Regression of pulmonary vascular changes following mitral valvuloplasty

Ramírez, Alberto; Grimes, Edward T.; Abelmann, Walter H.

doi:10.1016/0002-9343(68)90197-6

Cited by 16 publications

(5 citation statements)

References 17 publications

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“…As reported by increasing number of studies, pulmonary arterial remodeling of HPH would gradually reverse as hypoxia was withdrew. [38][39][40] More importantly, considerable evidence indicated that the thickened medial layer of HPH regressed most obviously during reoxygenation. 41 The present study showed that the reversal of thickened medial layer played a crucial role in the reversal of hypoxic pulmonary arterial remodeling.…”

Section: Discussionmentioning

confidence: 99%

Reoxygenation Reverses Hypoxic Pulmonary Arterial Remodeling by Inducing Smooth Muscle Cell Apoptosis via Reactive Oxygen Species–Mediated Mitochondrial Dysfunction

Chen

Wang

Dong

et al. 2017

JAHA

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BackgroundPulmonary arterial remodeling, a main characteristic of hypoxic pulmonary hypertension, can gradually reverse once oxygen has been restored. Previous studies documented that apoptosis increased markedly during the reversal of remodeled pulmonary arteries, but the types of cells and mechanisms related to the apoptosis have remained elusive. This study aimed to determine whether pulmonary artery smooth muscle cell (PASMC)‐specific apoptosis was involved in the reoxygenation‐induced reversal of hypoxic pulmonary arterial remodeling and elucidate the underlying mechanism.Methods and ResultsHypoxic pulmonary hypertension was induced in adult male Sprague‐Dawley rats (n=6/group) by chronic hypobaric hypoxia. and the hypoxic pulmonary hypertension rats were then transferred to a normoxia condition. During reoxygenation, hypoxia‐induced pulmonary arterial remodeling gradually reversed. The reversal of remodeled pulmonary arteries was associated with increased H2O2 and with changes in lung expression of cleaved caspase3/PARP, Bax, and Bcl‐2, consistent with increased apoptosis. The PASMC apoptosis, in particular, increased remarkably during this reversal. In vitro, reoxygenation induced the apoptosis of cultured rat primary PASMCs accompanied by increased mitochondrial reactive oxygen species, mitochondrial dysfunction, and the release of cytochrome C from mitochondria to cytoplasm. Clearance of reactive oxygen species alleviated mitochondrial dysfunction as well as the release of cytochrome C and, finally, decreased PASMC apoptosis.ConclusionsReoxygenation‐induced apoptosis of PASMCs is implicated in the reversal of hypoxic pulmonary arterial remodeling, which may be attributed to the mitochondrial reactive oxygen species–mediated mitochondrial dysfunction.

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Section: Discussionmentioning

confidence: 99%

Reoxygenation Reverses Hypoxic Pulmonary Arterial Remodeling by Inducing Smooth Muscle Cell Apoptosis via Reactive Oxygen Species–Mediated Mitochondrial Dysfunction

Chen

Wang

Dong

et al. 2017

JAHA

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“…Following surgical banding of pulmonary arteries in congenital pulmonary hypertension, vascular resistance returns to normal and lung biopsies show regression of medial hypertrophy. 6 Similar changes occur after correction of mitral stenosis 7 and when high altitude dwellers move to sea level. 8 The walls of blood vessels appear to revert to normal when hemodynamic stress is reduced.…”

Section: Mechanical Forcesmentioning

confidence: 85%

Effects of Mechanical Forces on Lung Vascular Remodeling

Riley

Thakker‐Varia

Poiani³

et al. 1994

Semin Respir Crit Care Med

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Pulmonary hypertension is a feature common to many chronic lung diseases. Hypertension may be reversible if the provoking stimulus is removed. If the disease is advanced, however, the changes are irreversible and often progress despite therapy. Advanced pulmonary hypertension is often irreversible due to fixed structural changes in the walls of "remodeled" pulmonary arteries. Remodeled arteries are thickened by increased amounts of smooth muscle and connective tissue. Vascular remodeling is a common sequel to several processes. One process is altered hemodynamics caused by increased blood pressure or high flow. 1 Another is vascular injury as the result of inflammation or direct toxic effects of drugs. 2 Remodeling appears to be a general response to many disorders affecting pulmonary arteries.The major physiological consequence of remodeling is narrowing of the vascular lumen and decreased distensibility of the vascular wall. These changes lead to increased pulmonary vascular resistance and further increases in pulmonary artery pressure. If not reversed, continual remodeling results in progression to cor pulmonale and right heart failure.To develop strategies to prevent progressive pulmonary hypertension, it is essential to understand the processes that stimulate vascular remodeling. Several stimuli have been proposed based on animal models and in vitro experiments. Of the various stimuli of remodeling, mechanical forces are considered to be central to many forms of pulmonary hypertension. 3 Thickening of vascular walls is an expected adaptation to high stress imposed on blood vessels by hemodynamic forces. It is logical therefore that mechanical stimuli would be closely linked to vascular remodeling. Interest in mechanical forces has increased greatly in the past several years, particularly as it affects the cardiovascular system. 4 There is now understanding of how physical forces are perceived by cells and how these mechanical signals are transduced into biochemical and molecular alterations in cells. Insights into this field may bring progress in our understanding of pulmonary vascular remodeling.

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“…The rise in left atrial pressure in mitral valve disease has been described as the most significant factor in the development of pulmonary hypertension with consequent vasoconstriction of the pulmonary arterioles (Wood, 1958). Some cases are further complicated by organic changes in the pulmonary vasculature, but these changes are moderate (Harris and Heath, 1962) and are probably reversible after mitral valve surgery (Ramirez, Grimes, and Abelmann, 1968). Even severe degrees of pulmonary hypertension can regress markedly following adequate decompression of the left atrium after closed mitral valvotomy (Werko et al, 1953;MacKinnon, Wade, and Vickers, 1956;Emanuel, 1963), open mitral valvotomy (Zener et al, 1972), and mitral replacement (Dalen et al, 1967;Zener et al, 1972).…”

Section: Resultsmentioning

confidence: 99%

Mitral valve replacement in the presence of severe pulmonary hypertension.

Kaul¹,

Bain²,

Sandoval³

et al. 1976

Thorax

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. (1976). Thorax, 31,[332][333][334][335][336] (Emanuel, 1963). In general, it has been held that severe pulmonary hypertension was associated with greater operative risk, higher operative mortality, and a poorer long-term prognosis.However, a significant reduction in the level of pulmonary hypertension in some patients after mitral valve surgery and a more favourable longterm outlook have been reported (Dalen et al., 1967;Zener et al., 1972). Furthermore, Ward and Hancock (1975) suggested that extreme pulmonary hypertension should be regarded as a positive indication for early operation. In their series there was a high mortality in this group, but the prognosis was nonetheless considerably better than the natural history of the disease without surgical intervention. In our series in the last five years, only one of 16

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Regression of pulmonary vascular changes following mitral valvuloplasty

Cited by 16 publications

References 17 publications

Reoxygenation Reverses Hypoxic Pulmonary Arterial Remodeling by Inducing Smooth Muscle Cell Apoptosis via Reactive Oxygen Species–Mediated Mitochondrial Dysfunction

Reoxygenation Reverses Hypoxic Pulmonary Arterial Remodeling by Inducing Smooth Muscle Cell Apoptosis via Reactive Oxygen Species–Mediated Mitochondrial Dysfunction

Effects of Mechanical Forces on Lung Vascular Remodeling

Mitral valve replacement in the presence of severe pulmonary hypertension.

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