Right ventricular hypertrophy in animals at high altitude

The weight of the ventricles and septum in formalin-fixed hearts were determined in six animal species living continuously at altitudes between 10,000 and 15,400 ft in the central Peruvian Andes. Control studies were made of a similar number of hearts obtained from sea-level animals. Guinea pigs, rabbits, dogs, lambs, pigs, and steers all exhibited a moderate hypertrophy of the right ventricle roughly equivalent to a 25% increase in weight. A lesser degree of septal hypertrophy occurred in all animals except steers. The data suggest that a moderate degree of pulmonary hypertension is the probable cause of the right ventricular hypertrophy. In steers this would be roughly the equivalent of a mean pressure of 35 mm Hg at 11,800 ft compared with sea-level pressures of 24 mm Hg. ventricular hypertrophy; altitude; pulmonary hypertension; lambs; pigs; steers Submitted on December 3, 1962

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Transient severe isolated right ventricular hypertrophy in neonates

Cardiology in the Young ◽

10.1017/s1047951103000799 ◽

2003 ◽

Vol 13 (4) ◽

pp. 384-386 ◽

Cited By ~ 2

Author(s):

Munesh Tomar ◽

Sitaraman Radhakrishnan ◽

Savitri Shrivastava

Keyword(s):

Pulmonary Hypertension ◽

Right Ventricular ◽

Ventricular Function ◽

Ventricular Hypertrophy ◽

Pressure Overload ◽

Posterior Wall ◽

Right Ventricular Hypertrophy ◽

Pulmonary Vasculature ◽

Normal Thickness ◽

The Right

We report two instances of transient isolated right-sided myocardial hypertrophy in patients with an intact ventricular septum, normal thickness of the posterior wall of the left ventricle, and normal ventricular function, diagnosed by echocardiography on the third day of life. The two neonates, born at 36 and 38 weeks gestation respectively, had perinatal distress. Both were diagnosed as having isolated right ventricular hypertrophy with mild pulmonary hypertension, which disappeared in both cases within 8 weeks without any specific therapy. Though the cause of the ventricular hypertrophy remains unclear, we believe that it is the consequence of remodeling of pulmonary vasculature secondary to acute perinatal distress, resulting in persistent pulmonary hypertension and producing pressure overload on the right ventricle, and hence right ventricular hypertrophy. The finding of early and transient right ventricular hypertrophy, with normal left-sided structures and normal ventricular function, has thus far failed to gain attention in the paediatric cardiologic literature.

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Activation of the right ventricular endothelin (ET) system in the monocrotaline model of pulmonary hypertension: response to chronic ETA receptor blockade

Clinical Science ◽

10.1042/cs20030139 ◽

2003 ◽

Vol 105 (6) ◽

pp. 647-653 ◽

Cited By ~ 26

Author(s):

Jean-François JASMIN ◽

Peter CERNACEK ◽

Jocelyn DUPUIS

Keyword(s):

Pulmonary Hypertension ◽

Right Ventricle ◽

Right Ventricular ◽

Ventricular Hypertrophy ◽

Right Ventricular Hypertrophy ◽

Lower Percentage ◽

Receptor Blockade ◽

Eta Receptor ◽

Eta Receptor Antagonist ◽

The Right

Although activation of the endothelin (ET) system contributes to pulmonary hypertension, modifications of the cardiopulmonary ET system and its responses to chronic ET receptor blockade are not well known. To investigate this, rats were injected with monocrotaline (60 mg/kg intraperitoneal) or saline, followed with treatment with the selective ETA receptor antagonist LU135252 (LU; 50 mg·kg-1·day-1) or with saline. After 3 weeks, haemodynamics, cardiac hypertrophy, ET-1 levels and cardiopulmonary ET-receptor-binding profile were evaluated. Monocrotaline (n=7) elicited marked pulmonary hypertension and right ventricular hypertrophy compared with controls (n=8). Both variables were substantially attenuated by LU therapy (n=8; P<0.05 for both). After monocrotaline, right ventricular ET-1 levels were more significantly increased than in the left ventricle (+198% compared with +127%; P<0.05). ETB receptor density was augmented (3-fold) in the right ventricle, whereas that of ETA receptors was not affected. LU treatment also significantly attenuated these alterations (P<0.05). In the lungs, ET-1 levels were not increased after monocrotaline, whereas the balance of ETB to ETA receptors was altered, with a trend toward a lower percentage of ETB than in the control rats. LU treatment did not affect these variables in the lungs. Therefore monocrotaline-induced pulmonary hypertension and right ventricular hypertrophy are associated with the up-regulation of ET-1 and ETB receptors in the right ventricle. These alterations are attenuated with the reduction of pulmonary hypertension and right ventricular hypertrophy after chronic blockade of the ETA receptors, supporting the role of the ET system in right ventricular hypertrophy.

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Cystamine Treatment Fails to Prevent the Development of Pulmonary Hypertension in Chronic Hypoxic Rats

Journal of Vascular Research ◽

10.1159/000515511 ◽

2021 ◽

pp. 1-15

Author(s):

Lars K. Markvardsen ◽

Lene D. Sønderskov ◽

Christine Wandall-Frostholm ◽

Estéfano Pinilla ◽

Judit Prat-Duran ◽

...

Keyword(s):

Pulmonary Hypertension ◽

Right Ventricle ◽

Right Ventricular ◽

Lung Tissue ◽

Ventricular Hypertrophy ◽

Systolic Pressure ◽

Right Ventricular Hypertrophy ◽

Ventricular Systolic Pressure ◽

Pulmonary Arterial ◽

The Right

Introduction: Pulmonary hypertension is characterized by vasoconstriction and remodeling of pulmonary arteries, leading to right ventricular hypertrophy and failure. We have previously found upregulation of transglutaminase 2 (TG2) in the right ventricle of chronic hypoxic rats. The hypothesis of the present study was that treatment with the transglutaminase inhibitor, cystamine, would inhibit the development of pulmonary arterial remodeling, pulmonary hypertension, and right ventricular hypertrophy. Methods: Effect of cystamine on transamidase activity was investigated in tissue homogenates. Wistar rats were exposed to chronic hypoxia and treated with vehicle, cystamine (40 mg/kg/day in mini-osmotic pumps), sildenafil (25 mg/kg/day), or the combination for 2 weeks. Results: Cystamine concentration-dependently inhibited TG2 transamidase activity in liver and lung homogenates. In contrast to cystamine, sildenafil reduced right ventricular systolic pressure and hypertrophy and decreased pulmonary vascular resistance and muscularization in chronic hypoxic rats. Fibrosis in the lung tissue decreased in chronic hypoxic rats treated with cystamine. TG2 expression was similar in the right ventricle and lung tissue of drug and vehicle-treated hypoxic rats. Discussion/Conclusions: Cystamine inhibited TG2 transamidase activity, but cystamine failed to prevent pulmonary hypertension, right ventricular hypertrophy, and pulmonary arterial muscularization in the chronic hypoxic rat.

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Lung vessel leak precedes right ventricular hypertrophy in monocrotaline-treated rats

Journal of Applied Physiology ◽

10.1152/jappl.1983.54.2.371 ◽

1983 ◽

Vol 54 (2) ◽

pp. 371-374 ◽

Cited By ~ 64

Author(s):

T. Sugita ◽

T. M. Hyers ◽

I. M. Dauber ◽

W. W. Wagner ◽

I. F. McMurtry ◽

...

Keyword(s):

Pulmonary Hypertension ◽

Right Ventricular ◽

Ventricular Hypertrophy ◽

Dry Weight ◽

Lavage Fluid ◽

Right Ventricular Hypertrophy ◽

Lung Water ◽

Cell Hyperplasia ◽

Albumin Content ◽

The Right

Monocrotaline induces microvascular leak and pulmonary hypertension in rats. We have hypothesized that the leak is related in some way to the pulmonary hypertension and precedes it. In rats given 40 mg monocrotaline/kg body wt subcutaneously, lung wet weight-to-dry weight ratios and lung albumin content began to increase within the first 3 days and became maximal at 1 wk. Alveolar lavage fluid showed little or no increase in protein. Right ventricular hypertrophy increased progressively from 2 through 3 wk. An increase in lung dry weight paralleled the right ventricular hypertrophy. The amount of blood retained in the lung did not account for the increased lung water, albumin, or weight. We considered that microvascular leak without leak into the alveolar space preceded pulmonary hypertension, right ventricular hypertrophy, and increased lung dry weight. In rats not given monocrotaline but exposed for 3 wk to hypobaric hypoxia, lung albumin, lung dry weight, and right ventricular weight increased. Increased lung dry weight probably reflects hyperplasia of lung cells. If so, an association of microvascular leak, lung cell hyperplasia, and right ventricular hypertrophy may occur in both monocrotaline- and hypoxia-induced pulmonary hypertension.

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Neither anticoagulant nor nonanticoagulant heparin affects monocrotaline lung injury

Journal of Applied Physiology ◽

10.1152/jappl.1987.62.2.816 ◽

1987 ◽

Vol 62 (2) ◽

pp. 816-820 ◽

Cited By ~ 5

Author(s):

J. W. Fasules ◽

K. R. Stenmark ◽

P. M. Henson ◽

N. F. Voelkel ◽

J. T. Reeves

Keyword(s):

Pulmonary Hypertension ◽

Lung Injury ◽

Right Ventricular ◽

Ventricular Hypertrophy ◽

Right Ventricular Hypertrophy ◽

Vascular Leak ◽

Hypoxic Pulmonary Hypertension ◽

Antiproliferative Agent ◽

The Right ◽

Insight Into

The administration of monocrotaline to rats causes pulmonary vascular leak within 1 wk followed in 2–3 wk by perivascular proliferation and fatal pulmonary hypertension. Possibly blocking the proliferation might block the pulmonary hypertension, providing insight into its mechanism. Because heparin, given as an antiproliferative agent, reduced hypoxic pulmonary hypertension in mice, it might also block monocrotaline-induced pulmonary hypertension. Alternatively, anticoagulation could worsen the lung injury. We found that heparin (300 and 600 U/kg sc twice daily) inhibited clotting in rats given monocrotaline but did not change the vascular leak, the right ventricular pressure, the right ventricular hypertrophy, the increased medial thickness of the pulmonary arterioles, or the production of a slow-reacting substance of anaphylaxis-like material by the lungs. A nonanticoagulant heparin fragment (2 mg/kg sc twice daily), given to avoid anticoagulation also did not influence the monocrotaline injury. Thus neither anticoagulant nor nonanticoagulant heparin either attenuated or worsened the measured effects of monocrotaline.

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