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Robert Naeije - One of the best experts on this subject based on the ideXlab platform.
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exercise stress echocardiography of the Pulmonary circulation and right ventricular arterial coupling in healthy adolescents
European Journal of Echocardiography, 2020Co-Authors: Yoshiki Motoji, Kevin Forton, Sergio Caravita, Vitalie Faoro, Robert NaeijeAbstract:AIMS : To explore the effects of age and sex in adolescents vs. young or middle-aged adults on Pulmonary Vascular function and right ventricular-arterial (RV-PA) coupling as assessed by exercise stress echocardiography. METHODS AND RESULTS : Forty healthy adolescents aged 12-15 years were compared with 40 young adults aged 17-22 years and 40 middle-aged adults aged 30-50 years. Sex distribution was equal in the three groups. All the subjects underwent an exercise stress echocardiography. A Pulmonary Vascular distensibility coefficient α was determined from multipoint Pulmonary Vascular Pressure-flow relationships. RV-PA coupling was assessed by the tricuspid annular plane systolic excursion (TAPSE) to systolic Pulmonary artery Pressure (PASP) ratio, who has been previously validated by invasive study. While cardiac index and mean PAP were not different, adolescents compared to young and middle-aged adults, respectively had higher Pulmonary Vascular distensibility coefficients α (1.60 ± 0.31%/mmHg vs. 1.39 ± 0.29%/mmHg vs. 1.20 ± 0.35%/mmHg, P < 0.00001). Adolescents and young adults compared to middle-aged adults, respectively had higher TAPSE/PASP ratios at rest (1.24 ± 0.18 mm/mmHg and 1.22 ± 0.17 mm/mmHg vs. 1.07 ± 0.18 mm/mmHg, P < 0.008) and during exercise (0.86 ± 0.24, 0.80 ± 0.15 and 0.72 ± 0.15 mm/mmHg, P < 0.04). The TAPSE/PASP ratio decreased with exercise. There were no sex differences in α or TAPSE/PASP. CONCLUSION : Compared to adults, adolescents present with a sex-independent more distensible Pulmonary circulation. Resting and exercise RV-PA coupling is decreased in middle-aged adults.
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effects of body position on exercise capacity and Pulmonary Vascular Pressure flow relationships
Journal of Applied Physiology, 2016Co-Authors: Kevin Forton, Robert Naeije, Yoshiki Motoji, Vitalie Faoro, Gael DeboeckAbstract:Body position does not affect exercise stress echocardiography of the Pulmonary circulation or aerobic exercise capacity as measured by a maximum oxygen uptake. However, the semirecumbent position ...
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exercise capacity and Pulmonary Vascular Pressure flow relationshipsin different body positions
European Respiratory Journal, 2016Co-Authors: Yoshiki Motoji, Robert Naeije, Kevin Forton, Vitalie Faoro, Gael DeboeckAbstract:Background: There has been recent revival of interest in exercise testing of the Pulmonary circulation for the diagnosis of Pulmonary Vascular disease, but whether body position affects the results remains uncertain. Aims: The aim of this study is to compare the Pulmonary circulation during exercise in different body positions. Methods: Twenty-six healthy volunteers (13 women) performed a cardioPulmonary exercise tests with echocardiography. Mean Pulmonary artery Pressure (mPAP) and cardiac output (CO) were estimated at rest and during exercise in upright, semi-recumbent and supine positions. Results: At maximum workload, oxygen uptake (43 ± 10 vs 43 ± 10 vs 42 ± 9 ml/kg / min, respectively), respiratory exchange ratio, ventilatory equivalent for carbon dioxide were not significantly different among 3 body positions. Similarly, mPAP, CO, mPAP-CO slope and total Pulmonary Vascular resistance (TPR) were similar. However, the maximum workload was 10% decreased in semi-recumbent position. Furthermore, CO-workload or CO-VO 2 relationships were nonlinear and too variable for a reliable prediction of CO. Conclusions: These results suggest that body position does not affect mPAP, CO, mPAP-CO slope, TPR or VO 2 at maximum exercise. Maximum workload is low in semi-recumbent as compared to upright exercise, and workload or VO 2 cannot be reliable as surrogates for CO at higher work load.
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reading Pulmonary Vascular Pressure tracings how to handle the problems of zero leveling and respiratory swings
American Journal of Respiratory and Critical Care Medicine, 2014Co-Authors: Gabor Kovacs, Robert Naeije, Alexander Avian, Michael Pienn, Horst OlschewskiAbstract:The accuracy of Pulmonary Vascular Pressure measurements is of great diagnostic and prognostic relevance. However, there is variability of zero leveling procedures, and the current recommendation of end-expiratory reading may not always be adequate. A review of physiological and anatomical data, supported by recent imaging, leads to the practical recommendation of zero leveling at the cross-section of three transthoracic planes, which are, respectively midchest frontal, transverse through the fourth intercostal space, and midsagittal. As for the inevitable respiratory Pressure swings, end-expiratory reading at functional residual capacity allows for minimal influence of elastic lung recoil on Pulmonary Pressure reading. However, hyperventilation is associated with changes in end-expiratory lung volume and increased intrathoracic Pressure, eventually exacerbated by expiratory muscle contraction and dynamic hyperinflation, all increasing Pulmonary Vascular Pressures. This problem is amplified in patients with obstructed airways. With the exception of dynamic hyperinflation states, it is reasonable to assume that negative inspiratory and positive expiratory intrathoracic Pressures cancel each other out, so averaging Pulmonary Vascular Pressures over several respiratory cycles is most often preferable. This recommendation may be generalized for the purpose of consistency and makes sense, as Pulmonary blood flow measurements are not corrected for phasic inspiratory and expiratory changes in clinical practice.
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Pulmonary circulation at exercise
Comprehensive Physiology, 2012Co-Authors: Robert Naeije, Naomi C CheslerAbstract:The Pulmonary circulation is a high-flow and low-Pressure circuit, with an average resistance of 1 mmHg/min/L in young adults, increasing to 2.5 mmHg/min/L over four to six decades of life. Pulmonary Vascular mechanics at exercise are best described by distensible models. Exercise does not appear to affect the time constant of the Pulmonary circulation or the longitudinal distribution of resistances. Very high flows are associated with high capillary Pressures, up to a 20 to 25 mmHg threshold associated with interstitial lung edema and altered ventilation/perfusion relationships. Pulmonary artery Pressures of 40 to 50 mmHg, which can be achieved at maximal exercise, may correspond to the extreme of tolerable right ventricular afterload. Distension of capillaries that decrease resistance may be of adaptative value during exercise, but this is limited by hypoxemia from altered diffusion/perfusion relationships. Exercise in hypoxia is associated with higher Pulmonary Vascular Pressures and lower maximal cardiac output, with increased likelihood of right ventricular function limitation and altered gas exchange by interstitial lung edema. Pharmacological interventions aimed at the reduction of Pulmonary Vascular tone have little effect on Pulmonary Vascular Pressure-flow relationships in normoxia, but may decrease resistance in hypoxia, unloading the right ventricle and thereby improving exercise capacity. Exercise in patients with Pulmonary hypertension is associated with sharp increases in Pulmonary artery Pressure and a right ventricular limitation of aerobic capacity. Exercise stress testing to determine multipoint Pulmonary Vascular Pressures-flow relationships may uncover early stage Pulmonary Vascular disease.
Paul A Murray - One of the best experts on this subject based on the ideXlab platform.
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attenuated hypoxic Pulmonary vasoconstriction during isoflurane anesthesia is abolished by cyclooxygenase inhibition in chronically instrumented dogs
Anesthesiology, 1996Co-Authors: Paul F Lennon, Paul A MurrayAbstract:BACKGROUND: Hypoxic Pulmonary vasoconstriction (HPV) is a homeostatic mechanism whereby gas exchange is improved through the diversion of blood flow away from poorly oxygenated regions of the lung. The effect of isoflurane anesthesia on HPV is unclear. Using a chronically instrumented canine model, it was hypothesized that isoflurane anesthesia would attenuate HPV compared to the response measured in the same animal in the conscious state. Moreover, because volatile anesthetics increase the production of cyclooxygenase metabolites, it was hypothesized that attenuation of HPV during isoflurane anesthesia would be abolished by cyclooxygenase inhibition. METHODS: Left Pulmonary Vascular Pressure-flow plots were generated in chronically instrumented dose by measuring the Pulmonary Vascular Pressure gradient (Pulmonary arterial Pressure-left atrial Pressure) and left Pulmonary blood flow during inflation of a hydraulic occluder implanted around the right main Pulmonary artery. In protocol 1 (n - 7), left Pulmonary Vascular Pressure-flow plots were generated during normoxia and hypoxia (systemic arterial PO2 approximately 50 mmHg) in the conscious and isoflurane-anesthetized states. In protocol 2 (n = 7), left Pulmonary Vascular Pressure-flow plots were generated during normoxia and hypoxia (1) in the conscious state, (2) in the conscious state after inhibition of the cyclooxygenase pathway with indomethacin, and (3) during isoflurane anesthesia after cyclooxygenase inhibition. RESULTS: In both the conscious and isoflurane-anesthetized states, the magnitude of HPV was dependent on the level of left Pulmonary blood flow. Compared to the response measured in the conscious state, the magnitude of HPV was attenuated during isoflurane anesthesia over the empirically measured range of left Pulmonary blood flow. Cyclooxygenase inhibition abolished the isoflurane-induced attenuation of HPV. CONCLUSIONS: This is the first study to demonstrate that isoflurane anesthesia attenuates the magnitude of HPV compared to the response measured in the same animal in the conscious state. Cyclooxygenase inhibition potentiated the magnitude of HPV in both the conscious and isoflurane-anesthetized states, which indicates that vasodilator metabolites of the cyclooxygenase pathways modulate HPV under these conditions. Importantly, the finding that the magnitude of HPV is flow-dependent in both the conscious and isoflurane-anesthetized states may explain conflicting reports in the literature concerning the effects of isoflurane anesthesia on the HPV response.
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isoflurane and the Pulmonary Vascular Pressure flow relation at baseline and during sympathetic α and β adrenoreceptor activation in chronically instrumented dogs
Anesthesiology, 1995Co-Authors: Paul F Lennon, Paul A MurrayAbstract:BACKGROUND The extent to which isoflurane anesthesia alters systemic Vascular regulation has received considerable attention. In contrast, the Pulmonary Vascular effects of isoflurane have not been elucidated. Our initial objective was to investigate the net effect of isoflurane on the baseline left Pulmonary Vascular Pressure-flow (LPQ) relation compared with values measured in the conscious state. In addition, we assessed the extent to which isoflurane alters the Pulmonary Vascular responses to sympathetic alpha- and beta-adrenoreceptor activation. METHODS Twelve conditioned mongrel dogs were chronically instrumented to measure the LPQ relation. LPQ plots were generated by continuously measuring the Pulmonary Vascular Pressure gradient (Pulmonary arterial Pressure--left atrial Pressure) and left Pulmonary blood flow during gradual (approximately 1 min) inflation of a hydraulic occluder implanted around the right main Pulmonary artery. LPQ plots were generated at baseline in the conscious and isoflurane-anesthetized states (n = 12). The Pulmonary Vascular dose-response relation to the sympathetic alpha-adrenoreceptor agonist phenylephrine also was investigated in conscious and isoflurane-anesthetized dogs (n = 6). Finally, after preconstriction with the thromboxane analogue U46619, the dose-response relation to the sympathetic beta-adrenoreceptor agonist isoproterenol was assessed in the conscious and isoflurane-anesthetized states (n = 8). RESULTS Compared with values measured in the conscious state, isoflurane anesthesia had no net effect on the baseline LPQ relation. The magnitude of the Pulmonary vasoconstrictor response to phenylephrine observed in conscious dogs was not altered during isoflurane anesthesia. In contrast, the Pulmonary vasodilator response to isoproterenol was markedly potentiated (P < 0.01) during isoflurane anesthesia compared with that in the conscious state. CONCLUSIONS These results indicate that isoflurane does not exert a net vasodilator influence on the Pulmonary circulation at baseline. In contrast to the systemic circulation, the Pulmonary vasoconstrictor response to sympathetic alpha-adrenoreceptor activation is maintained during isoflurane anesthesia. Surprisingly, the Pulmonary vasodilator response to sympathetic beta-adrenoreceptor activation is actually potentiated during isoflurane. Thus, isoflurane anesthesia has differential effects on the canine Pulmonary Vascular responses to sympathetic alpha- and beta-adrenoreceptor activation.
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amrinone and the Pulmonary Vascular Pressure flow relationship in conscious control dogs and following left lung autotransplantation
Anesthesiology, 1993Co-Authors: Daniel Nyhan, Kimitoshi Nishiwaki, Peter Rock, P M Desai, W P Peterson, Charles G Pribble, Gregory A Trempy, Paul A MurrayAbstract:Background: Amrinone, a bipyridine compound, is known to improve left ventricular function via its positive inotropic and afterload-reducing effects. The goal of this study was to assess the efficacy of amrinone as a Pulmonary vasodilator, an effect that could be beneficial in the setting of right heart failure associated with Pulmonary hypertension. Methods: investigated were the effects of intravenous amrinone (750 μg/kg loading dose plus 1-20 μg.kg -1 .min -1 maintenance dose) on the left Pulmonary Vascular Pressure-flow (LPQ) relationship in chronically instrumented, conscious dogs
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acute and chronic Pulmonary vasoconstriction after left lung autotransplantation in conscious dogs
Journal of Applied Physiology, 1992Co-Authors: Paul A Murray, Peter Rock, R S Stuart, Charles D Fraser, D M Fehr, B B Chen, P M Desai, Daniel NyhanAbstract:: We investigated the acute and chronic effects of left lung autotransplantation (LLA) on the left Pulmonary Vascular Pressure-flow (LP/Q) relationship in conscious dogs. Continuous LP/Q plots were generated in chronically instrumented conscious dogs 2 days, 2 wk, 1 mo, and 2 mo after LLA. Identically instrumented normal conscious dogs were studied at equal time points post-surgery. LLA had little or no effect on baseline systemic hemodynamics or blood gases. In contrast, compared with normal conscious dogs, striking active flow-independent Pulmonary vasoconstriction was observed 2 days post-LLA. The slope of the LP/Q relationship was increased from a normal value of 0.275 +/- 0.021 to 0.699 +/- 0.137 mmHg.ml-1.min-1.kg-1 2 days post-LLA. Pulmonary vasoconstriction of similar magnitude was also observed on a chronic basis at 2 wk, 1 mo, and even 2 mo post-LLA. Pulmonary vasoconstriction post-LLA was not due to fixed resistance at the left Pulmonary arterial or venous anastomotic sites. Finally, systemic arterial blood gases were unchanged when total Pulmonary blood flow was directed to exclusively perfuse the transplanted left lung. Thus, LLA results in both acute and chronic Pulmonary vasoconstriction in conscious dogs. LLA should serve as a useful stable experimental model to assess the specific effects of surgical transplantation on Pulmonary Vascular regulation.
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n omega nitro l arginine and Pulmonary Vascular Pressure flow relationship in conscious dogs
American Journal of Physiology-heart and Circulatory Physiology, 1992Co-Authors: Kimitoshi Nishiwaki, Daniel Nyhan, Peter Rock, P M Desai, W P Peterson, Charles G Pribble, Paul A MurrayAbstract:We investigated the effects of an inhibitor of nitric oxide (NO) synthesis, N omega-nitro-L-arginine (L-NNA), on the Pulmonary Vascular Pressure-flow relationship in chronically instrumented conscious dogs. The L-arginine analogue L-NNA (20 mg/min for 60 min iv) had no effect on the baseline Pressure-flow relationship. This result indicates that tonic release of endothelium-derived relaxing factor (EDRF), which is thought to be NO or a labile NO-generating molecule, is not responsible for low resting Pulmonary vasomotor tone in conscious dogs. In contrast, L-NNA caused a leftward shift in the dose-response relationship to the thromboxane mimetic U-46619, indicating that the endogenous release of EDRF modulates the Pulmonary Vascular response to this vasoconstrictor. Finally, after preconstriction with U-46619, L-NNA abolished the Pulmonary vasodilator response to bradykinin (1-10 micrograms.kg-1.min-1) but had no effect on the Pulmonary vasodilator response to sodium nitroprusside (1-10 micrograms.kg-1.min-1). Thus EDRF does not appear to tonically regulate the baseline Pulmonary Vascular Pressure-flow relationship in conscious dogs. However, EDRF does act to attenuate the magnitude of U-46619-induced Pulmonary vasoconstriction. Moreover, the Pulmonary vasodilator response to bradykinin is entirely mediated by EDRF in conscious dogs.
Marc Leeman - One of the best experts on this subject based on the ideXlab platform.
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inhibition of cyclooxygenase and nitric oxide synthase in hypoxic vasoconstriction and oleic acid induced lung injury
American Journal of Respiratory and Critical Care Medicine, 1999Co-Authors: Marc Leeman, Christian Melot, Valerie Zegers De Beyl, Dominique Biarent, Marco Maggiorini, Robert NaeijeAbstract:Cyclooxygenase (COX) products and nitric oxide (NO) inhibit hypoxic Pulmonary vasoconstriction (HPV), and their release could contribute to alterations in gas exchange in lung injury. We tested the hypothesis that combined blockade of COX and NO synthase (NOS) could further increase HPV and better protect gas exchange in lung injury than could blockade of either COX or NOS alone. We determined Pulmonary Vascular Pressure‐flow relationships in pentobarbital-anesthetized and ventilated dogs submitted to hypoxic challenges before and after administration of solvent (n 5 4), indomethacin alone (2 mg/kg intravenously, n 5 8), N v -nitro- L -arginine ( L -NA) alone (10 mg/kg intravenoulsy, n 5 8), indomethacin followed by L -NA (n 5 8), and L -NA followed by indomethacin (n 5 8). All of the dogs so treated then received oleic acid (0.06 ml/kg intravenously) to induce lung injury. Blood flow was manipulated by establishing a femoral arteriovenous bypass or by inflating an inferior vena caval balloon. Gas exchange was evaluated by measuring arterial P O2 and intraPulmonary shunt (using the inert gas sulfur hexafluoride) at identical cardiac outputs. The magnitude of HPV was not affected by solvent. Indomethacin and L -NA given separately enhanced HPV. L -NA added to indomethacin further enhanced HPV, as did indomethacin added to L -NA. After oleic acid‐induced lung injury, gas exchange deteriorated less in dogs pretreated with indomethacin than in dogs pretreated with solvent or with L -NA alone. These results suggest that in pentobarbital-anesthetized dogs: ( 1 ) the magnitude of HPV is limited by the corelease of COX metabolites and of NO; and ( 2 ) inhibition of COX, but not of NOS, attenuates the deterioration of gas exchange in oleic acid‐induced lung injury. Leeman M, Zegers de Beyl V, Biarent D, Maggiorini M, Melot C, Naeije R. Inhibition of cyclooxygenase and nitric oxide synthase in hypoxic vasoconstriction and oleic acid‐ induced lung injury. AM J RESPIR CRIT CARE MED 1999;159:1383‐1390.
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inhibition of cyclooxygenase and nitric oxide synthase in hypoxic vasoconstriction and oleic acid induced lung injury
American Journal of Respiratory and Critical Care Medicine, 1999Co-Authors: Marc Leeman, Christian Melot, Valerie Zegers De Beyl, Dominique Biarent, Marco Maggiorini, Robert NaeijeAbstract:Cyclooxygenase (COX) products and nitric oxide (NO) inhibit hypoxic Pulmonary vasoconstriction (HPV), and their release could contribute to alterations in gas exchange in lung injury. We tested the hypothesis that combined blockade of COX and NO synthase (NOS) could further increase HPV and better protect gas exchange in lung injury than could blockade of either COX or NOS alone. We determined Pulmonary Vascular Pressure‐flow relationships in pentobarbital-anesthetized and ventilated dogs submitted to hypoxic challenges before and after administration of solvent (n 5 4), indomethacin alone (2 mg/kg intravenously, n 5 8), N v -nitro- L -arginine ( L -NA) alone (10 mg/kg intravenoulsy, n 5 8), indomethacin followed by L -NA (n 5 8), and L -NA followed by indomethacin (n 5 8). All of the dogs so treated then received oleic acid (0.06 ml/kg intravenously) to induce lung injury. Blood flow was manipulated by establishing a femoral arteriovenous bypass or by inflating an inferior vena caval balloon. Gas exchange was evaluated by measuring arterial P O2 and intraPulmonary shunt (using the inert gas sulfur hexafluoride) at identical cardiac outputs. The magnitude of HPV was not affected by solvent. Indomethacin and L -NA given separately enhanced HPV. L -NA added to indomethacin further enhanced HPV, as did indomethacin added to L -NA. After oleic acid‐induced lung injury, gas exchange deteriorated less in dogs pretreated with indomethacin than in dogs pretreated with solvent or with L -NA alone. These results suggest that in pentobarbital-anesthetized dogs: ( 1 ) the magnitude of HPV is limited by the corelease of COX metabolites and of NO; and ( 2 ) inhibition of COX, but not of NOS, attenuates the deterioration of gas exchange in oleic acid‐induced lung injury. Leeman M, Zegers de Beyl V, Biarent D, Maggiorini M, Melot C, Naeije R. Inhibition of cyclooxygenase and nitric oxide synthase in hypoxic vasoconstriction and oleic acid‐ induced lung injury. AM J RESPIR CRIT CARE MED 1999;159:1383‐1390.
Marco Maggiorini - One of the best experts on this subject based on the ideXlab platform.
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inhibition of cyclooxygenase and nitric oxide synthase in hypoxic vasoconstriction and oleic acid induced lung injury
American Journal of Respiratory and Critical Care Medicine, 1999Co-Authors: Marc Leeman, Christian Melot, Valerie Zegers De Beyl, Dominique Biarent, Marco Maggiorini, Robert NaeijeAbstract:Cyclooxygenase (COX) products and nitric oxide (NO) inhibit hypoxic Pulmonary vasoconstriction (HPV), and their release could contribute to alterations in gas exchange in lung injury. We tested the hypothesis that combined blockade of COX and NO synthase (NOS) could further increase HPV and better protect gas exchange in lung injury than could blockade of either COX or NOS alone. We determined Pulmonary Vascular Pressure‐flow relationships in pentobarbital-anesthetized and ventilated dogs submitted to hypoxic challenges before and after administration of solvent (n 5 4), indomethacin alone (2 mg/kg intravenously, n 5 8), N v -nitro- L -arginine ( L -NA) alone (10 mg/kg intravenoulsy, n 5 8), indomethacin followed by L -NA (n 5 8), and L -NA followed by indomethacin (n 5 8). All of the dogs so treated then received oleic acid (0.06 ml/kg intravenously) to induce lung injury. Blood flow was manipulated by establishing a femoral arteriovenous bypass or by inflating an inferior vena caval balloon. Gas exchange was evaluated by measuring arterial P O2 and intraPulmonary shunt (using the inert gas sulfur hexafluoride) at identical cardiac outputs. The magnitude of HPV was not affected by solvent. Indomethacin and L -NA given separately enhanced HPV. L -NA added to indomethacin further enhanced HPV, as did indomethacin added to L -NA. After oleic acid‐induced lung injury, gas exchange deteriorated less in dogs pretreated with indomethacin than in dogs pretreated with solvent or with L -NA alone. These results suggest that in pentobarbital-anesthetized dogs: ( 1 ) the magnitude of HPV is limited by the corelease of COX metabolites and of NO; and ( 2 ) inhibition of COX, but not of NOS, attenuates the deterioration of gas exchange in oleic acid‐induced lung injury. Leeman M, Zegers de Beyl V, Biarent D, Maggiorini M, Melot C, Naeije R. Inhibition of cyclooxygenase and nitric oxide synthase in hypoxic vasoconstriction and oleic acid‐ induced lung injury. AM J RESPIR CRIT CARE MED 1999;159:1383‐1390.
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inhibition of cyclooxygenase and nitric oxide synthase in hypoxic vasoconstriction and oleic acid induced lung injury
American Journal of Respiratory and Critical Care Medicine, 1999Co-Authors: Marc Leeman, Christian Melot, Valerie Zegers De Beyl, Dominique Biarent, Marco Maggiorini, Robert NaeijeAbstract:Cyclooxygenase (COX) products and nitric oxide (NO) inhibit hypoxic Pulmonary vasoconstriction (HPV), and their release could contribute to alterations in gas exchange in lung injury. We tested the hypothesis that combined blockade of COX and NO synthase (NOS) could further increase HPV and better protect gas exchange in lung injury than could blockade of either COX or NOS alone. We determined Pulmonary Vascular Pressure‐flow relationships in pentobarbital-anesthetized and ventilated dogs submitted to hypoxic challenges before and after administration of solvent (n 5 4), indomethacin alone (2 mg/kg intravenously, n 5 8), N v -nitro- L -arginine ( L -NA) alone (10 mg/kg intravenoulsy, n 5 8), indomethacin followed by L -NA (n 5 8), and L -NA followed by indomethacin (n 5 8). All of the dogs so treated then received oleic acid (0.06 ml/kg intravenously) to induce lung injury. Blood flow was manipulated by establishing a femoral arteriovenous bypass or by inflating an inferior vena caval balloon. Gas exchange was evaluated by measuring arterial P O2 and intraPulmonary shunt (using the inert gas sulfur hexafluoride) at identical cardiac outputs. The magnitude of HPV was not affected by solvent. Indomethacin and L -NA given separately enhanced HPV. L -NA added to indomethacin further enhanced HPV, as did indomethacin added to L -NA. After oleic acid‐induced lung injury, gas exchange deteriorated less in dogs pretreated with indomethacin than in dogs pretreated with solvent or with L -NA alone. These results suggest that in pentobarbital-anesthetized dogs: ( 1 ) the magnitude of HPV is limited by the corelease of COX metabolites and of NO; and ( 2 ) inhibition of COX, but not of NOS, attenuates the deterioration of gas exchange in oleic acid‐induced lung injury. Leeman M, Zegers de Beyl V, Biarent D, Maggiorini M, Melot C, Naeije R. Inhibition of cyclooxygenase and nitric oxide synthase in hypoxic vasoconstriction and oleic acid‐ induced lung injury. AM J RESPIR CRIT CARE MED 1999;159:1383‐1390.
Valerie Zegers De Beyl - One of the best experts on this subject based on the ideXlab platform.
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inhibition of cyclooxygenase and nitric oxide synthase in hypoxic vasoconstriction and oleic acid induced lung injury
American Journal of Respiratory and Critical Care Medicine, 1999Co-Authors: Marc Leeman, Christian Melot, Valerie Zegers De Beyl, Dominique Biarent, Marco Maggiorini, Robert NaeijeAbstract:Cyclooxygenase (COX) products and nitric oxide (NO) inhibit hypoxic Pulmonary vasoconstriction (HPV), and their release could contribute to alterations in gas exchange in lung injury. We tested the hypothesis that combined blockade of COX and NO synthase (NOS) could further increase HPV and better protect gas exchange in lung injury than could blockade of either COX or NOS alone. We determined Pulmonary Vascular Pressure‐flow relationships in pentobarbital-anesthetized and ventilated dogs submitted to hypoxic challenges before and after administration of solvent (n 5 4), indomethacin alone (2 mg/kg intravenously, n 5 8), N v -nitro- L -arginine ( L -NA) alone (10 mg/kg intravenoulsy, n 5 8), indomethacin followed by L -NA (n 5 8), and L -NA followed by indomethacin (n 5 8). All of the dogs so treated then received oleic acid (0.06 ml/kg intravenously) to induce lung injury. Blood flow was manipulated by establishing a femoral arteriovenous bypass or by inflating an inferior vena caval balloon. Gas exchange was evaluated by measuring arterial P O2 and intraPulmonary shunt (using the inert gas sulfur hexafluoride) at identical cardiac outputs. The magnitude of HPV was not affected by solvent. Indomethacin and L -NA given separately enhanced HPV. L -NA added to indomethacin further enhanced HPV, as did indomethacin added to L -NA. After oleic acid‐induced lung injury, gas exchange deteriorated less in dogs pretreated with indomethacin than in dogs pretreated with solvent or with L -NA alone. These results suggest that in pentobarbital-anesthetized dogs: ( 1 ) the magnitude of HPV is limited by the corelease of COX metabolites and of NO; and ( 2 ) inhibition of COX, but not of NOS, attenuates the deterioration of gas exchange in oleic acid‐induced lung injury. Leeman M, Zegers de Beyl V, Biarent D, Maggiorini M, Melot C, Naeije R. Inhibition of cyclooxygenase and nitric oxide synthase in hypoxic vasoconstriction and oleic acid‐ induced lung injury. AM J RESPIR CRIT CARE MED 1999;159:1383‐1390.
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inhibition of cyclooxygenase and nitric oxide synthase in hypoxic vasoconstriction and oleic acid induced lung injury
American Journal of Respiratory and Critical Care Medicine, 1999Co-Authors: Marc Leeman, Christian Melot, Valerie Zegers De Beyl, Dominique Biarent, Marco Maggiorini, Robert NaeijeAbstract:Cyclooxygenase (COX) products and nitric oxide (NO) inhibit hypoxic Pulmonary vasoconstriction (HPV), and their release could contribute to alterations in gas exchange in lung injury. We tested the hypothesis that combined blockade of COX and NO synthase (NOS) could further increase HPV and better protect gas exchange in lung injury than could blockade of either COX or NOS alone. We determined Pulmonary Vascular Pressure‐flow relationships in pentobarbital-anesthetized and ventilated dogs submitted to hypoxic challenges before and after administration of solvent (n 5 4), indomethacin alone (2 mg/kg intravenously, n 5 8), N v -nitro- L -arginine ( L -NA) alone (10 mg/kg intravenoulsy, n 5 8), indomethacin followed by L -NA (n 5 8), and L -NA followed by indomethacin (n 5 8). All of the dogs so treated then received oleic acid (0.06 ml/kg intravenously) to induce lung injury. Blood flow was manipulated by establishing a femoral arteriovenous bypass or by inflating an inferior vena caval balloon. Gas exchange was evaluated by measuring arterial P O2 and intraPulmonary shunt (using the inert gas sulfur hexafluoride) at identical cardiac outputs. The magnitude of HPV was not affected by solvent. Indomethacin and L -NA given separately enhanced HPV. L -NA added to indomethacin further enhanced HPV, as did indomethacin added to L -NA. After oleic acid‐induced lung injury, gas exchange deteriorated less in dogs pretreated with indomethacin than in dogs pretreated with solvent or with L -NA alone. These results suggest that in pentobarbital-anesthetized dogs: ( 1 ) the magnitude of HPV is limited by the corelease of COX metabolites and of NO; and ( 2 ) inhibition of COX, but not of NOS, attenuates the deterioration of gas exchange in oleic acid‐induced lung injury. Leeman M, Zegers de Beyl V, Biarent D, Maggiorini M, Melot C, Naeije R. Inhibition of cyclooxygenase and nitric oxide synthase in hypoxic vasoconstriction and oleic acid‐ induced lung injury. AM J RESPIR CRIT CARE MED 1999;159:1383‐1390.
