Resolution of Hypoxic Changes in the Heart and Pulmonary Arterioles of Rats during Intermittent Correction of Hypoxia

1977 ◽  
Vol 52 (2) ◽  
pp. 153-162 ◽  
Author(s):  
Enid Leach ◽  
P. Howard ◽  
R. Barer Gwenda
Keyword(s):  
Right Ventricular ◽  
Ventricular Hypertrophy ◽  
Oxygen Therapy ◽  
Cor Pulmonale ◽  
Right Ventricular Hypertrophy ◽  
Airways Obstruction ◽  
Hypoxic Environment ◽  
Normal Environment

1. Rats kept in a hypoxic chamber (10% O2) for 3 or more weeks developed right ventricular hypertrophy, muscularization of pulmonary arterioles and polycythaemia. These changes resemble those found in human hypoxic disease and, in particular, in patients dying from chronic airways obstruction. 2. Resolution of these changes was studied in a normal environment and in an intermittently normal, intermittently hypoxic environment. The latter regimen modelled the situation of patients with cor pulmonale receiving long-term intermittent oxygen therapy. 3. In a normal environment right ventricular hypertrophy and polycythaemia were resolved in 6 weeks but vessel changes were not resolved in 12 weeks. 4. In the intermittently normoxic environment (40 or 80 h in air per week) there was some resolution of right ventricular hypertrophy in 6 weeks but no significant reduction in vessel thickening or in polycythaemia in 12 weeks.

The Electrocardiographic Pattern of Right Ventricular Hypertrophy in Cor Pulmonale (due to Pulmonary Tuberculosis)

Cardiology ◽  
1960 ◽  
Vol 36 (5) ◽  
pp. 287-308 ◽  
Author(s):  
J. Widimský ◽  
A. Valach ◽  
R. Dejdar ◽  
Z. Fejfar ◽  
Z. Vysloužil ◽  
...  
Keyword(s):  
Pulmonary Tuberculosis ◽  
Right Ventricular ◽  
Ventricular Hypertrophy ◽  
Cor Pulmonale ◽  
Right Ventricular Hypertrophy

scholarly journals Nox2 Upregulation and p38α MAPK Activation in Right Ventricular Hypertrophy of Rats Exposed to Long-Term Chronic Intermittent Hypobaric Hypoxia

2020 ◽  
Vol 21 (22) ◽  
pp. 8576
Author(s):  
Eduardo Pena ◽  
Patricia Siques ◽  
Julio Brito ◽  
Silvia M. Arribas ◽  
Rainer Böger ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Nadph Oxidase ◽  
Right Ventricular ◽  
Hypobaric Hypoxia ◽  
Ventricular Hypertrophy ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Right Ventricular Hypertrophy ◽  
Mapk Activation ◽  
Intermittent Hypobaric Hypoxia

One of the consequences of high altitude (hypobaric hypoxia) exposure is the development of right ventricular hypertrophy (RVH). One particular type of exposure is long-term chronic intermittent hypobaric hypoxia (CIH); the molecular alterations in RVH in this particular condition are less known. Studies show an important role of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase complex-induced oxidative stress and protein kinase activation in different models of cardiac hypertrophy. The aim was to determine the oxidative level, NADPH oxidase expression and MAPK activation in rats with RVH induced by CIH. Male Wistar rats were randomly subjected to CIH (2 days hypoxia/2 days normoxia; n = 10) and normoxia (NX; n = 10) for 30 days. Hypoxia was simulated with a hypobaric chamber. Measurements in the RV included the following: hypertrophy, Nox2, Nox4, p22phox, LOX-1 and HIF-1α expression, lipid peroxidation and H2O2 concentration, and p38α and Akt activation. All CIH rats developed RVH and showed an upregulation of LOX-1, Nox2 and p22phox and an increase in lipid peroxidation, HIF-1α stabilization and p38α activation. Rats with long-term CIH-induced RVH clearly showed Nox2, p22phox and LOX-1 upregulation and increased lipid peroxidation, HIF-1α stabilization and p38α activation. Therefore, these molecules may be considered new targets in CIH-induced RVH.

E-4010, a selective phosphodiesterase 5 inhibitor, attenuates hypoxic pulmonary hypertension in rats

1999 ◽  
Vol 277 (2) ◽  
pp. L225-L232 ◽  
Author(s):  
Norihisa Hanasato ◽  
Masahiko Oka ◽  
Masashi Muramatsu ◽  
Mayu Nishino ◽  
Hideyuki Adachi ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Right Ventricular ◽  
Ventricular Hypertrophy ◽  
Chronic Hypoxia ◽  
Systemic Arterial Pressure ◽  
Right Ventricular Hypertrophy ◽  
Pulmonary Arterial

The purpose of this study was to determine whether E-4010, a newly synthesized potent and selective orally active phosphodiesterase (PDE) 5 inhibitor, would prevent the development of chronic hypoxia-induced pulmonary hypertension in rats. In conscious, pulmonary hypertensive rats, a single oral administration of E-4010 (1.0 mg/kg) caused an acute, long-lasting reduction in mean pulmonary arterial pressure (PAP), with no significant effects on systemic arterial pressure, cardiac output, and heart rate. In rats that received food containing 0.01 or 0.1% E-4010 during the 3-wk exposure to hypoxia, mean PAP was significantly decreased (mean PAP 24.0 ± 0.9, 16.2 ± 0.8, and 12.8 ± 0.5 mmHg in rats treated with 0, 0.01, and 0.1% E-4010-containing food, respectively), whereas mean systemic arterial pressure was unchanged and cardiac output was slightly increased compared with chronically hypoxic control rats. Right ventricular hypertrophy, medial wall thickness in pulmonary arteries corresponding to the respiratory and terminal bronchioles, and the degree of muscularization of more distal arteries were less severe in E-4010-treated rats. Long-term treatment with E-4010 caused an increase in cGMP levels in lung tissue and plasma but not in aortic tissue and no significant change in cAMP levels in either lung, aorta, or plasma. These results suggest that long-term oral treatment with E-4010 reduced the increase in PAP, right ventricular hypertrophy, and pulmonary arterial remodeling induced by exposure to chronic hypoxia, probably through increasing cGMP levels in the pulmonary vascular smooth muscle.

scholarly journals Stage IV Sarcoidosis with Cor pulmonale: A Case Report

2016 ◽  
Vol 30 (1) ◽  
pp. 37-42
Author(s):  
Mostashirul Haque ◽  
Tunaggina Afrin Khan ◽  
Md Rasul Amin ◽  
Montasin Rezwan ◽  
Md Rashidul Hasan ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Ventricular Hypertrophy ◽  
Systolic Pressure ◽  
Stage Iv ◽  
Pulmonary Involvement ◽  
Cor Pulmonale ◽  
Right Ventricular Hypertrophy ◽  
Pulmonary Artery Systolic Pressure ◽  
Strain Pattern

Sarcoidosis is a well known systemic disorder that invariably involves lungs. However, pulmonary hypertension and cor-pulmanle are not common due to pulmonary involvement of sarcoidosis. We report a case of pulmonary hypertension leading to corpulmonale due to sarcoidosis. An elderly female suffering from hypertension & sarcoidosis developed complications and arrived at the diagnosis by correlating various investigations. X-ray chest (P/A) showed cardiomegaly (right ventricular type), reticulo-nodular shadow involving both mid and lower zone; characteristic high resolution CT (HRCT) scan appearances include reticulonodular opacities; pulmonary function test showed restrictive type of defect; ECG showed right ventricular hypertrophy with strain pattern; in echocardiogram there were right ventricular hypertrophy (RVH) with pulmonary artery systolic pressure (PASP) of 63 mmHg indicating severe pulmonary arterial hypertension (PH); along with significantly elevated B-type natriuretic peptide(BNP) level.Bangladesh Heart Journal 2015; 30(1) : 37-42

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