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.

Effect of Norepinephrine on Circulation of the Dog in Hemorrhagic Shock

1956 ◽  
Vol 186 (1) ◽  
pp. 74-78 ◽  
Author(s):  
E. D. Frank ◽  
H. A. Frank ◽  
S. Jacob ◽  
H. A. E. Weizel ◽  
H. Korman ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Hemorrhagic Shock ◽  
Renal Blood Flow ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Arterial Pressure ◽  
Norepinephrine Infusion ◽  
Pulmonary Arterial

Norepinephrine infusion did not prolong the survival or effect the recovery of dogs in hemorrhagic shock unresponsive to replacement transfusion. During its pressor action in shock, either before or after replacement transfusion, norepinephrine infusion increased coronary, cerebral and adrenal blood flow, reduced renal blood flow, and did not change hepatic blood flow. Cardiac output was increased in oligemic shock but not after blood replacement. Pulmonary arterial pressure and right and left auricular pressures were raised by norepinephrine infusion in all phases of hemorrhagic shock, and calculated pulmonary vascular resistance was reduced.

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 pressor response after prostaglandin synthesis inhibition in conscious dogs

1982 ◽  
Vol 52 (3) ◽  
pp. 705-709 ◽  
Author(s):  
B. R. Walker ◽  
N. F. Voelkel ◽  
J. T. Reeves
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Pressor Response ◽  
Conscious Dogs ◽  
Pulmonary Pressure ◽  
Time Control ◽  
Mean Pulmonary Arterial Pressure ◽  
Before And After ◽  
Pulmonary Arterial

Recent studies have shown that vasodilator prostaglandins are continually produced by the isolated rat lung. We postulated that these vasodilators may contribute to maintenance of normal low pulmonary arterial pressure. Pulmonary pressure and cardiac output were measured in conscious dogs prior to and 30 to 60 min following administration of meclofenamate (2 mg/kg iv, followed by infusion at 2 mg . kg-1 . h-1) or the structurally dissimilar inhibitor RO–20–5720 (1 mg/kg iv, followed by infusion at 1 mg . kg-1 . h-1). The animals were also made hypoxic with inhalation of 10% O2 before and after inhibition. Time-control experiments were conducted in which only the saline vehicle was administered. Meclofenamate or RO–20–5720 caused an increase in mean pulmonary arterial pressure and total pulmonary resistance. Cardiac output and systemic pressure were unaffected. The mild hypoxic pulmonary pressor response observed was not affected by meclofenamate. Animals breathing 30% O2 to offset Denver's altitude also demonstrated increased pulmonary pressure and resistance when given meclofenamate. It is concluded that endogenous vasodilator prostaglandins may contribute to normal, low vascular tone in the pulmonary circulation.

Rho kinase and Ca2+ entry mediate increased pulmonary and systemic vascular resistance in l-NAME-treated rats

2007 ◽  
Vol 293 (5) ◽  
pp. L1306-L1313 ◽  
Author(s):  
Jasdeep S. Dhaliwal ◽  
David B. Casey ◽  
Anthony J. Greco ◽  
Adeleke M. Badejo ◽  
Thomas B. Gallen ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Arterial Pressure ◽  
Rho Kinase ◽  
Systemic Arterial Pressure ◽  
Intravenous Injections ◽  
Pulmonary Arterial ◽  
Dose Dependent

The small GTP-binding protein and its downstream effector Rho kinase play an important role in the regulation of vasoconstrictor tone. Rho kinase activation maintains increased pulmonary vascular tone and mediates the vasoconstrictor response to nitric oxide (NO) synthesis inhibition in chronically hypoxic rats and in the ovine fetal lung. However, the role of Rho kinase in mediating pulmonary vasoconstriction after NO synthesis inhibition has not been examined in the intact rat. To address this question, cardiovascular responses to the Rho kinase inhibitor fasudil were studied at baseline and after administration of an NO synthesis inhibitor. In the intact rat, intravenous injections of fasudil cause dose-dependent decreases in systemic arterial pressure, small decreases in pulmonary arterial pressure, and increases in cardiac output. l-NAME caused a significant increase in pulmonary and systemic arterial pressures and a decrease in cardiac output. The intravenous injections of fasudil after l-NAME caused dose-dependent decreases in pulmonary and systemic arterial pressure and increases in cardiac output, and the percent decreases in pulmonary arterial pressure in response to the lower doses of fasudil were greater than decreases in systemic arterial pressure. The Ca++ entry blocker isradipine also decreased pulmonary and systemic arterial pressure in l-NAME-treated rats. Infusion of sodium nitroprusside restored pulmonary arterial pressure to baseline values after administration of l-NAME. These data provide evidence in support of the hypothesis that increases in pulmonary and systemic vascular resistance following l-NAME treatment are mediated by Rho kinase and Ca++ entry through L-type channels, and that responses to l-NAME can be reversed by an NO donor.

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.

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

1994 ◽  
Vol 77 (3) ◽  
pp. 1333-1340 ◽  
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)

Hemodynamic response to hypoxia in dogs with chronic pulmonary hypertension

1964 ◽  
Vol 207 (3) ◽  
pp. 650-652 ◽  
Author(s):  
Dusan Kentera ◽  
Charles R. Wallace ◽  
William F. Hamilton ◽  
Lois T. Ellison
Keyword(s):  
Pulmonary Hypertension ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Sodium Pentobarbital ◽  
Pulmonary Resistance ◽  
Chronic Pulmonary Hypertension ◽  
Pulmonary Arterial ◽  
Clear Increase ◽  
Sodium Pentobarbital Anesthesia

Control dogs showed a clear increase in pulmonary resistance, in cardiac output, and in pulmonary arterial pressure when artifically ventilated with 10% O2 under sodium pentobarbital anesthesia. Dogs with pulmonary hypertension from Dirofilariasis showed the same increase in pulmonary arterial resistance but no statistically significant change in pulmonary arterial pressure or in cardiac output when ventilated in the same manner and under the same anesthesia. The anoxia produced a greater lowering of arterial saturation in the hypertensive dogs but this is not enough to explain the clear differences in the response of cardiac output and pulmonary arterial pressure to the anoxic stimulus. It is hypothesized that failure of blood flow and pressure to increase significantly in the hypertensive animals is due to the inability of the chronically overloaded heart to increase its performance in response to anoxia and the accompanying sympathetic stimulation.

Cardiorespiratory Disturbances Associated with Infective Fever in Man: Studies of Ethiopian Louse-Borne Relapsing Fever

1970 ◽  
Vol 39 (1) ◽  
pp. 123-145 ◽  
Author(s):  
D. A. Warrell ◽  
Helen M. Pope ◽  
E. H. O. Parry ◽  
P. L. Perine ◽  
A.D.M. Bryceson
Keyword(s):  
Cardiac Output ◽  
Body Temperature ◽  
Arterial Pressure ◽  
Metabolic Rate ◽  
Vascular Resistance ◽  
Pulmonary Arterial Pressure ◽  
Pulmonary Ventilation ◽  
Systemic Arterial Pressure ◽  
Relapsing Fever ◽  
Pulmonary Arterial

1. Nineteen patients with louse-borne relapsing fever were studied in Addis Abeba (altitude 2285 m). 2. Following treatment with tetracycline a febrile Jarisch—Herxheimer-like reaction developed which showed the phases described in artificially-induced endotoxin fever. 3. During the chill phase body temperature, metabolic rate and pulmonary ventilation increased. Despite alveolar hyperventilation pulmonary venous admixture was high. Cardiac output, heart rate and systemic arterial pressure increased but pulmonary arterial pressure decreased. 4. During the flush phase systemic arterial pressure fell and remained low for many hours due to reduced vascular resistance, but pulmonary arterial pressure and inflow resistance increased. Small increases in glucose, lactate, and pyruvate concentrations were prevented by inhaling oxygen. 5. Stimulation of metabolic rate, ventilation and cardiac output during the reaction was not due simply to increased body temperature, hypoxia, or acidosis but was probably attributable to spirochaetal endotoxin. 6. Limitation of pulmonary oxygen diffusion may have been responsible for the impaired pulmonary oxygen uptake in these patients. 7. During the prolonged flush phase a greatly increased cardiac output is necessary to maintain systemic arterial pressure because of the very low vascular resistance. Prevention of extracellular fluid volume depletion, early detection and prompt treatment of cardiac failure and oxygen therapy may reduce fatalities during this critical period but hydrocortisone in large doses failed to reduce the severity of the reaction.

Pregnancy-induced pulmonary hypertension in cows susceptible to high mountain disease

1979 ◽  
Vol 46 (1) ◽  
pp. 184-188 ◽  
Author(s):  
L. G. Moore ◽  
J. T. Reeves ◽  
D. H. Will ◽  
R. F. Grover
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Vascular Reactivity ◽  
Pulmonary Arterial Pressure ◽  
Pressor Response ◽  
Acute Hypoxia ◽  
High Mountain ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Arterial

Observations in several species suggest that pulmonary vascular reactivity may be reduced during pregnancy. We tested this hypothesis in two groups of unanesthetized cows, one “susceptible” and one “resistant” to high mountain or brisket disease. At the altitude of residence (1,524 m), mean pulmonary arterial pressure was elevated during pregnancy by 18% and total pulmonary vascular resistance by 32% in susceptible but not in resistant cows. During acute exposure to simulated altitudes of 2,120--4,550 m, pulmonary arterial pressure was increased by 16% and total pulmonary resistance by 28% during pregnancy in susceptible cows. The pulmonary pressor response to a 5 microgram/kg bolus of prostaglandin FIalpha was not different during pregnancy in either group. Resistant cows hyperventilated while pregnant, raising arterial partial pressure of oxygen (PaO2) by 6 Torr both at 1,524 m and, on the average, by 7 Torr at altitudes of 2,120--4,550 m. Susceptible cows increased their PaO2 less than did the resistant cows during pregnancy. The results indicated that pregnancy was associated with a greater rise in pulmonary arterial pressure and total pulmonary vascular resistance during acute hypoxia and failed to elicit as great a ventilatory response in susceptible than in resistant cows.

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