Regression of altitude-produced cardiac hypertrophy.

Sizemore, David A.; McIntyre, Thom; Liere, Edward J. Van; Wilson, M F

doi:10.1152/jappl.1973.35.4.518

Cited by 16 publications

(13 citation statements)

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“…Severe hypoxia was applied in a hypobaric chamber for 4-8 h?day -1 , 5-7 days a week, with a total of 13-24 exposures. Oxygen pressure in the inspired air ranged from 56 mmHg [30] to 70 mmHg [31]. The results were fairly uniform.…”

Section: Intermittent Hypoxia In Animal Modelsmentioning

confidence: 89%

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Effects of intermittent hypoxia on pulmonary haemodynamics: animal modelsversusstudies in humans

Zieliński¹

2005

Eur Respir J

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The aim of this review was to analyse the effects of intermittent hypoxia (IH) on pulmonary haemodynamics, comparing results of animal experiments with results of clinical studies.In animal investigations even short hypoxic exposure, continuously or in short repeated episodes mimicking obstructive sleep apnoea (OSA), leads to pulmonary artery remodelling and to pulmonary hypertension (PH). Results of investigations on effects of nocturnal IH on pulmonary haemodynamics in patients with chronic obstructive pulmonary disease (COPD) are discordant. Earlier studies reported the development of mild PH in subjects desaturating during sleep, while more recent investigations did not confirm those findings.Alveolar IH developing during apnoeic episodes during sleep in OSA patients is a diseaseinduced model to study its effects on pulmonary haemodynamics. In the majority of studies in OSA patients pulmonary arterial pressure remained within normal values. PH was found in patients with OSA accompanied by COPD and/or extreme obesity.People commuting between lowland and high altitude due to their employment, are also repeatedly exposed to IH. Results of clinical investigations suggest that it did not lead to the development of permanent PH.The mechanisms of discrepancies between effects of intermittent hypoxia in animal models and in humans remain to be studied.

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Section: Intermittent Hypoxia In Animal Modelsmentioning

confidence: 89%

“…Several investigations have been performed in rats, evaluating effects of intermittent hypoxia (IH) on pulmonary haemodynamics [27][28][29][30][31]. Severe hypoxia was applied in a hypobaric chamber for 4-8 h?day -1 , 5-7 days a week, with a total of 13-24 exposures.…”

Section: Intermittent Hypoxia In Animal Modelsmentioning

confidence: 99%

Effects of intermittent hypoxia on pulmonary haemodynamics: animal modelsversusstudies in humans

Zieliński¹

2005

Eur Respir J

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“…RVH is observed in most ani mals exposed to high altitude [1-3, 6, 13, 15,25, 26], Several studies have been conducted to characterize the regression of hypoxia-in duced pulmonary circulatory changes fol lowing return to normoxic conditions. RVH appears to resolve rapidly [1,9,11,14,27]; however, the regression of pul monary hypertension [1,10] and vascular muscularization [1,4,7,9,12] seems to be a much slower process. Vascular respon siveness has not been characterized in lungs of animals recovering from chronic hypoxia.…”

Section: Introductionmentioning

confidence: 99%

Pulmonary Vascular Changes in Young and Aging Rats Exposed to 5,486 m Altitude

et al. 1984

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Young (YNG) and middle-aged (MA) male rats were exposed to 5,486 m for durations ranging from 1 to 42 days to determine the effect of age on the progression of polycythemia, right ventricular hypertrophy (RVH), lung vascular muscularization, and pulmonary vascular responsiveness. Other rats were exposed for 42 days at 5,486 m and were then allowed to recover at 1,520 m for periods up to 42 days. The progression and subsequent regression of polycythemia and RVH with altitude exposure were similar for YNG and MA rats. However, YNG rats exhibited vascular muscularization during the altitude exposure, characterized by hypertrophy of smooth muscle cells, whereas MA rats exhibited little or no change in vascular morphology. Lungs from both altitude-exposed YNG and MA rats exhibited blunting of acute hypoxic pulmonary vasoconstriction upon exposure to 5,486 m, with more severe blunting apparent in MA rats. Pressor responses to angiotensin II (All) were potentiated in lungs from high altitude rats, particularly in the YNG rats, and this increased responsiveness persisted during the recovery period. A positive correlation was found in YNG rats between the degree of vascular muscularization and the pressor response to All, suggesting that increased muscle mass was partially responsible for the potentiated Allresponses. However, MA rats did not exhibit the same correlation for All, and neither YNG nor MA rats exhibited increased responsiveness to 5-hydroxytryptamine. The results indicate that age influences the morphologic responses to altitude exposure and vascular responsiveness to All, but does not affect the polycythemic response or the degree of RVH

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“…The only data regarding regression of altitude-induced cardiac hypertrophy in rats come from intermittent high-altitude exposure (4-8 h/day, 5 or 6 days/week, stepwise up to 7,000 m, 24 exposures). Reported results vary from 2 to 4 wk (14,22). Regression of heart weight to control values in our model is longer than these latter ones.…”

Section: Discussionmentioning

confidence: 81%

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

Chouabe

Amsellem

Espinosa

et al. 2002

American Journal of Physiology-Heart and Circulatory Physiology

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Chouabe, C., J. Amsellem, L. Espinosa, P. Ribaux, S. Blaineau, P. Mé gas, and R. Bonvallet. Reversibility of electrophysiological changes induced by chronic high-altitude hypoxia in adult rat heart. Am J Physiol Heart Circ Physiol 282: H1452-H1460, 2002; 10.1152/ajpheart.00286. 2001.-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.hypertrophy; right ventricular myocytes; fibrosis; action potential; ionic currents RECENT EVIDENCE in animal models of left ventricular (LV) hypertrophy (LVH) suggests that LVH regression is associated with normalization of ventricular electrophysiology (18,19,28). Chronic hypoxia is the main pathophysiological factor in severe disturbances of the cardiovascular system, represented by pulmonary, ischemic, and congenital heart disease and in cardiopulmonary changes induced by exposure to a high-altitude environment (17). Development of right ventricular (RV) hypertrophy (RVH) is a common consequence of increased pulmonary vascular resistance in most mammals (including humans) living at high altitudes (25). This phenomenon also occurs in experimental animal models during exposure to either normobaric or hypobaric high-altitude hypoxia simulated under laboratory conditions (21). One of the most typical characteristics of phenotypical adaptations is their reversible nature. It has been shown that even severe chronic hypoxia-induced changes, such as pulmonary hypertension and RVH, are completely reversible after removal of the animals from the hypoxic atmosphere for a sufficiently long period of time (15). Recently, we demonstrated that chronic hypobaric high-altitude hypoxia induced true RV myocyte hypertrophy in rats and that hypertrophied cells showed prolongation of their action potential duration (APD) compared with control cells (4, 5). Moreover, we showed that the decrease of the transient outward current (I to1 ) a...

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Regression of altitude-produced cardiac hypertrophy.

Cited by 16 publications

References 0 publications

Effects of intermittent hypoxia on pulmonary haemodynamics: animal modelsversusstudies in humans

Effects of intermittent hypoxia on pulmonary haemodynamics: animal modelsversusstudies in humans

Pulmonary Vascular Changes in Young and Aging Rats Exposed to 5,486 m Altitude

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

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