scholarly journals Expression and Correlation of Hypoxia-Inducible Factor-1α (HIF-1α) with Pulmonary Artery Remodeling and Right Ventricular Hypertrophy in Experimental Pulmonary Embolism

2017 ◽  
Vol 23 ◽  
pp. 2083-2088 ◽  
Author(s):  
Wenjuan Liu ◽  
Yimei Zhang ◽  
Liwen Lu ◽  
Liling Wang ◽  
Mingxin Chen ◽  
...  
Keyword(s):  
Pulmonary Embolism ◽  
Pulmonary Artery ◽  
Right Ventricular ◽  
Ventricular Hypertrophy ◽  
Hypoxia Inducible Factor ◽  
Right Ventricular Hypertrophy ◽  
Hypoxia Inducible Factor 1Α ◽  
Artery Remodeling ◽  
Pulmonary Artery Remodeling

Effect of right ventricular hypertrophy on infundibular pressure gradients in dogs

1965 ◽  
Vol 209 (3) ◽  
pp. 513-518
Author(s):  
Peter E. Blundell ◽  
John R. Tobin ◽  
H. J. C. Swan
Keyword(s):  
Pulmonary Artery ◽  
Pressure Gradient ◽  
Right Ventricular ◽  
Arteriovenous Fistula ◽  
Ventricular Hypertrophy ◽  
Pressure Overload ◽  
Volume Overload ◽  
Right Ventricular Hypertrophy ◽  
Pulmonary Artery Banding ◽  
Pressure Gradients

Right ventricular hypertrophy was produced in normal dogs: in six by means of pressure overload (pulmonary artery banding) and in six by means of volume overload (systemic arteriovenous fistula). A greater degree of hypertrophy resulted from the latter procedure. Right ventricular hypertrophy due to chronic pressure overload causes a greater degree of infundibular constriction and much higher pressure gradient than in normal animals or in animals with volume overload. Infundibular pressure gradients associated with severe hypertrophy due to volume overload are not significantly greater than those observed in normal dogs. Infundibular gradients are dominantly related to narrowing of the outflow tract.

Astragalus Polysaccharides Attenuate Monocrotaline-Induced Pulmonary Arterial Hypertension in Rats

2017 ◽  
Vol 45 (04) ◽  
pp. 773-789 ◽  
Author(s):  
Lin-Bo Yuan ◽  
Chun-Yan Hua ◽  
Sheng Gao ◽  
Ya-Ling Yin ◽  
Mao Dai ◽  
...  
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Pulmonary Artery ◽  
Arterial Hypertension ◽  
Right Ventricular ◽  
Ventricular Hypertrophy ◽  
Biological Activities ◽  
Right Ventricular Hypertrophy ◽  
Astragalus Polysaccharides ◽  
Pulmonary Hemodynamic ◽  
Pulmonary Arterial

Astragalus polysaccharides (APS) have been shown to possess a variety of biological activities including anti-oxidant and anti-inflammation functions in a number of diseases. However, their function in pulmonary arterial hypertension (PAH) is still unknown. Rats received APS (200[Formula: see text]mg/kg once two days) for 2 weeks after being injected with monocrotaline (MCT; 60[Formula: see text]mg/kg). The pulmonary hemodynamic index, right ventricular hypertrophy, and lung morphological features of the rat models were examined, as well as the NO/eNOS ratio of wet lung and dry lung weight and MPO. A qRT-PCR and p-I[Formula: see text]B was used to assess IL-1[Formula: see text], IL-6 and TNF-[Formula: see text] and WB was used to detect the total I[Formula: see text]B. Based on these measurements, it was found that APS reversed the MCT-induced increase in mean pulmonary arterial pressure (mPAP) (from 32.731[Formula: see text]mmHg to 26.707[Formula: see text]mmHg), decreased pulmonary vascular resistance (PVR) (from 289.021[Formula: see text]mmHg[Formula: see text][Formula: see text] min/L to 246.351[Formula: see text]mmHg[Formula: see text][Formula: see text][Formula: see text]min/L), and reduced right ventricular hypertrophy (from 289.021[Formula: see text]mmHg[Formula: see text][Formula: see text][Formula: see text]min/L to 246.351 mmHg[Formula: see text][Formula: see text][Formula: see text]min/L) ([Formula: see text]0.05). In terms of pulmonary artery remodeling, the WT% and WA% decreased with the addition of APS. In addition, it was found that APS promoted the synthesis of eNOS and the secretion of NO, promoting vasodilation and APS decreased the MCT-induced elevation of MPO, IL-1[Formula: see text], IL-6 and TNF-[Formula: see text], reducing inflammation. Furthermore, APS was able to inhibit the activation of pho-I[Formula: see text]B[Formula: see text]. In couclusion, APS ameliorates MCT-induced pulmonary artery hypertension by inhibiting pulmonary arterial remodeling partially via eNOS/NO and NF-[Formula: see text]B signaling pathways.

scholarly journals Right ventricular hypertrophy and diastolic dysfunction in arterial switch patients without pulmonary artery stenosis

Heart ◽  
2006 ◽  
Vol 93 (12) ◽  
pp. 1604-1608 ◽  
Author(s):  
H B Grotenhuis ◽  
L J M Kroft ◽  
S G C van Elderen ◽  
J J M Westenberg ◽  
J Doornbos ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Right Ventricular ◽  
Diastolic Dysfunction ◽  
Ventricular Hypertrophy ◽  
Right Ventricular Hypertrophy ◽  
Artery Stenosis ◽  
Pulmonary Artery Stenosis ◽  
Arterial Switch

Effects of exercise on monocrotaline-induced changes in right heart function and pulmonary artery remodeling in rats

2013 ◽  
Vol 91 (1) ◽  
pp. 38-44 ◽  
Author(s):  
Rafael Colombo ◽  
Rafaela Siqueira ◽  
Cristiano Urbano Becker ◽  
Tânia Gatelli Fernandes ◽  
Karla Maria Pires ◽  
...  
Keyword(s):  
Exercise Training ◽  
Pulmonary Artery ◽  
Right Ventricle ◽  
Right Ventricular ◽  
Right Heart ◽  
Interstitial Volume ◽  
Artery Remodeling ◽  
Gsk 3Β ◽  
The Right ◽  
Pulmonary Artery Remodeling

Pulmonary arterial hypertension (PAH) induced by monocrotaline (MCT) is an experimental protocol of right heart failure. We analyzed the role of exercise training on the right ventricle structure and function, pulmonary artery remodeling, and GSK-3β expression. Rats were divided among the following groups: sedentary control (SC), sedentary monocrotaline (SM), trained control (TC), and trained monocrotaline (TM). Rats underwent exercise training for a period of 5 weeks, with 3 weeks post-MCT injection. Rats in the SM and TM groups presented with an increase in right ventricle hypertrophy indexes and lung congestion. The right ventricular end diastolic pressure (RVEDP), right ventricular systolic pressure (RVSP), and its minimum and maximal pressure derivates were increased in the SM and TM groups. The right ventricle interstitial volume pulmonary artery thickness and p-GSK-3β/GSK-3β were increased in the MCT groups as compared with the control groups. The TM group had a reduction in interstitial volume, p-GSK-3β/GSK-3β ratio, pulmonary artery thickness, RVEDP, and an increase in intramyocardial vessels volume as compared with the SM group. The overall results have shown that the exercise protocol used promoted positive changes in right ventricle and pulmonary artery remodeling. These observations also suggest that structural remodeling may be influenced by signaling proteins, such as GSK-3β.

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