Vectorcardiographic Criteria in Right Ventricular Hypertrophy Related to Pulmonary Artery Mean Pressure

2015 ◽  
pp. 76-84
Author(s):  
V. Král ◽  
V. Je�ek ◽  
A. Michaljanic ◽  
P. Fr�dl ◽  
R. Jandová ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Right Ventricular ◽  
Ventricular Hypertrophy ◽  
Right Ventricular Hypertrophy ◽  
Mean Pressure

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

Hypoxic exposure time dependently modulates endothelininduced contraction of pulmonary artery smooth muscle

1998 ◽  
Vol 274 (4) ◽  
pp. L552-L559 ◽  
Author(s):  
Russell A. Bialecki ◽  
Carol S. Fisher ◽  
Wallace W. Murdoch ◽  
Herbert G. Barthlow ◽  
Richard B. Stow ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Pulmonary Artery ◽  
Right Ventricular ◽  
Exposure Time ◽  
Ventricular Hypertrophy ◽  
Plasma Concentrations ◽  
Right Ventricular Hypertrophy ◽  
Hypoxic Exposure ◽  
Pulmonary Artery Smooth Muscle ◽  
Induced Changes

Endothelins (ETs) have been implicated in the pathogenesis of hypoxia-induced pulmonary hypertension. We determined whether hypoxic exposure of rats (10% O2-90% N2, 1 atm, 1–48 days) altered contraction to ET in isolated segments of endothelium-denuded extralobar branch pulmonary artery (PA) and aorta. Hypoxic exposure increased hematocrit, right ventricular hypertrophy, and ET-1 plasma concentration. Hypoxia also caused a sustained decrease in PA but not in aorta sensitivity to ET-1. In comparison, hypoxic exposure throughout 12 days decreased time dependently the maximum contraction of PA to ET-1, BaCl2, and KCl. The hypoxia-induced decrease in maximum contraction of PA to ET-1 returned toward normal levels by 21 days and approximated control levels by 48 days. After 14 days of hypoxia, right ventricular hypertrophy correlated with decreased sensitivity of PA to ET-1. After 21 days of hypoxia, PA sensitivity to ET-2 and ET-3 was decreased, and sarafotoxin S6c-induced contraction was abolished. In conclusion, hypoxic exposure time dependently modulates the responsiveness of PA smooth muscle to ETs, BaCl2, and KCl. The hypoxia-induced changes in tissue responsiveness to ET-1 may be associated with increased plasma concentrations of this peptide.

Changes in pulmonary structure and function induced by monocrotaline intoxication

1981 ◽  
Vol 240 (2) ◽  
pp. H149-H155 ◽  
Author(s):  
F. Ghodsi ◽  
J. A. Will
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Right Ventricular ◽  
Ventricular Hypertrophy ◽  
Pyrrolizidine Alkaloid ◽  
Histological Study ◽  
Right Ventricular Hypertrophy ◽  
Laboratory Animals ◽  
Functional Relationships ◽  
And Function

Monocrotaline, a pyrrolizidine alkaloid derived from Crotalaria spectabilis, is known to be toxic to a variety of domestic and laboratory animals and to humans. Major pathological effects induced by monocrotaline poisoning include hepatic cirrhosis and megalocytosis, venocclusive disease, pulmonary hypertension, and right ventricular hypertrophy. The present investigation explored the structural and functional relationships that exist between pulmonary artery pressure, small pulmonary artery medial thickness, and right ventricular hypertrophy. The results of this physiological and histological study on monocrotaline-intoxicated rats has demonstrated that there is a positive correlation between progressive pulmonary hypertension, thickening of the medical wall of small pulmonary vessels, and right ventricular hypertrophy as a function of time.

Possible role of pulmonary blood volume in chronic hypoxic pulmonary hypertension

1993 ◽  
Vol 74 (6) ◽  
pp. 3020-3026 ◽  
Author(s):  
L. C. Ou ◽  
G. L. Sardella ◽  
N. S. Hill ◽  
C. D. Thron
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Right Ventricular ◽  
Blood Volume ◽  
Ventricular Hypertrophy ◽  
Chronic Hypoxia ◽  
Right Ventricular Hypertrophy ◽  
Hypoxic Pulmonary Hypertension ◽  
Pulmonary Blood Volume

Chronic hypoxia increases the total blood volume (TBV) and pulmonary arterial blood pressure (Ppa) and induces pulmonary vascular remodeling. The present study was undertaken to assess how the pulmonary blood volume (PBV) changes during hypoxia and the possible role of PBV in chronic hypoxic pulmonary hypertension. A novel method has been developed to measure the TBV, PBV, and Ppa in conscious rats. The method consists of chronic implantation of a loose ligature around the ascending aorta and pulmonary artery, so that when the ligature is drawn tightly, it traps the blood in the pulmonary vessels and left heart and simultaneously kills the rat. The pulmonary veins are then ligated to separate the left ventricular blood volume from the PBV. This surgical approach, together with chronic catheterization of the pulmonary artery and the use of 51Cr-labeled red blood cells, allows measurement of TBV, PBV, and Ppa. This method has been used to analyze the relationships between TBV and PBV and between Ppa or right ventricular hypertrophy and PBV in two rat strains with markedly different TBV and Ppa responses to chronic hypoxia. PBV per given lung weight did not increase and even decreased during hypoxia despite marked increases in TBV. There was a close correlation between Ppa or right ventricular hypertrophy and PBV in the two strains of chronically hypoxic animals, suggesting that a greater PBV plays a significant role in the development of severe chronic hypoxic pulmonary hypertension in the altitude-susceptible Hilltop rats.

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