scholarly journals EFFECTS OF LUNG SURGERY AND ONE-LUNG VENTILATION ON PULMONARY ARTERIAL PRESSURE, VENOUS ADMIXTURE AND IMMEDIATE POSTOPERATIVE LUNG FUNCTION

1989 ◽  
Vol 63 (6) ◽  
pp. 696-701 ◽  
Author(s):  
G. MALMKVIST ◽  
R. FLETCHER ◽  
L. NORDSTRÖM ◽  
O. WERNER
Keyword(s):  
Lung Function ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Lung Ventilation ◽  
Lung Surgery ◽  
Venous Admixture ◽  
One Lung Ventilation ◽  
Pulmonary Arterial ◽  
Postoperative Lung Function

Assessment of postpreservation rat lung function using a new model for extended venous reperfusion

1993 ◽  
Vol 75 (4) ◽  
pp. 1890-1896 ◽  
Author(s):  
K. N. DeCampos ◽  
T. K. Waddell ◽  
A. S. Slutsky ◽  
M. Post ◽  
G. A. Patterson
Keyword(s):  
Weight Gain ◽  
Lung Function ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Suitable Model ◽  
Rat Lung ◽  
Lung Dysfunction ◽  
Pulmonary Arterial ◽  
Group 3 ◽  
Group 1

Understanding the physiological significance of biochemical events after lung preservation in rats has been hampered by the lack of a suitable model for physiological assessment. We have developed an ex vivo paracorporeal rat lung perfusion model that permits hemodynamic and gas exchange evaluation of lung function. After anesthesia and heparinization, the heart-lung block was removed and the left lung was reperfused for 1 h at a constant flow of 4 ml/min with homologous venous blood drained from the inferior vena cava of the paracorporeal (host) rat. The lung effluent was returned at the same flow rate to the host distal aorta. The model was validated by the assessment of lung function after room temperature ischemia. Animals were allocated into three groups (n = 6) according to the ischemic interval (group 1, 20 min; group 2, 3 h; group 3, 4 h). In groups 1 and 2, PO2, PCO2, mean airway pressure, and pulmonary arterial pressure were within the normal ranges and stable throughout the experiment. In contrast, lungs in group 3 demonstrated higher pulmonary arterial pressure and lower blood effluent PO2 than were found in either group 1 or 2. A significant weight gain during reperfusion was observed only in group 3 (4.23 +/- 0.9 g; P < 0.002). For each lung, the final blood effluent PO2 correlated with the weight gain (R2 = 0.81; P < 0.0001). Our results indicate that this model can be used reliably to detect lung dysfunction after ischemic injury.

PAF increases vascular permeability without increasing pulmonary arterial pressure in the rat

2001 ◽  
Vol 90 (1) ◽  
pp. 261-268 ◽  
Author(s):  
Leonardo C. Clavijo ◽  
Mary B. Carter ◽  
Paul J. Matheson ◽  
Mark A. Wilson ◽  
William B. Wead ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Edema ◽  
Pulmonary Arterial Pressure ◽  
Ex Vivo ◽  
Platelet Activating Factor ◽  
Microvascular Permeability ◽  
Blue Dye ◽  
E Coli ◽  
Pulmonary Arterial

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.

scholarly journals 275 Phenotypic relationships between heart score and feed efficiency, carcass, and pulmonary arterial pressure traits

2020 ◽  
Vol 98 (Supplement_4) ◽  
pp. 204-205
Author(s):  
Kathryn R Heffernan ◽  
Scott Speidel ◽  
Milt Thomas ◽  
Mark Enns ◽  
Tim Holt
Keyword(s):  
Arterial Pressure ◽  
Feed Efficiency ◽  
Pulmonary Arterial Pressure ◽  
Carcass Traits ◽  
Multiple Linear Regression Model ◽  
Strong Relationship ◽  
Fixed Effect ◽  
Heart Score ◽  
Important Relationship ◽  
Pulmonary Arterial

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.

scholarly journals 265 Evaluation of the genetic relationship amongst high elevation pulmonary arterial pressure, feedlot and carcass performance traits

2020 ◽  
Vol 98 (Supplement_4) ◽  
pp. 197-197
Author(s):  
Emma A Briggs ◽  
Scott Speidel ◽  
Mark Enns ◽  
Milt Thomas ◽  
Tim Holt
Keyword(s):  
Arterial Pressure ◽  
Genetic Relationship ◽  
Feed Intake ◽  
Pulmonary Arterial Pressure ◽  
Carcass Traits ◽  
Genetic Correlations ◽  
High Elevation ◽  
Pulmonary Arterial ◽  
Carcass Performance ◽  
Moderate Elevation

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.

Regional pulmonary blood flow during 96 hours of hypoxia in conscious sheep

1986 ◽  
Vol 61 (6) ◽  
pp. 2136-2143 ◽  
Author(s):  
D. C. Curran-Everett ◽  
K. McAndrews ◽  
J. A. Krasney
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Pulmonary Blood Flow ◽  
Pulmonary Arterial Pressure ◽  
Pressor Response ◽  
Superior Vena ◽  
Acute Hypoxia ◽  
Vena Cava ◽  
Normobaric Hypoxia ◽  
Pulmonary Arterial

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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