The Influence of Hydrogen Ion in the Control of Pulmonary Artery Pressures in Patients with Obstructive Disease of the Lungs1

2015 ◽  
pp. 108-117
Author(s):  
R�jane M. Harvey
Keyword(s):  
Pulmonary Artery ◽  
Hydrogen Ion ◽  
Obstructive Disease

Efficacy of Pulmonary Artery Banding in the Prevention of Pulmonary Vascular Obstructive Disease

Cardiology ◽  
1994 ◽  
Vol 85 (3-4) ◽  
pp. 207-215 ◽  
Author(s):  
Andreas Borowski ◽  
Mathias Zeuchner ◽  
Sabine Schickendantz ◽  
Harald Korb
Keyword(s):  
Pulmonary Artery ◽  
Pulmonary Artery Banding ◽  
Obstructive Disease ◽  
Pulmonary Vascular Obstructive Disease

scholarly journals Truncus arteriosus with single pulmonary artery: Influence of pulmonary vascular obstructive disease on early and late operative results

1985 ◽  
Vol 5 (5) ◽  
pp. 1168-1172 ◽  
Author(s):  
Derek A. Fyfe ◽  
David J. Driscoll ◽  
Roberto M. Di Donato ◽  
Francisco J. Puga ◽  
Gordon K. Danielson ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Truncus Arteriosus ◽  
Operative Results ◽  
Obstructive Disease ◽  
Pulmonary Vascular Obstructive Disease

scholarly journals OBSERVATIONS ON RESISTANCE TO THE FLOW OF BLOOD TO AND FROM THE LUNGS

1927 ◽  
Vol 45 (4) ◽  
pp. 655-671 ◽  
Author(s):  
Richmond L. Moore ◽  
Carl A. L. Binger
Keyword(s):  
Pulmonary Artery ◽  
Pulmonary Veins ◽  
Hydrogen Ion ◽  
Ion Concentration ◽  
Tissue Elasticity ◽  
Hydrogen Ion Concentration ◽  
Starch Grains ◽  
Vascular Bed ◽  
Shallow Breathing ◽  
Pulmonary Vascular Bed

1. Embolism of pulmonary arterioles and capillaries produced by the intravenous injection of starch grains results in a dilatation of the pulmonary artery and the right chambers of the heart. This has been demonstrated both by x-ray studies and direct inspection. 2. The dilatation of the pulmonary artery and heart occurs synchronously with the acceleration of respirations. 3. Dilatation of these structures produced by other means, such as obstruction to the flow of blood to and from the lungs, by gradually clamping either the pulmonary artery (cat and dog) or pulmonary veins (cat) does not, however, give rise to rapid and shallow breathing. 4. The effect of these maneuvers on respiration does not become apparent until respirations suddenly cease. 5. Neither does sudden restriction of the pulmonary vascular bed by clamping the left branch of the pulmonary artery give rise to rapid and shallow breathing, though this procedure may cause an increase in CO2 tension and in hydrogen ion concentration of the blood. 6. Since rapid and shallow breathing is not the result of (1) anoxemia, (2) increased pCO2 and hydrogen ion concentration of the serum, (3) restriction of pulmonary vascular bed by nearly half, (4) increase in resistance to the flow of blood to and from the lungs) (5) the presence of starch grains in the lungs acting as a local irritant, it must be the result of the secondary pathological changes which occur in the pulmonary parenchyma following embolism. 7. The nature of these changes, congestion and edema, has been discussed elsewhere. Whether they operate directly on nerve endings or through their influence on lung volume and tissue elasticity is not certain. 8. Various important clinical analogies have been emphasized.

Anomalous origin of one pulmonary artery from the ascending aorta: 36 years' experience from one centre

1998 ◽  
Vol 8 (4) ◽  
pp. 449-454 ◽  
Author(s):  
Riyadh M. Abu-Sulaiman ◽  
Aijaz Hashmi ◽  
Brian W. McCrindle ◽  
William G. Williams ◽  
Robert M. Freedom
Keyword(s):  
Pulmonary Artery ◽  
Balloon Dilation ◽  
Total Mortality ◽  
Ascending Aorta ◽  
Arterial Stenosis ◽  
Anomalous Origin ◽  
Obstructive Disease ◽  
Mild Stenosis ◽  
Associated Lesions ◽  
Pulmonary Vascular Obstructive Disease

AbstractAnomalous origin of one pulmonary artery from the ascending aorta is an uncommon lesion with an uncertain outcome. We reviewed 16 consecutive children (9 males) presenting with this lesion over a 36 year period at a single institution. Median age at presentation was 2 days (range, birth to 3.2 years). The anomalous pulmonary was the right in 12 and the left in 4, all originating from the proximal ascending aorta, with no patient having stenosis at the origin of the anomalous pulmonary artery. Associated cardiac anomalies were noted in 9 patients. No intervention was attempted in 2 patients: one was deemed inoperable due to complex associated lesions and pulmonary vascular obstructive disease, while the other one died before repair. Surgical intervention was attempted in 14 patients, with 3 intraoperative deaths (21%). Of 11 operative survivors, 8 developed pulmonary arterial stenosis graded severe in 2, moderate in 1 and mild in 5. Patients with severe stenosis required surgical angioplasty, 1 after unsuccessful dilation combined with placement of an endovascular stent. One patient with moderate, and one with mild, stenosis underwent successful transcatheter balloon dilation. The remaining 4 patients with mild stenosis remain unchanged during follow-up. One patient had biopsy evidence of pulmonary vascular obstructive disease at 3.3 years of age. There were no late deaths, giving a total mortality of 25% (4/16).ConclusionWhile early diagnosis and repair of anomalous origin of one pulmonary artery from the ascending aorta is necessary, restenosis of the site of repair is common.

Endogenous hydrogen sulfide sulfhydrates IKKβ at cysteine 179 to control pulmonary artery endothelial cell inflammation

2019 ◽  
Vol 133 (20) ◽  
pp. 2045-2059 ◽  
Author(s):  
Da Zhang ◽  
Xiuli Wang ◽  
Siyao Chen ◽  
Selena Chen ◽  
Wen Yu ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Endothelial Cell ◽  
Pulmonary Artery ◽  
Cell Model ◽  
Site Directed Mutagenesis ◽  
Critical Event ◽  
Hypertensive Rats ◽  
Pulmonary Artery Endothelial Cell

Abstract Background: Pulmonary artery endothelial cell (PAEC) inflammation is a critical event in the development of pulmonary arterial hypertension (PAH). However, the pathogenesis of PAEC inflammation remains unclear. Methods: Purified recombinant human inhibitor of κB kinase subunit β (IKKβ) protein, human PAECs and monocrotaline-induced pulmonary hypertensive rats were employed in the study. Site-directed mutagenesis, gene knockdown or overexpression were conducted to manipulate the expression or activity of a target protein. Results: We showed that hydrogen sulfide (H2S) inhibited IKKβ activation in the cell model of human PAEC inflammation induced by monocrotaline pyrrole-stimulation or knockdown of cystathionine γ-lyase (CSE), an H2S generating enzyme. Mechanistically, H2S was proved to inhibit IKKβ activity directly via sulfhydrating IKKβ at cysteinyl residue 179 (C179) in purified recombinant IKKβ protein in vitro, whereas thiol reductant dithiothreitol (DTT) reversed H2S-induced IKKβ inactivation. Furthermore, to demonstrate the significance of IKKβ sulfhydration by H2S in the development of PAEC inflammation, we mutated C179 to serine (C179S) in IKKβ. In purified IKKβ protein, C179S mutation of IKKβ abolished H2S-induced IKKβ sulfhydration and the subsequent IKKβ inactivation. In human PAECs, C179S mutation of IKKβ blocked H2S-inhibited IKKβ activation and PAEC inflammatory response. In pulmonary hypertensive rats, C179S mutation of IKKβ abolished the inhibitory effect of H2S on IKKβ activation and pulmonary vascular inflammation and remodeling. Conclusion: Collectively, our in vivo and in vitro findings demonstrated, for the first time, that endogenous H2S directly inactivated IKKβ via sulfhydrating IKKβ at Cys179 to inhibit nuclear factor-κB (NF-κB) pathway activation and thereby control PAEC inflammation in PAH.

Symptom-free T4 lung cancer with bilateral pulmonary artery infiltration

2005 ◽  
Vol 6 (1) ◽  
pp. 64-64
Author(s):  
A CESARIO ◽  
D ONORATI ◽  
V CARDACI ◽  
S MARGARITORA ◽  
V PORZIELLA ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Pulmonary Artery ◽  
Free T4 ◽  
T4 Lung Cancer
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