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Side 1 fra 3629 resultater
Smooth muscle contractility. Effects of hypoxia.
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Mechanical perturbation of smooth muscle provides information about the mechanical properties of its crossbridges. We have developed a method for identifying: (1) that normally cycling and very slowly cycling are sequentially activated, (2) the moment of this transition, and (3) the proportions of
Smooth muscle myosin in precursor and mature smooth muscle cells in normal pulmonary arteries and the effect of hypoxia.
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Exposure to hypoxia increases pulmonary arterial muscularity-in the intra-acinar arteries "new" muscle appears in the normally nonmuscular regions and in the preacinar arteries, medial thickness increases. In the present study by immunofluorescence techniques, the myosin content of the pulmonary
Vascular smooth muscle ultrastructure in hypoxia [proceedings].
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[Effects of hypoxia on venous smooth muscle].
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Adaptation to hypoxia in vascular smooth muscle.
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Oxygen mediates vascular smooth muscle relaxation in hypoxia.
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The activation of soluble guanylate cyclase (sGC) by nitric oxide (NO) and other ligands has been extensively investigated for many years. In the present study we considered the effect of molecular oxygen (O2) on sGC both as a direct ligand and its affect on other ligands by measuring cyclic
Responses of systemic vascular smooth muscle to hypoxia.
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The rapidity and extent of hypoxic relaxation of vascular smooth muscle (VSM) from different systemic vessels is relevant to the study of mechanisms of vasodilation in different vascular beds. Variations between sites may also assist understanding of the link between oxygen tension and mechanical
Chronic hypoxia impairs pulmonary venous smooth muscle contraction.
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Chronic hypoxia increases total pulmonary vascular resistance and causes pulmonary hypertension. Although the effect of chronic hypoxia on pulmonary arterial tissue has been extensively studied, very little is known about the effects on the pulmonary vein. The purpose of the present investigation
Mechanical activity of vascular smooth muscle under anoxia.
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Prolonged hypoxia increases pulmonary vascular smooth muscle cytosolic calcium.
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Prolonged hypoxia increases pulmonary vascular smooth muscle cytosolic calcium.
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[Hypoxia induced the remodeling of pulmonary arterial smooth muscles and increased the pulmonary artery smooth muscle Krüppel-like zinc-finger transcription factor 5 expression].
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Objective: To study the effect of chronic hypoxia on pulmonary arterial remodeling and Krüppel-like zinc-finger transcription factor 5 (KLF5) protein expression in pulmonary artery smooth muscles in a hypoxia-induced pulmonary hypertension model. Methods: Totally 20 adult SD rats (200-250 g) were
Effects of hypoxia on rat airway smooth muscle cell proliferation.
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Although it is well known that hypoxemia induces pulmonary vasoconstriction and vascular remodeling, due to the proliferation of both vascular smooth muscle cells and fibroblasts, the effects of hypoxemia on airway smooth muscle cells are not well characterized. The present study was designed to
Pulmonary arterial smooth muscle contractility in hypoxia-induced pulmonary hypertension.
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The highly compliant low-resistance pulmonary vasculature is markedly altered with chronic hypoxia. Remodeling in response to hypoxia and/or hypertension involves hypertrophy and hyperplasia of smooth muscle and excessive deposition of connective tissue that likely contributes to the maintenance or
Intracellular pH in hypoxic smooth muscle.
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Hypoxia impairs contractility in canine tracheal smooth muscle (TSM). This is attributed to intracellular lactacidosis. The present studies were undertaken to confirm this. Lactate was found to be significantly increased in hypoxic TSM (65.36 +/- 7.37 mg/100 g wet tissue), compared to normoxic
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