scholarly journals PULMONARY HYPERTENSION IN RATS LIVING UNDER COMPRESSED AIR CONDITIONS

1934 ◽  
Vol 59 (2) ◽  
pp. 181-193 ◽  
Author(s):  
Granville A. Bennett ◽  
F. J. C. Smith
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Arterial Hypertension ◽  
Right Ventricle ◽  
Arterial Hypertension ◽  
Pulmonary Circulation ◽  
Barometric Pressure ◽  
Compressed Air ◽  
Perivascular Edema ◽  
Pulmonary Arterial ◽  
The Right

1. Pulmonary arterial hypertension was demonstrated in a series of rats that had been kept for 24–31 days in an environment of compressed air, having a barometric pressure of 3040 mm. Hg. The partial pressure of oxygen was 635 mm. Hg, which is equivalent to an 83.6 per cent oxygen mixture at normal barometric pressure. 2. Sclerosing changes in the pulmonary arterioles have been observed which precede the development of demonstrable hypertension in the pulmonary circulation. These vessels showed histological changes that were indicative of injury after 3 days of exposure. There was a thickening of the walls which stained more intensely with eosin, as well as marked perivascular edema and often a narrowing of the lumina. Progressive thickening, narrowing, and hyalinization of the pulmonary arterioles occurred later, after the disappearance of perivascular edema. These changes appeared very similar to the renal arterial lesions seen at autopsy in patients dying from malignant hypertension. 3. Pathological examination did not reveal significant or constant changes from normal in any organs except the lungs and heart. The blood vessels of the systemic circulation showed no pathological change. 4. The walls of the large pulmonary arteries increased in thickness rapidly after the 3rd day of exposure. This change was due to the progressive formation and condensation of fibrous tissue outside of the media and to a lesser extent to thickening of the alternate layers of elastic tissue and smooth muscle in the arterial wall. 5. Marked dilatation of the right ventricle and conus arteriosus as well as small areas of scar tissue formation in the right ventricle were present on prolonged exposure. A few hearts showed larger areas of fibrosis that were visible on macroscopic examination. 6. The systemic arterial blood pressure of a small series of rats exposed to compressed air for 38 days and examined 7 to 10 days after decompression was in each instance less than one-half the average normal pressure. 7. The findings in this study are consistent with the clinical and pathological signs of pulmonary hypertension in man. 8. The anatomical alterations observed in the alveolar units of the lungs were essentially the same as those previously described (1). 9. A method has been devised whereby pulmonary arterial hypertension, accompanied by important sclerotic changes in the arteries of the pulmonary circulation can be induced for investigation.

scholarly journals Comparison of vectorcardiographic parameters with structural-functional state of the right ventricle in patients with pulmonary hypertension

2015 ◽  
Vol 12 (4) ◽  
pp. 57-60
Author(s):  
E V Blinova ◽  
T A Sakhnova ◽  
M A Saidova ◽  
A S Loskutova ◽  
G V Ryabykina ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Arterial Hypertension ◽  
Right Ventricle ◽  
Arterial Hypertension ◽  
Functional State ◽  
Longitudinal Strain ◽  
Echocardiographic Parameters ◽  
Pulmonary Arterial ◽  
Moderate Negative Correlation ◽  
The Right

Changes of the vectrocardiographic ventricular gradient (VG) in patients with pulmonary arterial hypertension (PAH) are indicative of right ventricular (RV) overload and may be used to assess its severity. The study aim was to evaluate interrelations between vectrocardiographic VG, spatial QRS-T angle and echocardiographic parameters of structural-functional state of the RV.The following parameters were assessed in 30 PAH patients: RV dimensions; tricuspid annular plane systolic excursion (TAPSE); RV fractional area change (FAC); RV peak systolic annular velocity (TDI-S’), and longitudinal strain (LS). VG and spatial QRS-T angle were calculated using the orthogonal leads derived from standard echocardiography.Spatial component VG-Y had moderate negative correlation with LS (r=-0.62; p

scholarly journals Potts Shunt in Children With Familial Primary Pulmonary Hypertension: A Case Report and Brief Literature Review

2021 ◽  
Vol 9 (3) ◽  
pp. 247-254
Author(s):  
Mahya Mobinikhaledi ◽  
◽  
Ali Arjmand Shabestari ◽  
Yazdan Ghandi ◽  
◽  
...  
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Pulmonary Arterial Hypertension ◽  
Right Ventricle ◽  
Arterial Hypertension ◽  
Medical Treatment ◽  
Right Heart Failure ◽  
Right Heart ◽  
Pulmonary Arterial ◽  
The Right

Introduction: The primary concern about Familial Pulmonary Arterial Hypertension (FPAH) is the development of right heart failure, which ultimately leads to sudden death. Despite recent advances in pharmacological therapy, the mortality rate in children is still high, emphasizing the importance of novel treatments. Moreover, there is still no definitive treatment for children with severe pulmonary hypertension. The consequences of right heart failure led to the proposal of a surgical approach, the Potts shunt, to decompress the right ventricle, providing shunting of deoxygenated blood to lower extremities and improving overall cardiac output. This surgical technique creates an anastomosis between the left pulmonary artery and the descending aorta, providing a palliative treatment to off-load the right ventricle. Case Presentation: We report an 11-year-old girl with familial pulmonary arterial hypertension and right ventricular failure who benefited from a Potts shunt with good mid-term results. The patient was diagnosed at the age of 5 when she had a history of fainting and persistent syncope. The patient was under medical treatment therapy with bosentan, sildenafil, acetylsalicylic acid, and warfarin for six years. The results of molecular genetic testing, which was confirmed with direct sequencing of the Bone Morphogenetic Protein Receptor Type 2 (BMPR2) gene, revealed a heterozygous pathogenic mutation. Since she was diagnosed with Pulmonary Arterial Hypertension (PAH), she lost her grandmother, an aunt, and father because of PAH. Her 14-year-old sister also had mutated the BMPR2 gene without developing FPAH. Conclusions: The Potts shunt provides an interventional step for palliation of patients with familial pulmonary hypertension and severe right heart failure refractory to medical treatment. It opens the door to the possibility of lung transplantation in the future. We did not see any complications within 6 years after placing the Potts shunt.

scholarly journals Effects of ovariectomy on antioxidant defence systems in the right ventricle of female rats with pulmonary arterial hypertension induced by monocrotaline

2018 ◽  
Vol 96 (3) ◽  
pp. 295-303 ◽  
Author(s):  
Rafaela Siqueira ◽  
Rafael Colombo ◽  
Adriana Conzatti ◽  
Alexandre Luz de Castro ◽  
Cristina Campos Carraro ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Pulmonary Arterial Hypertension ◽  
Right Ventricle ◽  
Protein Expression ◽  
Arterial Hypertension ◽  
Female Rats ◽  
Antioxidant Defenses ◽  
Thioredoxin 1 ◽  
Pulmonary Arterial ◽  
The Right

The aim of this study was to evaluate the impact of ovariectomy on oxidative stress in the right ventricle (RV) of female rats with pulmonary arterial hypertension (PAH) induced by monocrotaline (MCT). Rats were divided into 4 groups (n = 6 per group): sham (S), sham + MCT (SM), ovariectomized (O), and ovariectomized + MCT (OM). MCT (60 mg·kg−1 i.p.) was injected 1 week after ovariectomy or sham surgery. Three weeks later, echocardiographic analysis and RV catheterisation were performed. RV morphometric, biochemical, and protein expression analysis through Western blotting were done. MCT promoted a slight increase in pulmonary artery pressure, without differences between the SM and OM groups, but did not induce RV hypertrophy. RV hydrogen peroxide increased in the MCT groups, but SOD, CAT, and GPx activities were also enhanced. Non-classical antioxidant defenses diminished in ovariectomized groups, probably due to a decrease in the nuclear factor Nrf2. Hemoxygenase-1 and thioredoxin-1 protein expression was increased in the OM group compared with SM, being accompanied by an elevation in the estrogen receptor β (ER-β). Hemoxygenase-1 and thioredoxin-1 may be involved in the modulation of oxidative stress in the OM group, and this could be responsible for attenuation of PAH and RV remodeling.

scholarly journals The striated muscles in pulmonary arterial hypertension: adaptations beyond the right ventricle

2015 ◽  
Vol 46 (3) ◽  
pp. 832-842 ◽  
Author(s):  
Emmy Manders ◽  
Silvia Rain ◽  
Harm-Jan Bogaard ◽  
M. Louis Handoko ◽  
Ger J.M. Stienen ◽  
...  
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Right Ventricle ◽  
Arterial Hypertension ◽  
Right Heart Failure ◽  
Exercise Intolerance ◽  
Muscle Dysfunction ◽  
Striated Muscles ◽  
Pulmonary Arterial ◽  
The Right ◽  
The Impact

Pulmonary arterial hypertension (PAH) is a fatal lung disease characterised by progressive remodelling of the small pulmonary vessels. The daily-life activities of patients with PAH are severely limited by exertional fatigue and dyspnoea. Typically, these symptoms have been explained by right heart failure. However, an increasing number of studies reveal that the impact of the PAH reaches further than the pulmonary circulation. Striated muscles other than the right ventricle are affected in PAH, such as the left ventricle, the diaphragm and peripheral skeletal muscles. Alterations in these striated muscles are associated with exercise intolerance and reduced quality of life. In this Back to Basics article on striated muscle function in PAH, we provide insight into the pathophysiological mechanisms causing muscle dysfunction in PAH and discuss potential new therapeutic strategies to restore muscle dysfunction.

scholarly journals MicroRNA-140 is elevated and mitofusin-1 is downregulated in the right ventricle of the Sugen5416/hypoxia/normoxia model of pulmonary arterial hypertension.

2016 ◽  
Vol 311 (3) ◽  
pp. H689-H698 ◽  
Author(s):  
Sachindra Raj Joshi ◽  
Vidhi Dhagia ◽  
Salina Gairhe ◽  
John G. Edwards ◽  
Ivan F. McMurtry ◽  
...  
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Right Ventricle ◽  
Arterial Hypertension ◽  
Systolic Pressure ◽  
Right Heart ◽  
Biochemical Processes ◽  
Pulmonary Arterial ◽  
Direct Target ◽  
The Right ◽  
Mitofusin 1

Heart failure, a major cause of morbidity and mortality in patients with pulmonary arterial hypertension (PAH), is an outcome of complex biochemical processes. In this study, we determined changes in microRNAs (miRs) in the right and left ventricles of normal and PAH rats. Using an unbiased quantitative miR microarray analysis, we found 1) miR-21-5p, miR-31-5 and 3p, miR-140-5 and 3p, miR-208b-3p, miR-221-3p, miR-222-3p, miR-702-3p, and miR-1298 were upregulated (>2-fold; P < 0.05) in the right ventricle (RV) of PAH compared with normal rats; 2) miR-31-5 and 3p, and miR-208b-3p were upregulated (>2-fold; P < 0.05) in the left ventricle plus septum (LV+S) of PAH compared with normal rats; 3) miR-187-5p, miR-208a-3p, and miR-877 were downregulated (>2-fold; P < 0.05) in the RV of PAH compared with normal rats; and 4) no miRs were up- or downregulated with >2-fold in LV+S compared with RV of PAH and normal. Upregulation of miR-140 and miR-31 in the hypertrophic RV was further confirmed by quantitative PCR. Interestingly, compared with control rats, expression of mitofusin-1 (MFN1), a mitochondrial fusion protein that regulates apoptosis, and which is a direct target of miR-140, was reduced in the RV relative to LV+S of PAH rats. We found a correlation between increased miR-140 and decreased MFN1 expression in the hypertrophic RV. Our results also demonstrated that upregulation of miR-140 and downregulation of MFN1 correlated with increased RV systolic pressure and hypertrophy. These results suggest that miR-140 and MFN1 play a role in the pathogenesis of PAH-associated RV dysfunction. Listen to this article's corresponding podcast at http://ajpheart.podbean.com/e/mir140-and-right-heart-hypertrophy/ .

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