Persistence of lung edema and arterial pressure rise in dogs after lung emboli

1964 ◽  
Vol 207 (3) ◽  
pp. 641-646 ◽  
Author(s):  
H. Weisberg ◽  
J. F. Lopez ◽  
M. H. Luria ◽  
L. N. Katz
Keyword(s):  
Pulmonary Artery ◽  
Arterial Pressure ◽  
Pulmonary Edema ◽  
Pulmonary Artery Pressure ◽  
Pressure Rise ◽  
Significant Rise ◽  
Lung Edema ◽  
Artery Pressure ◽  
Acute Elevation ◽  
Pulmonary Arterial

Bilateral pulmonary edema was present in dogs autopsied 24 hr after pulmonary embolization. Mean pulmonary artery pressure remained elevated during this period. Most others, which survived up to the 3rd day and died spontaneously after embolization, showed edema at autopsy. Longer survivors showed no edema. Edema severity during the first 2 days was roughly related to the pressure rise during the 1st hr after embolization. Immediate significant pulmonary artery pressure rise, predominant in dogs succumbing by the 3rd day, was not as common in those surviving longer. Thus, survival time showed an inverse relationship to immediate pulmonary artery pressure elevation. In another 17 dogs followed as long as 10–23 months after embolization, 53% showed a significant rise in pressure at the end and some animals also had histologic pulmonary vascular changes. In some instances acute elevation of pulmonary artery pressure at embolization may anticipate chronic pulmonary arterial hypertension. The problem is the creation of embolism which elevates pulmonary arterial pressure without animals succumbing acutely to the associated pulmonary edema.

Effect of hypoxia on pulmonary artery pressure of dogs

1964 ◽  
Vol 207 (6) ◽  
pp. 1314-1318 ◽  
Author(s):  
Benson R. Wilcox ◽  
W. Gerald Austen ◽  
Harvey W. Bender
Keyword(s):  
Pulmonary Artery ◽  
Arterial Pressure ◽  
Pulmonary Artery Pressure ◽  
Pulmonary Arterial Pressure ◽  
Venous Pressure ◽  
Artery Pressure ◽  
Pulmonary Vasoconstriction ◽  
Systemic Hypoxia ◽  
Pump Output ◽  
Pulmonary Arterial

The mechanism by which the pulmonary artery pressure rises in response to hypoxia has never been clearly demonstrated. This problem was reinvestigated in experiments utilizing separate pulmonary and systemic perfusion systems. These vascular beds were perfused in such a fashion that a change in pulmonary artery pressure could only result from changes in vasomotor tone. Alveolar-pulmonary vein hypoxia was usually associated with a slight fall in pulmonary artery pressure. Systemic hypoxia resulted in elevation of pulmonary arterial pressure in 10 of the 12 animals tested with a constant-flow and constant-pulmonary venous pressure. In addition, all animals with systemic desaturation showed an increased venous return. When the "cardiac output" (pump output) was increased to match this return, the elevation in pulmonary artery pressure increased. It was concluded that the pulmonary arterial pressure elevation seen with hypoxia is the result of active pulmonary vasoconstriction coupled with an increased pulmonary blood flow.

Stability of pulmonary artery pressure during emboli-induced pulmonary edema in dogs

1965 ◽  
Vol 208 (6) ◽  
pp. 1263-1266
Author(s):  
H. Weisberg ◽  
R. T. Jortner ◽  
I. K. Kline ◽  
A. Ellis ◽  
L. N. Katz
Keyword(s):  
Cardiac Output ◽  
Pulmonary Artery ◽  
Pulmonary Edema ◽  
Pulmonary Vascular Resistance ◽  
Pulmonary Artery Pressure ◽  
Vascular Resistance ◽  
Pressure Rise ◽  
Vascular Effects ◽  
Artery Pressure ◽  
Pressure Changes

Changes in some facets of cardiovascular hemodynamics occurring after acute unilateral pulmonary starch embolization were studied in the anesthetized closed-chest dog. While bilateral pulmonary edema and reduced cardiac output occurred in starch-embolized dogs, these phenomena were not seen in control animals. Pulmonary arterial pressure changes were not significant during the present experiments, but the consistent rise in pulmonary vascular resistance after embolization indicates that the latter may be a better index of pulmonary vascular effects of emboli than are pressure changes. The fall in cardiac output was of sufficient magnitude to more completely neutralize the pulmonary artery pressure rise usually expected with increased pulmonary vascular resistance following pulmonary embolization.

Effect of tonsillectomy and/or adenoidectomy on pulmonary arterial pressure in adults

Open Medicine ◽  
2008 ◽  
Vol 3 (4) ◽  
pp. 482-486
Author(s):  
Saeed Abdelwhab ◽  
Khaled. Dessoukey ◽  
Gamal Lotfy ◽  
Ashraf Alsaeed ◽  
Hesham Anwar
Keyword(s):  
Pulmonary Artery ◽  
Arterial Pressure ◽  
Pulmonary Artery Pressure ◽  
Pulmonary Arterial Pressure ◽  
Arterial Oxygen ◽  
Artery Pressure ◽  
Mean Pulmonary Arterial Pressure ◽  
Arterial Blood ◽  
Pulmonary Arterial ◽  
Group 1

AbstractThe aim of the study was to determine the mean pulmonary pressure in adult with hypertrophic tonsils and adenoids and to clarify whether tonsillectomy and adenoidectomy has any effect on mean pulmonary arterial pressure of these adult. The study was carried out on 50 patients with diagnosis of upper airway obstruction resulting from hypertrophied tonsils and adenoids (group1). 25 adults were assigned as control with similar age and sex distribution (group2). For study subjects Routine general Examinations, BMI, ECG, Chest X ray, Arterial blood gases and Echocardiography were done. Mean pulmonary arterial pressure was measured by using Doppler Echocardiography preoperatively and mean 3–4 months postoperatively in all subjects. Elevated PAP (pulmonary artery pressure) was found in 15 patients (30%) in group 1 preoperatively. Mean PAP was 28.34 ±5.11 mmHg preoperative in group 1 and 19.84 ± 5.0 mmHg in group 2 (p <0.001). PAP decrease to 22.38 ±4.28 mmHg postoperatively in group 1 (p <0.001). Arterial oxygen saturation (spo2%) increase from 93.5 ± 1.9% preoperatively to 95.3 ± 1.3% post operatively (p < 0.001). percent reduction of PAP postoperatively correlates to age (t=−2.3, p= 0.02), preoperative PAP (p =0.01) but no correlation was found with BMI. In conclusions, this Study showed that obstructed adenoid and hypertrophy of tonsils causes higher mean pulmonary artery pressure in adult & revealed that tonsil& adenoid is effective therapeutic measure in such patients. With early intervention is necessary to avoid progressive cardiopulmonary disease.

Inflammation and Congenital Heart Disease Associated Pulmonary Hypertension

2015 ◽  
Vol 18 (1) ◽  
pp. 038 ◽  
Author(s):  
Mete Gursoy ◽  
Ece Salihoglu ◽  
Ali Can Hatemi ◽  
A. Faruk Hokenek ◽  
Suleyman Ozkan ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Neutrophil To Lymphocyte Ratio ◽  
Cell Distribution ◽  
Inflammation Markers ◽  
Distribution Width ◽  
Artery Pressure ◽  
Lymphocyte Ratio ◽  
Mean Pulmonary Artery Pressure ◽  
Pulmonary Arterial

<strong>Background:</strong> Increased blood flow may trigger pulmonary arterial wall inflammation, which may influence progression of pulmonary artery hypertension in patients with congenital heart disease. In this study, we aimed to investigate the correlation between preoperative inflammation markers and pulmonary arterial hypertension. <br /><strong>Methods:</strong> A total of 201 patients with pulmonary hypertension were enrolled in this study retrospectively; they had undergone open heart surgery between January 2012 and December 2013. Patients’ preoperative C-reactive protein (CRP), neutrophil to lymphocyte ratio, red blood cell distribution width, pulmonary pressures, and postoperative outcomes were evaluated.<br /><strong>Results:</strong> Patient age, neutrophil to lymphocyte ratio, red blood cell distribution width, and CRP were found to be significantly correlated with both preoperative peak and mean pulmonary artery pressures. These data were entered into a linear logistic regression analysis. Patient age, neutrophil to lymphocyte ratio, and CRP were found to be independently correlated with peak pulmonary pressure (P &lt; .001, P &lt; .001, and P = .004) and mean pulmonary artery pressure (P &lt; .001, P &lt; .001, and P = .001), whereas preoperative mean pulmonary artery pressure was found to be independently correlated with intensive care unit stay (P &lt; .001). No parameter was found to be significantly correlated with extubation time and mortality. Eighteen patients had experienced pulmonary hypertensive crisis; in this subgroup, patients’ mean pulmonary artery pressure and neutrophil to lymphocyte ratio were found to be significant (P = .047, P = .003). <br /><strong>Conclusion:</strong> Preoperative inflammation markers may be correlated with the progression of pulmonary hypertensive disease, but further studies with larger sample size are needed to determine the predictive role of these markers for postoperative outcomes.<br /><br />

Pulmonary Hypertension

2013 ◽  
Author(s):  
George K Istaphanous ◽  
Andreas W Loepke
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Arterial Hypertension ◽  
Pulmonary Artery ◽  
Arterial Hypertension ◽  
Pulmonary Artery Pressure ◽  
Disease Process ◽  
Underlying Disease ◽  
Artery Pressure ◽  
Pulmonary Arterial ◽  
Made In

Pediatric pulmonary arterial hypertension (PAH) is characterized by a pathologically elevated pulmonary artery pressure in children. The etiology of PAH is multifactorial, and while its prognosis is closely related to the reversibility of the underlying disease process, much progress has recently been made in its diagnosis and treatment, significantly decreasing the associated morbidity and mortality.

Effect of repeated exercise on the lesser circulation

1963 ◽  
Vol 18 (5) ◽  
pp. 983-986 ◽  
Author(s):  
Jiri Widimsky ◽  
Erik Berglund ◽  
Rolf Malmberg
Keyword(s):  
Pulmonary Artery ◽  
Lung Disease ◽  
Pulmonary Artery Pressure ◽  
Healthy Subjects ◽  
Artery Pressure ◽  
Repeated Exercise ◽  
Exercise Period ◽  
Pulmonary Arterial ◽  
Lung Vessels ◽  
Wedge Pressure

In four healthy subjects and four patients with lung disease, hemodynamic studies were done during two periods of identical exercise, 1 hr apart. Pulmonary artery pressure was lower in the second exercise period in all subjects studied. Pulmonary arterial wedge pressure was measured in four cases and was unchanged or even slightly increased. The “total pulmonary” and pulmonary vascular resistances were markedly lower in the second exercise period. The decrease in pulmonary artery pressure was found also in the second postexercise period when compared with the starting resting level. It is believed that this fall in pulmonary artery pressure and resistance was due to opening or widening of previously closed or constricted lung vessels. Repeated exercise must be used with caution when studying the effect of pharmacological or physiological agents on the lesser circulation. Submitted on November 30, 1962

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