scholarly journals Changes in pulmonary arterial pressure in preterm infants with chronic lung disease

2000 ◽  
Vol 82 (3) ◽  
pp. 243F-247 ◽  
Author(s):  
N V Subhedar
2015 ◽  
Vol 46 (5) ◽  
pp. 1390-1396 ◽  
Author(s):  
Svenja L. Tiede ◽  
Henning Gall ◽  
Oliver Dörr ◽  
Marina dos Santos Guilherme ◽  
Christian Troidl ◽  
...  

This study aimed to determine whether the vascular endothelial growth factor (VEGF) family members soluble VEGF receptor 1 (also called soluble fms-like tyrosine kinase 1 (sFlt-1)) and placental growth factor (PlGF) could be used as biomarkers for pulmonary hypertension (PH).Consecutive patients undergoing right heart catheterisation were enrolled (those with mean pulmonary arterial pressure ≥25 mmHg were classed as having PH; those with mean pulmonary arterial pressure <25 mmHg acted as non-PH controls). Plasma from the time of PH diagnosis was analysed for PlGF and sFlt-1 using enzyme immunoassays.In total, 247 patients with PH were enrolled: 62 with idiopathic pulmonary arterial hypertension (IPAH), 14 with associated pulmonary arterial hypertension (APAH), 21 with collagen vascular disease (CVD), 26 with pulmonary venous hypertension, 67 with lung disease-associated PH and 57 with chronic thromboembolic PH. The non-PH control group consisted of 40 patients. sFlt-1 plasma levels were significantly higher in patients with IPAH, APAH, CVD and lung disease-associated PH versus controls; PlGF levels were significantly higher in all PH groups versus controls. The combination of sFlt-1 and PlGF resulted in a sensitivity of 83.7% with specificity of 100% for pulmonary arterial hypertension. There was no association between sFlt-1 or PlGF and haemodynamic parameters, 6-min walking distance or survival.In summary, PlGF and sFlt-1 are promising diagnostic biomarkers for PH.


1978 ◽  
Vol 55 (5) ◽  
pp. 485-490
Author(s):  
F. Schrijen ◽  
V. Ježek

1. Pulmonary and systemic haemodynamics during repeated exercise were studied in 28 patients with chronic lung disease of various etiology, 16 of whom suffered from chronic bronchitis. They performed a moderate exercise repeated after a 20 min rest period. Ventilatory variables, blood gas tensions, cardiac output and vascular pressures (right ventricular end-diastolic, pulmonary arterial, wedge and systemic arterial) were measured at rest, during exercise and again at rest and during the same exercise. 2. Ventilation and blood gas tensions were similar during the two rest and exercise periods; there was, however, a slightly significant difference in oxygen consumption and hydrogen ion concentration between the first and the second exercise period. Pulmonary arterial and wedge pressures were lower during the second rest and exercise, right ventricular filling pressure was lower at rest, and systemic arterial pressure during the second exercise. Cardiac output and pulmonary vascular resistance were unchanged. 3. Changes in systemic arterial pressure were significantly different in a group of patients with arterial oxygen desaturation or perfusion defects, compared with those patients without such impairment.


2001 ◽  
Vol 90 (1) ◽  
pp. 261-268 ◽  
Author(s):  
Leonardo C. Clavijo ◽  
Mary B. Carter ◽  
Paul J. Matheson ◽  
Mark A. Wilson ◽  
William B. Wead ◽  
...  

In vivo pulmonary arterial catheterization was used to determine the mechanism by which platelet-activating factor (PAF) produces pulmonary edema in rats. PAF induces pulmonary edema by increasing pulmonary microvascular permeability (PMP) without changing the pulmonary pressure gradient. Rats were cannulated for measurement of pulmonary arterial pressure (Ppa) and mean arterial pressure. PMP was determined by using either in vivo fluorescent videomicroscopy or the ex vivo Evans blue dye technique. WEB 2086 was administered intravenously (IV) to antagonize specific PAF effects. Three experiments were performed: 1) IV PAF, 2) topical PAF, and 3) Escherichia coli bacteremia. IV PAF induced systemic hypotension with a decrease in Ppa. PMP increased after IV PAF in a dose-related manner. Topical PAF increased PMP but decreased Ppa only at high doses. Both PMP (88 ± 5%) and Ppa (50 ± 3%) increased during E. coli bacteremia. PAF-receptor blockade prevents changes in Ppa and PMP after both topical PAF and E. coli bacteremia. PAF, which has been shown to mediate pulmonary edema in prior studies, appears to act in the lung by primarily increasing microvascular permeability. The presence of PAF might be prerequisite for pulmonary vascular constriction during gram-negative bacteremia.


2020 ◽  
Vol 98 (Supplement_4) ◽  
pp. 204-205
Author(s):  
Kathryn R Heffernan ◽  
Scott Speidel ◽  
Milt Thomas ◽  
Mark Enns ◽  
Tim Holt

Abstract Pulmonary hypertension (PH) can lead to premature mortality in fed cattle and is often called Feedlot Heart Disease (FHD). To date, pulmonary arterial pressure (PAP) has been the only indicator trait of PH that has been evaluated. The objective of this study was to evaluate relationships between heart score (using heart score as a phenotype for PH) and PAP, carcass, and feed efficiency traits in fattening Angus steers. Our hypothesis was that feed efficiency and carcass traits, along with PAP, would demonstrate a strong relationship with heart score. Feed efficiency, carcass, PAP and heart score data from 89 Black Angus steers from Colorado State University Beef Improvement Center were collected and used for this study. Evaluations were performed using a multiple linear regression model, which included heart score as a categorical fixed effect and age as a continuous fixed effect. Least Square Means, pairwise comparisons, and ANOVA tables were constructed per trait. PAP (P &lt; 0.001) showed an important relationship to heart score and average dry matter (P &lt; 0.10) intake approached importance to heart score. In general, feed efficiency and carcass traits decreased as heart score increased, but PAP was the only trait with a strong relationship to heart score (P &lt; 0.05). This led us to reject our hypothesis.


2020 ◽  
Vol 98 (Supplement_4) ◽  
pp. 197-197
Author(s):  
Emma A Briggs ◽  
Scott Speidel ◽  
Mark Enns ◽  
Milt Thomas ◽  
Tim Holt

Abstract The objective of the study was to evaluate if a genetic relationship exists between pulmonary arterial pressure (PAP) measured at high elevation with traits associated with moderate elevation feedlot and carcass traits. For this analysis, PAP, feed intake, and carcass data were taken from 6,898, 558, and 1,627 animals, respectively. At an elevation of 2,115 m, PAP measurements were collected, then a selective group of steers was relocated to a moderate elevation feedlot (1,500 m) where feed intake data were collected. Genetic relationships were evaluated with 5-trait animal models using REML statistical analysis. For all traits in the analysis, fixed effects and contemporary groups were assigned as well as a direct genetic random effect. For weaning weight, a maternal permanent environmental effect was applied in the analysis. For PAP, the heritability estimate was 0.29 ± 0.03. Genetic correlations between PAP with feedlot traits was positive, with estimates of 0.34 ± 0.20 (average dry matter intake) and 0.05 ± 17 (average daily gain). The strongest genetic correlation between PAP and carcass performance traits were those of rib eye area (-0.30 ± 0.12) and calculated yield grade (0.29 ± 0.13). Genetic correlations between PAP and marbling score, back fat, or hot carcass weight were 0.00 ± 0.13, -0.07 ± 0.13, and 0.14 ± 0.10, respectively. These results suggest a favorable genetic relationship exists between PAP with feedlot and carcass traits.


1986 ◽  
Vol 61 (6) ◽  
pp. 2136-2143 ◽  
Author(s):  
D. C. Curran-Everett ◽  
K. McAndrews ◽  
J. A. Krasney

The effects of acute hypoxia on regional pulmonary perfusion have been studied previously in anesthetized, artificially ventilated sheep (J. Appl. Physiol. 56: 338–342, 1984). That study indicated that a rise in pulmonary arterial pressure was associated with a shift of pulmonary blood flow toward dorsal (nondependent) areas of the lung. This study examined the relationship between the pulmonary arterial pressor response and regional pulmonary blood flow in five conscious, standing ewes during 96 h of normobaric hypoxia. The sheep were made hypoxic by N2 dilution in an environmental chamber [arterial O2 tension (PaO2) = 37–42 Torr, arterial CO2 tension (PaCO2) = 25–30 Torr]. Regional pulmonary blood flow was calculated by injecting 15-micron radiolabeled microspheres into the superior vena cava during normoxia and at 24-h intervals of hypoxia. Pulmonary arterial pressure increased from 12 Torr during normoxia to 19–22 Torr throughout hypoxia (alpha less than 0.049). Pulmonary blood flow, expressed as %QCO or ml X min-1 X g-1, did not shift among dorsal and ventral regions during hypoxia (alpha greater than 0.25); nor were there interlobar shifts of blood flow (alpha greater than 0.10). These data suggest that conscious, standing sheep do not demonstrate a shift in pulmonary blood flow during 96 h of normobaric hypoxia even though pulmonary arterial pressure rises 7–10 Torr. We question whether global hypoxic pulmonary vasoconstriction is, by itself, beneficial to the sheep.


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