Changes in Pulmonary Arterial Pressure and Pulmonary Vascular Resistance after Mitral Valve Replacement

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.

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

Journal of Applied Physiology ◽

10.1152/jappl.1992.73.4.1474 ◽

1992 ◽

Vol 73 (4) ◽

pp. 1474-1480 ◽

Cited By ~ 3

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.

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Pregnancy blunts pulmonary vascular reactivity in dogs

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1980.239.3.h297 ◽

1980 ◽

Vol 239 (3) ◽

pp. H297-H301 ◽

Cited By ~ 5

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.

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Effects of ONO-5046, a specific neutrophil elastase inhibitor, on endotoxin-induced lung injury in sheep

Journal of Applied Physiology ◽

10.1152/jappl.1994.77.3.1333 ◽

1994 ◽

Vol 77 (3) ◽

pp. 1333-1340 ◽

Cited By ~ 44

Author(s):

K. Kubo ◽

T. Kobayashi ◽

T. Hayano ◽

T. Koizumi ◽

T. Honda ◽

...

Keyword(s):

Lung Injury ◽

Arterial Pressure ◽

Pulmonary Vascular Resistance ◽

Vascular Resistance ◽

Neutrophil Elastase ◽

Pulmonary Arterial Pressure ◽

Pulmonary Vascular Permeability ◽

Lung Dysfunction ◽

Pulmonary Arterial ◽

Lung Lymph

The purpose of the present study was to assess the role of polymorphonuclear leukocyte (neutrophil) elastase in endotoxin-induced acute lung injury in sheep with lung lymph fistula. We studied the effects of ONO-5046, a specific inhibitor of neutrophil elastase, on the lung dysfunction induced by the intravenous infusion of 1 microgram/kg of Escherichia coli endotoxin. Endotoxin alone produced a biphasic response as previously reported. Early (0.5–1 h) after endotoxin, pulmonary arterial pressure increased from 19.5 +/- 0.9 cmH2O at baseline to a peak of 46.8 +/- 2.4 cmH2O (P > 0.05). Pulmonary vascular resistance increased from 3.03 +/- 0.17 cmH2O.l–1.min at baseline to a peak of 9.77 +/- 0.70 cmH2O.l–1.min (P < 0.05). Circulating neutrophils decreased from 7,355 +/- 434/mm3 at baseline to a nadir of 1,762 +/- 32/mm3 (P < 0.05). Thromboxane B2 and 6-ketoprostaglandin F1 alpha concentrations in plasma and lung lymph were significantly increased. Late (3–5 h) after endotoxin, pulmonary arterial pressure and pulmonary vascular resistance returned to baseline levels, but lung lymph flow remained increased from 4.2 +/- 0.3 ml/0.5 h at baseline to 7.3 +/- 0.7 ml/0.5 h (P < 0.05), with a slight increase in lung lymph-to-plasma protein concentration ratio, suggesting increased pulmonary vascular permeability. The histopathological features of the lungs during the early period in sheep treated with endotoxin alone revealed a large increase in neutrophils per 100 alveoli and changes of pulmonary edema such as thickening of the interstitium of the lung and alveolar flooding.(ABSTRACT TRUNCATED AT 250 WORDS)

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