Значения термина chronic hypoxia на английском

No significant right atrial hypertrophy was observed under these conditions of chronic hypoxia.

This study investigated the inflammatory and metabolic profile of AT after chronic hypoxia.

CLIC4 gene deletion markedly attenuated the development of chronic hypoxia-induced pulmonary hypertension in mice.

Rats treated with the combination of SU5416 and chronic hypoxia also developed pulmonary endothelial hyperproliferative lesions.

We examined cardioprotective effect of chronic hypoxia and the time course of its recovery under normoxic conditions.

Concomitantly, chronic hypoxia increased AT expression of regulators of oxidative metabolism and markers of mitochondrial function and lipolysis.

Adaptation to chronic hypoxia involves immune cell invasion and increased expression of inflammatory cytokines in rat carotid body.

In this study, we test the hypothesis that ARC expression is essential for the development of chronic hypoxia-induced PH.

Lungs from piglets raised in chronic hypoxia exhibited greater SNAT1 expression and higher l-citrulline levels than lungs from controls.

Conclusions: This is the first effort to separate acute and chronic hypoxia from serial PET images of cancer patients.

Inhibition of ACE by captopril during chronic hypoxia attenuated pulmonary hypertension and markedly reduced distal muscularization of small pulmonary arteries.

Methods and results: We found that apelin-null mice developed more severe PH compared with wild-type mice when exposed to chronic hypoxia.

These results suggest that different strains use different gene expression mechanisms to adapt to the challenge of chronic hypoxia, resulting in modified phenotypic changes.

Furthermore, our data indicate that chronic hypoxia is accompanied by significant alterations in AT metabolic gene expression, pointing toward an enhanced AT metabolic rate.

These stem cells give rise to increased circulating monocytes and macrophages and contribute to the pathogenesis of chronic hypoxia-induced pulmonary artery remodeling and hypertension.

To track circulating fibrocytes in vivo, we transplanted wild-type mice with bone marrow from ubiquitously eGFP expressing mice and subjected them to chronic hypoxia.