Life-long consequences of postnatal normoxia exposure in rats raised at high altitude

2012 ◽  
Vol 112 (1) ◽  
pp. 33-41 ◽  
Author(s):  
Delphine Lumbroso ◽  
Alexandra Lemoine ◽  
Marcelino Gonzales ◽  
Gabriela Villalpando ◽  
Tommy Seaborn ◽  
...  
Keyword(s):  
Right Ventricular ◽  
High Altitude ◽  
Ventricular Hypertrophy ◽  
Minute Ventilation ◽  
Right Ventricular Hypertrophy ◽  
Male Rats ◽  
Whole Body ◽  
La Paz ◽  
Respiratory Parameters ◽  
Air Space

We tested the hypothesis that exposure of high-altitude (HA) rats to a period of postnatal normoxia has long-term consequences on the ventilatory and hematological acclimatization in adults. Male and female HA rats (3,600 m, Po2 ≃ 100 Torr; La Paz, Bolivia) were exposed to normal room air [HA control (HACont)] or enriched oxygen (32% O2; Po2 ≃ 160 Torr) from 1 day before to 15 days after birth [HA postnatal normoxia (HApNorm)]. Hematocrit and hemoglobin values were assessed at 2, 12, and 32 wk of age. Cardiac and lung morphology were assessed at 12 wk by measuring right ventricular hypertrophy (pulmonary hypertension index) and lung air space-to-tissue ratio (indicative of alveolarization). Respiratory parameters under baseline conditions and in response to 32% O2 for 10 min (relieving the ambient hypoxic stimulus) were measured by whole body plethysmography at 12 wk. Finally, we performed a survival analysis up to 600 days of age. Compared with HACont, HApNorm rats had reduced hematocrit and hemoglobin levels at all ages (both sexes); reduced right ventricular hypertrophy (both sexes); lower air space-to-tissue ratio in the lungs (males only); reduced CO2 production rate, but higher oxygen uptake (males only); and similar respiratory frequency, tidal volume, and minute ventilation. When breathing 32% O2, HApNorm male rats had a stronger decrease of minute ventilation than HACont. HApNorm rats had a marked tendency toward longer survival throughout the study. We conclude that exposure to ambient hypoxia during postnatal development in HA rats has deleterious consequences on acclimatization to hypoxia as adults.

Further evidence for the involvement of anatomical parameters of the cardiopulmonary system in the development of ascites syndrome in broiler chickens

2008 ◽  
Vol 56 (1) ◽  
pp. 71-80 ◽  
Author(s):  
Mohammad Hassanzadeh ◽  
Johan Buyse ◽  
Eddy Decuypere
Keyword(s):  
Right Ventricular ◽  
High Altitude ◽  
Broiler Chickens ◽  
Ventricular Hypertrophy ◽  
Developmental Trajectories ◽  
Right Ventricular Hypertrophy ◽  
Thoracic Cavity ◽  
Low Altitude ◽  
Cardiopulmonary System ◽  
Anatomical Parameters

Eggs from a broiler line were incubated at two different altitudes and hatched. Relative heart and lung weights, volumes of the heart, lung and thoracic cavity, incidence of right ventricular hypertrophy and ascites, and related physiological parameters were followed in the day-old chickens hatched from the above eggs. Lung and heart weights as a percentage of body weight, lung and heart volumes relative to the volume of the thoracic cavity after removing the heart and lungs were higher in chickens hatched at high altitude. Additionally, embryonic triiodothyronine (T3) and thyroxine (T4) levels relative to cardiopulmonary parameters were higher in day-old chickens that hatched at high altitude as compared with chickens hatched at low altitude. This was associated with a lower incidence of right ventricular hypertrophy and ascites in chickens hatched at high altitude. Our data indicate that chronic hypoxia interacting with the endogenous functions of embryos during embryonic development at high altitude, as adaptation mechanisms, changed the developmental trajectories of cardiopulmonary parameters in postnatal chickens. This important development facilitates an increase in the gas exchange area in broiler chickens, thus lowering their susceptibility to pulmonary hypertension and ascites.

Chronic propranolol treatment blunts right ventricular hypertrophy in rats at high altitude

1980 ◽  
Vol 48 (3) ◽  
pp. 473-478 ◽  
Author(s):  
N. F. Voelkel ◽  
I. F. McMurtry ◽  
J. T. Reeves
Keyword(s):  
Right Ventricular ◽  
High Altitude ◽  
Ventricular Hypertrophy ◽  
Pressor Response ◽  
Acute Hypoxia ◽  
Right Ventricular Hypertrophy ◽  
Receptor Blockade ◽  
Beta Receptor ◽  
Propranolol Treatment ◽  
Beta Receptor Blockade

Chronic beta-receptor blockade has been reported to inhibit right ventricular hypertrophy in rats at high altitude. If so, we wanted to determine whether beta-receptor blockade or some other drug action were involved and whether the heart, the lung vessels, or blood alterations were affected. In rats, chronic treatment with DL-propranolol (2 mg/kg ip once daily) reduced right ventricular hypertrophy and polycythemia of chronic high altitude. D-Propranolol and metoprolol did not reduce hypoxia-induced right ventricular hypertrophy or polycythemia. In isolated lungs from low-altitude rats treated chronically with DL-propranolol or with D-propranolol the pressor response to acute hypoxia was blunted. Chronic DL-propranolol blunted the acute hypoxic pressor response and angiotensin II induced vasoconstriction in lungs from high-altitude rats. Two effects of DL-propranolol treatment were seen: 1) blockade of beta 2-adrenergic receptors, which reduced the right ventricular hypertrophy of high altitude through reduction of hematocrit; and 2) a non-beta-effect, which reduced vascular responsiveness to acute hypoxia in the isolated lung preparation.

Lung vascular smooth muscle as a determinant of pulmonary hypertension at high altitude

1975 ◽  
Vol 228 (3) ◽  
pp. 762-767 ◽  
Author(s):  
A Tucker ◽  
IF McMurtry ◽  
JT Reeves ◽  
AF Alexander ◽  
DH Will ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Right Ventricular ◽  
High Altitude ◽  
Ventricular Hypertrophy ◽  
Mammalian Species ◽  
Systolic Pressure ◽  
Right Ventricular Hypertrophy ◽  
Ventricular Systolic Pressure

The pulmonary hypertensive response to chronic hypoxia varies markedly among mammalian species. An explanation for this variability was sought by exposing seven species to hypobaric hypoxia (PB equal to 435 mmHg) for 19-48 days. Control animals were studied at 1,600 m (PB equal to 630 mmHg). The pulmonary hypertension that developed varied in the following order of decreasing severity: calf and pig (severe); rat and rabbit (moderate); sheep, guinea pig, and dog (mild). Right ventricular hypertrophy developed in proportion to the elevation in right ventricular systolic pressure. These interspecies variations in response were not correlated with the degree of arterial hypoxemia, degree of polycythemia, elevation in heart rate, or postnatal age. However, the medial thickness of the small pulmonary arteries in control animals was highly correlated with the development of pulmonary hypertension and right ventricular hypertrophy in hypoxic animals. Thus, the amount of lung vascular smooth muscle inherent within each species is a major determinant of the pulmonary hypertensive response to high altitude and contributes to the interspecies variability in this response.

Reversibility of electrophysiological changes induced by chronic high-altitude hypoxia in adult rat heart

2002 ◽  
Vol 282 (4) ◽  
pp. H1452-H1460 ◽  
Author(s):  
C. Chouabe ◽  
J. Amsellem ◽  
L. Espinosa ◽  
P. Ribaux ◽  
S. Blaineau ◽  
...  
Keyword(s):  
Right Ventricular ◽  
High Altitude ◽  
Current Density ◽  
Ventricular Hypertrophy ◽  
Right Ventricular Hypertrophy ◽  
Heart Weight ◽  
Altitude Hypoxia ◽  
Altitude Exposure ◽  
High Altitude Hypoxia ◽  
The Right

Recent studies indicate that regression of left ventricular hypertrophy normalizes membrane ionic current abnormalities. This work was designed to determine whether regression of right ventricular hypertrophy induced by permanent high-altitude exposure (4,500 m, 20 days) in adult rats also normalizes changes of ventricular myocyte electrophysiology. According to the current data, prolonged action potential, decreased transient outward current density, and increased inward sodium/calcium exchange current density normalized 20 days after the end of altitude exposure, whereas right ventricular hypertrophy evidenced by both the right ventricular weight-to-heart weight ratio and the right ventricular free wall thickness measurement normalized 40 days after the end of altitude exposure. This morphological normalization occurred at both the level of muscular tissue, as shown by the decrease toward control values of some myocyte parameters (perimeter, capacitance, and width), and the level of the interstitial collagenous connective tissue. In the chronic high-altitude hypoxia model, the regression of right ventricular hypertrophy would not be a prerequisite for normalization of ventricular electrophysiological abnormalities.

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