Pulmonary Vasculopathy in Idiopathic Spontaneous Pneumothorax in Young Subjects

2000 ◽  
Vol 124 (5) ◽  
pp. 717-720 ◽  
Author(s):  
Pamela V. Cyr ◽  
Lydia Vincic ◽  
J. Michael Kay
Keyword(s):  
Pulmonary Artery ◽  
Chronic Inflammation ◽  
Spontaneous Pneumothorax ◽  
Lung Resection ◽  
Pulmonary Veins ◽  
Pulmonary Arteries ◽  
Vascular Lesions ◽  
Pulmonary Vascular Disease ◽  
Young Subjects ◽  
Medial Hypertrophy

Abstract Background.—We have encountered instances where young subjects with idiopathic spontaneous pneumothorax have been needlessly referred for investigation of pulmonary hypertension because surgical pathologists have misinterpreted the significance of medial hypertrophy and intimal fibrosis of muscular pulmonary arteries in lung resection specimens. Methods.—We reviewed 20 cases of idiopathic spontaneous pneumothorax and determined the prevalence and severity of medial and intimal lesions in the pulmonary arteries and pulmonary veins. We correlated the vascular changes with inflammation and fibrosis in the lung. Results.—Pulmonary artery medial hypertrophy was seen in 15% of cases, pulmonary artery intimal fibrosis in 90% of cases, and pulmonary vein intimal fibrosis in 80% of cases. In 95% of cases, the lung showed some fibrosis and chronic inflammation. There was a significant positive correlation between pulmonary artery medial thickness and lung fibrosis and inflammation scores. Conclusions.—Pulmonary artery medial hypertrophy and intimal fibrosis of pulmonary arteries and pulmonary veins are commonly seen in resected lung tissue from patients with idiopathic spontaneous pneumothorax. The vascular lesions are probably secondary to chronic inflammation and fibrosis in the adjacent lung. They are not clinically significant and do not represent hypertensive pulmonary vascular disease.

Double outlet right atrium and complete atrioventricular septal defect with abnormal findings of the biopsied lung

1994 ◽  
Vol 4 (4) ◽  
pp. 402-404 ◽  
Author(s):  
Kiyoshi Suzuki ◽  
Toshio Kikuchi ◽  
Shigekazu Mimori
Keyword(s):  
Septal Defect ◽  
Pulmonary Veins ◽  
Pulmonary Arteries ◽  
Atrioventricular Septal Defect ◽  
Pulmonary Trunk ◽  
Atrial Septum ◽  
Corrective Surgery ◽  
Rare Type ◽  
Medial Hypertrophy ◽  
Complete Atrioventricular

SummaryWe describe a rare type of atrioventricular septal defect with common atrioventricular orifice and malaligned atrial septum, the latter feature resulting in severe obstruction of the left atrial egress. Excision of the atrial septum and banding of the pulmonary trunk was performed at the age of thirteen months. Lung biopsy demonstrated marked medial hypertrophy with severe intimal fibrosis in the small pulmonary arteries and mild thickening of the pulmonary veins, considered contraindications for corrective surgery.

Measurements of Mouse Pulmonary Artery Biomechanics

2004 ◽  
Vol 126 (2) ◽  
pp. 309-313 ◽  
Author(s):  
Naomi C. Chesler ◽  
John Thompson-Figueroa and ◽  
Ken Millburne
Keyword(s):  
High Pressure ◽  
Pulmonary Artery ◽  
Vascular Disease ◽  
Measurement Techniques ◽  
Circumferential Stress ◽  
Pulmonary Arteries ◽  
Biomechanical Properties ◽  
Pulmonary Vascular Disease ◽  
Internal Diameter ◽  
Stress Strain

Background: Robust techniques for characterizing the biomechanical properties of mouse pulmonary arteries will permit exciting gene-level hypotheses regarding pulmonary vascular disease to be tested in genetically engineered animals. In this paper, we present the first measurements of the biomechanical properties of mouse pulmonary arteries. Method of Approach: In an isolated vessel perfusion system, transmural pressure, internal diameter and wall thickness were measured during inflation and deflation of mouse pulmonary arteries over low (5–40 mmHg) and high (10–120 mmHg) pressure ranges representing physiological pressures in the pulmonary and systemic circulations, respectively. Results: During inflation, circumferential stress versus strain showed the nonlinear “J”-shape typical of arteries. Hudetz’s incremental elastic modulus ranged from 27±13kPan=7 during low-pressure inflation to 2,700±1,700kPan=9 during high-pressure inflation. The low and high-pressure testing protocols yielded quantitatively indistinguishable stress-strain and modulus-strain results. Histology performed to assess the state of the tissue after mechanical testing showed intact medial and adventitial architecture with some loss of endothelium, suggesting that smooth muscle cell contractile strength could also be measured with these techniques. Conclusions: The measurement techniques described demonstrate the feasibility of quantifying mouse pulmonary artery biomechanical properties. Stress-strain behavior and incremental modulus values are presented for normal, healthy arteries over a wide pressure range. These techniques will be useful for investigations into biomechanical abnormalities in pulmonary vascular disease.

Pulmonary vascular remodeling in rats with unilaterally banded lobar pulmonary veins

1992 ◽  
Vol 2 (2) ◽  
pp. 121-128 ◽  
Author(s):  
Carol M. Cottrill ◽  
William N. O'Connor ◽  
Robert Fitz ◽  
Mark N. Gillespie
Keyword(s):  
Vascular Disease ◽  
Pulmonary Veins ◽  
Pulmonary Arteries ◽  
Group Versus ◽  
Laboratory Animals ◽  
Pulmonary Venous Obstruction ◽  
Pulmonary Vascular Disease ◽  
External Diameter ◽  
Pulmonary Arterial ◽  
Medial Area

AbstractAlthough pulmonary vascular disease occurs in association with pulmonary venous obstruction, a model of pulmonary vascular lesions in this setting in small laboratory animals has yet to be described. The objective of this study was to determine if unilateral banding of pulmonary veins in the rat would produce pulmonary vascular disease that mimicked key aspects of the human disorder. Rats were anesthetized and, after mechanical ventilation and thoracotomy, one of the four pulmonary veins was banded to reduce its external diameter by approximately 65–75% to 0.8 mm. Additional animals, sham-operated controls, were treated identically except for venous banding. Mortality did not differ between groups and was less than 20%. Eight weeks after surgical preparation, moderate pulmonary hypertension was demonstrated with a mean pressure in the pulmonary artery of 24.9 mm Hg (range 19.25 – 30.0) in the banded group versus 18.7 mm Hg (range 16.6 – 19.3) for sham-operated animals. Pulmonary cineangiography in rats with banded pulmonary veins demonstrated marked pulmonary congestion and a prolonged residence time of contrast medium in the capillary circulation of the lung region subjected to banding. Angiographically, non-banded lungs were similar to shams. Histopathology of the vein-banded region revealed venous congestion, arterialization of veins, perivenular edema, and sparse to moderate inflammation. Prominent bronchial vessels, pulmonary arterial medial and occasional intimal thickening, and periarterial inflammation were also observed in banded regions. Similar inflammation around pulmonary arterial and pulmonary venous vessels was noted in contralateral lung lobes but not in sham-operated control rats. Morphometric evaluation of all muscular pulmonary arteries from 50–200μ external diameter accompanying airways to the level of terminal and respiratory bronchioles indicated that the medial area in lung regions subjected to venous banding was over three times greater than in shams. Pulmonary arteries from the contralateral, unbanded lungs of treated animals also exhibited a two-fold increase in medial area. These findings indicate that a modest degree of pulmonary venous banding in rats produces congestion and causes alterations in lung vessels which are reminiscent of those observed in humans with pulmonary venous outflow obstruction. Such a model in a cost-effective laboratory animal should be useful for delineating the specific mechanisms underlying these alterations.

The Physical Properties of Human Pulmonary Arteries and Veins

1978 ◽  
Vol 55 (5) ◽  
pp. 477-484 ◽  
Author(s):  
J. Banks ◽  
F. V. McL. Booth ◽  
E. H. MacKay ◽  
B. Rajagopalan ◽  
G. De J. Lee
Keyword(s):  
Pulmonary Artery ◽  
Physical Properties ◽  
Lung Disease ◽  
Left Atrium ◽  
Pulmonary Veins ◽  
Main Pulmonary Artery ◽  
Pulmonary Arteries ◽  
Post Mortem ◽  
Arteries And Veins

1. We have studied the extensibility of circumferential strips of main pulmonary artery and large pulmonary veins obtained at post mortem from patients of all ages, dying from conditions other than heart and lung disease. 2. The vessel strips were submitted to increasing loads in a tension balance. The pulmonary arteries were found to be readily extensible. This extensibility became less with increasing age. The pulmonary veins were virtually inextensible at all ages. 3. It is postulated that the large extraparenchymal pulmonary veins have a capacitative role in supplying blood from the lungs to the left atrium. This may be accomplished by their collapsible nature, as they have little capability of distension.

scholarly journals Vascular Lesions in Lungs of Bali Cattle with Jembrana Disease

1992 ◽  
Vol 29 (3) ◽  
pp. 210-215 ◽  
Author(s):  
I. T. Budiarso ◽  
Y. Rikihisa
Keyword(s):  
Plasma Cells ◽  
Pulmonary Veins ◽  
Pulmonary Arteries ◽  
Vascular Lesion ◽  
Vascular Lesions ◽  
Unknown Etiology ◽  
Postmortem Diagnosis ◽  
Bos Javanicus ◽  
Acute Infectious Disease ◽  
Bali Cattle

Jembrana disease is an acute infectious disease of unknown etiology enzootic among Bali cattle ( Bos javanicus) in Indonesia. Morphologic examination of 75 female Bali cattle between 18 months and 4 years old affected with Jembrana disease consistently revealed pulmonary granulomatous vascular lesions. The lesions were diffusely distributed throughout the lung. The principal lesion was the presence of a large number of intravascular macrophages that filled the lumina of pulmonary veins and pulmonary arteries of a vascular diameter of 20–200 μm, excluding the rest of blood cellular components. Concentric layers of perithelia] cells also with plasma cells and macrophages were occasionally present around both veins and arteries. Infiltration of polymorphonuclear leukocytes or small lymphocytes was not seen. Destruction or necrosis of tissues or blood vessels was rarely seen. Because this vascular lesion was found in the lungs of all affected cattle examined, this change is useful for the postmortem diagnosis of Jembrana disease. Moreover, its presence could be used to distinguish Jembrana disease from malignant catarrhal fever and other lymphoreticular proliferative conditions that are frequently found among cattle in Indonesia.

THE EFFECTS OF MATERNAL HYPOXIA AND HYPEROXIA UPON THE NEONATAL PULMONARY VASCULATURE

PEDIATRICS ◽  
1971 ◽  
Vol 48 (4) ◽  
pp. 528-533 ◽  
Author(s):  
Stanley J. Goldberg ◽  
Richard A. Levy ◽  
Bijan Siassi ◽  
Joanne Betten
Keyword(s):  
Pulmonary Artery ◽  
Pulmonary Arteries ◽  
Pulmonary Vasculature ◽  
External Diameter ◽  
Pulmonary Arterial ◽  
The Mean ◽  
Medial Hypertrophy ◽  
Maternal Hypoxia ◽  
Relationship Of ◽  
Hypoxic Group

The fetal and newborn pulmonary artery has thickened media by comparison to that of the older infant. In this study we investigated the proposition that chronic maternal hypoxia during the latter part of gestation might induce further thickening of the neonatal pulmonary artery media. Relative medial thickness was determined by the ratio of the arterial media to external diameter. The mean ratio of small pulmonary arteries of progeny of hypoxic mothers was significantly thicker in each size group between 50 and 150 microns as compared to those born to mothers who spent their gestation in air or hyperoxic environments. Medial hypertrophy was most pronounced in the smaller arteries of the hypoxic group; no intersize variations were found between the control or hyperoxic groups. Medial thickness decreased in all arteries through 2 weeks of age; this decrease was greatest in control and hyperoxic arteries. The possible relationship of hypertrophied pulmonary arterial media and abnormally increased neonatal pulmonary vascular resistance is discussed.

scholarly journals P720 Antenatal and postnatal echocardiographic diagnosis of Truncus Arteriosus III (TAIII) complicated by spontaneous PDA (patent ductus arteriosus) closure and LPA (left pulmonary artery) disconnection

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
N Alabdulkarim ◽  
A T I F Asahari ◽  
A M Alotay ◽  
SHERIF Thabet ◽  
TURKI Alqahtani
Keyword(s):  
Pulmonary Artery ◽  
Aortic Arch ◽  
Fetal Echocardiography ◽  
Ductus Arteriosus ◽  
Pulmonary Veins ◽  
Pulmonary Arteries ◽  
Left Pulmonary Artery ◽  
Truncus Arteriosus ◽  
Arterial Trunk ◽  
Ductal Closure

Abstract Introduction TA III is a rare form of truncus arteriosus when the branch pulmonary arteries originate independently from the common arterial trunk or aortic arch, with origin of one pulmonary artery from the underside of the aortic arch from a ductus arteriosus. Accurate diagnosis and timing of surgery is essential for survival of neonates affected. Purpose Illustration of various imaging modalities utilized to diagnose and manage this lesion and the importance of spontaneous PDA closure. Results TAIII diagnosed at 24 weeks gestation by fetal echocardiography images 1,2,3. Baby was spontaneously delivered at term with 3 Kg weight and 8,9 Apgar score. Diagnosis was confirmed by transthoracic echocardiography images 4,5 , however on 7th day of life routine echocardiogram was performed to assess PDA , markedly decreased flow noted in LPA/left pulmonary veins and no PDA could be seen at that time images 5,6. Spontaneous ductal closure was confirmed by tomography image 7 then cardiac intervention performed to establish LPA patency image 8,9. Successful total repair was done within the neonatal period with excellent results at follow up ( image 10 at 3 years old). Conculsions 1- TAIII can can be diagnosed and assessed by echocardiography. 2- PDA patency to maintain LPA continuity is essential in TAIII management. 3- Successful total surgical repair with good outcomes can be achieved for neonates with this rare complex cyanotic CHD. Abstract P720 Figure. Images

Surgical management of iatrogenic occluded left pulmonary artery

2018 ◽  
Vol 27 (5) ◽  
pp. 396-399
Author(s):  
Ali Sadeghpour Tabaie ◽  
Mohaddeseh Behjati ◽  
Hojjat Mortezaeian ◽  
Hamid Reza Pouraliakbar ◽  
Behshid Ghadrdoost ◽  
...  
Keyword(s):  
Computed Tomography ◽  
Pulmonary Artery ◽  
Patent Ductus Arteriosus ◽  
Computed Tomography Angiography ◽  
Ductus Arteriosus ◽  
Pulmonary Veins ◽  
Pulmonary Arteries ◽  
Left Pulmonary Artery ◽  
Artery Occlusion ◽  
Patent Ductus

A 4-year-old boy developed dyspnea 18 months after attempted surgical patent ductus arteriosus closure using a clip that was inadvertently placed on the left pulmonary artery, followed by reoperation to repair the left pulmonary artery with a patch and re-close the ductus. Computed tomography angiography confirmed a large patent ductus arteriosus, left pulmonary artery occlusion, and patent left pulmonary veins. Therefore, a third surgery was performed for suture closure of the ductus and left pulmonary artery repair with an interposition tube graft. Follow-up by transthoracic echocardiography and computed tomography angiography showed good flow in the left and right pulmonary arteries.

Inhibition of elastolysis by SC-37698 reduces development and progression of monocrotaline pulmonary hypertension

1991 ◽  
Vol 261 (4) ◽  
pp. H1255-H1267 ◽  
Author(s):  
C. L. Ye ◽  
M. Rabinovitch
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Vascular Lesions ◽  
Constant Infusion ◽  
Peripheral Arteries ◽  
Vascular Changes ◽  
Elastase Inhibitor ◽  
Indwelling Catheters ◽  
Elastolytic Activity ◽  
Medial Hypertrophy

Our previous studies showed that increased pulmonary artery elastolytic activity is associated with monocrotaline-induced pulmonary hypertension in rats, and the latter is reduced by the elastase inhibitor SC-39026. This agent, given orally, decreases monocrotaline-induced muscularization of normally nonmuscular peripheral arteries but not medial hypertrophy of muscular arteries. To establish whether constant infusion of an elastase inhibitor would reduce both vascular lesions induced by monocrotaline injection, SC-37698 (an analogue of SC-39026) was given intravenously by osmopump. To separately assess whether SC-37698 would inhibit development of the vascular changes as well as their progression, SC-37698 or vehicle was infused for the first 2 wk (2-wk study) or was delayed until 1 wk after monocrotaline injection (3-wk study). Hemodynamic data were recorded from indwelling catheters, and the lungs were evaluated morphologically. Saline-injected control rats given SC-37698 or vehicle were similar at both time points. Monocrotaline-injected rats given SC-37698 compared with those given vehicle alone had lower pulmonary artery pressures, 17.9 +/- 0.5 vs. 23.7 +/- 0.8 mmHg (P less than 0.01) in the 2-wk study and 24.0 +/- 1.8 vs. 33.5 +/- 3.1 mmHg (P less than 0.05) in the 3-wk study. This was associated with significant decreases in muscularization of peripheral arteries and reductions in medial hypertrophy of muscular arteries. In the hilar pulmonary arteries assessed at 3 wk only, SC-37698 significantly decreased monocrotaline-induced endothelial injury, subendothelial edema, migration of smooth muscle cells into subendothelium, medial hypertrophy, collagen accumulation, and abnormal distribution of elastin as interlamellar islands. Pulmonary artery elastolytic activity was reduced in SC-37698-treated compared with untreated monocrotaline-injected rats (P less than 0.05). Thus infusion of SC-37698 reduces monocrotaline-induced pulmonary hypertension when administered before or even after development of early vascular changes.

PREOPERATIVE EVALUATION OF THE PULMONARY VASCULAR BED IN PATIENTS WITH PULMONARY HYPERTENSION ASSOCIATED WITH LEFT TO RIGHT SHUNTS

PEDIATRICS ◽  
1959 ◽  
Vol 24 (3) ◽  
pp. 448-454
Author(s):  
I. Hunter Crittenden ◽  
Forrest H. Adams ◽  
Harrison Latta
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Vascular Disease ◽  
Preoperative Evaluation ◽  
Pulmonary Arteries ◽  
Operative Risk ◽  
Pulmonary Vascular Disease ◽  
Vascular Bed ◽  
The Media ◽  
Index Of Severity

Eighteen patients with pulmonary hypertension associated with left to right cardiac shunts have been studied using acetylcholine injected into the pulmonary artery to determine the distensibility of the vascular bed. The response is considered as an index of severity of vascular disease and of operative risk. Six cases failed to respond to the drug. One of these had received atropine, and the data may not be reliable. Five were 6 years of age or older and had relatively less left to right shunting than the others. Surgery was performed in two of this group of six, and it proved fatal. The small pulmonary arteries in both patients had marked intimal disease. All of the 12 cases that responded to acetylcholine had shunting of at least 140% of the systemic flow, and in five patients tested the shunt increased following injection of the drug. The five cases operated upon from this group had hypertrophy of the media of the small pulmonary arteries and in two cases minimal proliferation of the intima was present. The pulmonary artery pressures were similar in both groups. These observations suggest that the severity of pulmonary vascular disease may be predicted by the method described.

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