to the same animals postpartum. Mean pulmonary arterial pressure (Ppa) and PVR during infusion of prostaglandin (PG) F2 alpha were also reduced during pregnancy. Nonpregnant female dogs (n = 5) treated with estrogen (0.001 mg x kg-1 x da-1) for 2 wk had decreased Ppa (P < 0.01) during acute hypoxia compared to control measurements, but PVR was unchanged during hypoxia and PGF2 alpha infusion. Treatment with progesterone in four dogs had no effect on pulmonary vascular reactivity to hypoxia or PGF2 alpha. Inhibition of circulating PG with meclofenamate in four dogs during pregnancy did not appear to restore pulmonary vascular reactivity. Blunted pulmonary vascular reactivity is suggested by the limited data available for women, but is not seen in pregnant cows. We conclude that pregnancy decreases pulmonary as well as systemic vascular reactivity in the dog, but the mechanism is unclear.

Effects of lung volume and alveolar surface tension on pulmonary vascular resistance

1987 ◽  
Vol 62 (4) ◽  
pp. 1622-1626 ◽  
Author(s):  
R. Y. Sun ◽  
G. F. Nieman ◽  
T. S. Hakim ◽  
H. K. Chang
Keyword(s):  
Surface Tension ◽  
Lung Volume ◽  
Pulmonary Arterial Pressure ◽  
Lower Lobe ◽  
Venous Occlusion ◽  
Alveolar Pressure ◽  
Lung Inflation ◽  
Occlusion Technique ◽  
Pulmonary Arterial ◽  
Alveolar Surface

Utilizing the arterial and venous occlusion technique, the effects of lung inflation and deflation on the resistance of alveolar and extraalveolar vessels were measured in the dog in an isolated left lower lobe preparation. The lobe was inflated and deflated slowly (45 s) at constant speed. Two volumes at equal alveolar pressure (Palv = 9.9 +/- 0.6 mmHg) and two pressures (13.8 +/- 0.8 mmHg, inflation; 4.8 +/- 0.5 mmHg, deflation) at equal volumes during inflation and deflation were studied. The total vascular pressure drop was divided into three segments: arterial (delta Pa), middle (delta Pm), and venous (delta Pv). During inflation and deflation the changes in pulmonary arterial pressure were primarily due to changes in the resistance of the alveolar vessels. At equal Palv (9.9 mmHg), delta Pm was 10.3 +/- 1.2 mmHg during deflation compared with 6.8 +/- 1.1 mmHg during inflation. At equal lung volume, delta Pm was 10.2 +/- 1.5 mmHg during inflation (Palv = 13.8 mmHg) and 5.0 +/- 0.7 mmHg during deflation (Palv = 4.8 mmHg). These measurements suggest that the alveolar pressure was transmitted more effectively to the alveolar vessels during deflation due to a lower alveolar surface tension. It was estimated that at midlung volume, the perimicrovascular pressure was 3.5–3.8 mmHg greater during deflation than during inflation.

Effects of Hemoglobin on Pulmonary Arterial Pressure and Pulmonary Vascular Resistance in Patients with Chronic Emphysema

Respiration ◽  
2000 ◽  
Vol 67 (5) ◽  
pp. 502-506 ◽  
Author(s):  
Akira Nakamura ◽  
Norio Kasamatsu ◽  
Ikko Hashizume ◽  
Takushi Shirai ◽  
Suguru Hanzawa ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Arterial Pressure ◽  
Pulmonary Arterial

PULMONARY VASCULAR ADJUSTMENTS IN THE NEONATAL PERIOD

PEDIATRICS ◽  
1961 ◽  
Vol 28 (1) ◽  
pp. 28-34 ◽  
Author(s):  
Abraham M. Rudolph ◽  
Peter A. M. Auld ◽  
Richard J. Golinko ◽  
Milton H. Paul
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Circulation ◽  
Neonatal Period ◽  
Pulmonary Arterial Pressure ◽  
Systolic Pressure ◽  
Indwelling Catheters ◽  
Pulmonary Vessels ◽  
Pulmonary Arterial ◽  
Unanesthetized Animals ◽  
Young Puppy

Pulmonary arterial or right ventricular pressures were measured repeatedly in 18 puppies and 2 goats, from 1 to 36 days of age; these pressures were measured with the use of indwelling catheters in unanesthetized animals. In puppies the systolic pressure in the pulmonary circulation decreased rapidly to near adult levels in 5 to 10 days after birth, and then more slowly to adult levels by 5 to 6 weeks of age. In goats the pressures decreased more slowly, reaching near adult levels in about 12 to 14 days. Acetylcholine produced a decrease in pulmonary arterial pressure in the puppy in the first 5 days of life, but an increase in pulmonary pressure after that time in the resting animal. In the hypoxic puppy, a reduction in pulmonary arterial pressure was induced by acetylcholine. These findings suggest that the pulmonary vessels in the young puppy are actively constricted but that relaxation occurs after the first few days of life.

Low exercise pulmonary resistance is not dependent on vasodilator prostaglandins

1983 ◽  
Vol 55 (2) ◽  
pp. 558-561 ◽  
Author(s):  
J. Lindenfeld ◽  
J. T. Reeves ◽  
L. D. Horwitz
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Arterial Pressure ◽  
Cyclooxygenase Inhibitors ◽  
Pulmonary Resistance ◽  
Before And After ◽  
Pulmonary Arterial

In resting conscious dogs, administration of cyclooxygenase inhibitors results in modest increases in pulmonary arterial pressure and pulmonary vascular resistance, suggesting that vasodilator prostaglandins play a role in maintaining the low vascular resistance in the pulmonary bed. To assess the role of these vasodilator prostaglandins on pulmonary vascular resistance during exercise, we studied seven mongrel dogs at rest and during exercise before and after intravenous meclofenamate (5 mg/kg). Following meclofenamate, pulmonary vascular resistance rose both at rest (250 24 vs. 300 +/- 27 dyn . s . cm-5, P less than 0.01) and with exercise (190 +/- 9 vs. 210 +/- 12 dyn . s . cm-5, P less than 0.05). Systemic vascular resistance rose slightly following meclofenamate both at rest and during exercise. There were no changes in cardiac output. The effects of cyclooxygenase inhibition, although significant, were less during exercise than at rest. This suggests that the normal fall in pulmonary vascular resistance during exercise depends largely on factors other than vasodilator prostaglandins.

Pulmonary vascular reactivity and hemodynamic changes in elastase-induced emphysema in hamsters

1992 ◽  
Vol 73 (4) ◽  
pp. 1474-1480 ◽  
Author(s):  
C. M. Tseng ◽  
S. Qian ◽  
W. Mitzner
Keyword(s):  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Right Ventricular ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Ventricular Hypertrophy ◽  
Vascular Reactivity ◽  
Pulmonary Arterial Pressure ◽  
Pressor Responses ◽  
Pulmonary Arterial

Changes in pulmonary hemodynamics and vascular reactivity in emphysematous hamsters were studied in an isolated lung preparation perfused at constant flow with blood and 3% dextran. Hamsters were treated with intratracheal porcine pancreatic elastase at 70 days of age, and experimental studies were conducted at 1, 3, and 8 mo after treatment. Baseline pulmonary arterial pressure in elastase-treated lungs was increased compared with saline-treated control lungs 1 mo after treatment, but this increase did not progress at 3 and 8 mo. Increases in pulmonary arterial pressure in elastase-treated lungs were temporally correlated with the morphological development of emphysema and right ventricular hypertrophy; both of these were evident at 1 mo after treatment and showed little change thereafter. Pressor responses to hypoxia and angiotensin II were not different between elastase-treated and control lungs at 1 and 3 mo. At 8 mo, however, pressor responses in emphysematous lungs to 0% O2 (but not to angiotensin II) were significantly increased. This was the result of a lack of the normal age-related fall in the hypoxic pressor response. Our results suggest that the right ventricular hypertrophy found in these emphysematous animals results from a chronically increased pulmonary vascular resistance. Furthermore, increases in pulmonary vascular resistance in the early development of emphysema are likely a result of the loss of vascular beds and supporting connective tissue.

Distribution of lung vascular resistance after chronic systemic-to-pulmonary shunts

1985 ◽  
Vol 249 (6) ◽  
pp. H1106-H1113 ◽  
Author(s):  
R. P. Michel ◽  
T. S. Hakim ◽  
R. E. Hanson ◽  
A. R. Dobell ◽  
F. Keith ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Vascular Resistance ◽  
Pulmonary Circulation ◽  
Pulmonary Arterial Pressure ◽  
Lower Lobe ◽  
Venous Occlusion ◽  
Morphometric Measurements ◽  
Arterial Resistance ◽  
Pulmonary Arterial ◽  
The Right

Congenital cardiac shunts produce pathological lesions on the arterial side of the lung vasculature. We examined the effects of chronic shunts (14.2 +/- 1.2 mo) in 10 young dogs, between the left subclavian and the left lower lobe (LLL) artery, on pulmonary vascular pressure and flow (P-Q) relationships, segmental resistance with arterial and venous occlusion (AVO), and sensitivity to drugs. At final thoracotomy, mean LLL pulmonary arterial pressure (Ppa) was 23.2 +/- 4.3 mmHg compared with 11.9 +/- 0.9 in the right lung (P less than 0.05); two animals had LLL Ppa of 41 and 48 mmHg. The LLL artery and vein were cannulated, and pressure-flow (P-Q) and AVO measurements were made and compared with previous control LLL (n = 11) and contralateral right lower lobe (RLL, n = 5). Responses to serotonin, histamine, and vasodilators (diltiazem and isoproterenol) were evaluated. Comparisons of morphometric measurements were made between LLL and RLL. We found a significant increase in arterial resistance as measured with AVO and a hypersensitivity to serotonin in the shunt LLL, without changes in total pulmonary vascular resistance or P-Q measurements; vasodilators had a small effect only in the hypertensive lobes. Our data suggest that chronic shunts to the pulmonary circulation increase arterial resistance and sensitivity to serotonin, even in the absence of discernible morphometric changes, and that vasoconstriction may be an important precursor to the development of morphological lesions.

Hyperventilation, alkalosis, prostaglandins, and pulmonary circulation of the newborn

1986 ◽  
Vol 61 (6) ◽  
pp. 2088-2094 ◽  
Author(s):  
F. C. Morin
Keyword(s):  
Carbon Dioxide ◽  
Arterial Pressure ◽  
Pulmonary Circulation ◽  
Pulmonary Arterial Pressure ◽  
Respiratory Alkalosis ◽  
Newborn Lamb ◽  
Mechanical Factors ◽  
Pulmonary Arterial ◽  
Carbon Dioxide Co2 ◽  
Normal Ventilation

This study was designed to determine whether the effects of hyperventilation on the pulmonary circulation of the newborn lamb were 1) due to mechanical factors or to respiratory alkalosis; and 2) mediated by prostaglandins. Six control lambs were studied during normal ventilation and during hyperventilation with, and without, decreased carbon dioxide (CO2). Five lambs were given indomethacin and studied similarly. In control lambs, hyperventilation with decreased CO2 decreased pulmonary arterial pressure from 26 +/- 2.2 to 18 +/- 1.0 (SE) Torr (P less than or equal to 0.005) and pulmonary vascular resistance from 0.099 +/- 0.035 to 0.070 +/- 0.011 Torr X kg-1 X min-1 (P less than or equal to 0.015). Hyperventilation with normal CO2 did not affect the pulmonary circulation. Hyperventilation with decreased CO2 increased pulmonary arterial concentrations of 6-ketoprostaglandin F1 alpha, a major metabolite of prostacyclin, in control lambs but not in the indomethacin-treated lambs. However, it affected the pulmonary circulation of the control- and indomethacin-treated lambs similarly. In conclusion, hyperventilation affected the pulmonary circulation by respiratory alkalosis not by mechanical factors and prostaglandins did not mediate its effects.

Effects of lung inflation on pulmonary arterial blood volume in intact dogs

1975 ◽  
Vol 38 (4) ◽  
pp. 675-680 ◽  
Author(s):  
A. Wanner ◽  
S. Zarzecki ◽  
M. A. Sackner
Keyword(s):  
Arterial Pressure ◽  
Blood Volume ◽  
Lung Volume ◽  
Pulmonary Arterial Pressure ◽  
Valsalva Maneuver ◽  
Lung Inflation ◽  
Arterial Blood ◽  
Mueller Maneuver ◽  
Pulmonary Arterial ◽  
Arterial Blood Volume

The isolated effects of alterations of lung inflation and transmural pulmonary arterial pressure (pressure difference between intravascular and pleural pressure) on pulmonary arterial blood volume (Vpa) were investigated in anesthetized intact dogs. Using transvenous phrenic nerve stimulation, changes in transmural pulmonary arterial pressure (Ptm) at a fixed transpulmonary pressure (Ptp) were produced by the Mueller maneuver, and increases in Ptp at relatively constant Ptm by a quasi-Valsalva maneuver. Also, both Ptm and Ptp were allowed to change during open airway lung inflation. Vpa was determined during these three maneuvers by multiplying pulmonary blood flow by pulmonary arterial mean transit time obtained by an ether plethysmographic method. During open airway lung inflation, mean (plus or minus SD) Ptp increased by 7.2 (plus or minus 3.7) cmH2O and Ptm by 4.3 (plus or minus 3.4) cmH2O for a mean increase in Vpa by 26.2 (plus or minus 10.7) ml. A pulmonary arterial compliance term (Delta Vpa/Delta Ptm) calculated from the Mueller maneuver was 3.9 ml/cmH2O and an interdependence term (Delta Vpa/Delta Ptp) calculated from the quasi-Valsalva maneuver was 2.5 ml/cmH2O for a 19% increase in lung volume, and 1.2 ml/cmH2O for an increase in lung volume from 19% to 35%. These findings indicate that in normal anesthetized dogs near FRC for a given change in Ptp and Ptm the latter results in a greater increase of Vpa.

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