Thiosulfate: a readily accessible source of hydrogen sulfide in oxygen sensing

AJP Regulatory Integrative and Comparative Physiology, Journal Year: 2013, Volume and Issue: 305(6), P. R592 - R603

Published: June 27, 2013

H2S derived from organic thiol metabolism has been proposed serve as an oxygen sensor in a variety of systems because its susceptibility to oxidation and ability mimic hypoxic responses numerous oxygen-sensing tissues. Thiosulfate, intermediate oxidative can alternatively be reduced regenerate H2S. We propose that this contributes the H2S-mediated mechanism. formation thiosulfate buffers mammalian tissues lamprey dorsal aorta was examined real time using polarographic sensor. Inferences intracellular production were made by examining pulmonary vasoconstriction (HPV) bovine arteries under conditions which increased would expected mouse rat aortas, where reducing should mediate vasorelaxation. In Krebs-Henseleit (mammalian) Cortland (lamprey) buffers, generated presence exogenous agent, DTT, or endogenous reductant dihydrolipoic acid (DHLA). Both magnitude rate greatly these reductants tissue, with most notable effects occurring liver. only observed when hypoxic; exposure room air, injecting inhibited resulted net consumption. DTT DHLA augmented HPV, dose-dependently relaxed precontracted aortas. These results indicate contribute signaling is not ready source but also serves means recycling sulfur thereby conserving biologically relevant thiols.

Language: Английский

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Oxygen sensing and signal transduction in hypoxic pulmonary vasoconstriction

European Respiratory Journal, Journal Year: 2015, Volume and Issue: 47(1), P. 288 - 303

Published: Oct. 22, 2015

Hypoxic pulmonary vasoconstriction (HPV), also known as the von Euler-Liljestrand mechanism, is an essential response of vasculature to acute and sustained alveolar hypoxia. During local hypoxia, HPV matches perfusion ventilation maintain optimal arterial oxygenation. In contrast, during global leads hypertension. The oxygen sensing signal transduction machinery located in smooth muscle cells (PASMCs) pre-capillary vessels, albeit physiological may be modulated vivo by endothelium. While factors such nitric oxide modulate HPV, reactive species (ROS) have been suggested act mediators HPV. ROS originate from mitochondria and/or NADPH oxidases but exact mechanisms, well question whether increased or decreased cause are under debate. induce intracellular calcium increase subsequent contraction PASMCs via direct indirect interactions with protein kinases, phospholipases, sarcoplasmic channels, transient receptor potential voltage-dependent potassium channels L-type whose relevance vary different experimental conditions. Successful identification regulating allow development novel therapeutic approaches for conditions disturbed

Language: Английский

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Pathophysiology and Treatment of High-Altitude Pulmonary Vascular Disease

Circulation, Journal Year: 2015, Volume and Issue: 131(6), P. 582 - 590

Published: Feb. 9, 2015

Language: Английский

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Postoperative Critical Care of the Adult Cardiac Surgical Patient. Part I

Critical Care Medicine, Journal Year: 2015, Volume and Issue: 43(7), P. 1477 - 1497

Published: May 9, 2015

Cardiac surgery, including coronary artery bypass, cardiac valve, and aortic procedures, is among the most common surgical procedures performed in United States. Successful outcomes after surgery depend on optimum postoperative critical care. The intensivist must have a comprehensive understanding of cardiopulmonary physiology sequelae bypass. In this concise review, targeted at intensivists surgeons, we discuss routine management patient.Narrative review relevant English-language peer-reviewed medical literature.Critical care patient complex dynamic endeavor. Adequate fluid resuscitation, appropriate inotropic support, attention to rewarming, ventilator are key components. Patient safety enhanced by experienced personnel, structured handover between operating room ICU teams, transfusion strategies.

Language: Английский

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Reactive Oxygen Species in Pulmonary Vascular Remodeling

Comprehensive physiology, Journal Year: 2013, Volume and Issue: unknown, P. 1011 - 1034

Published: July 1, 2013

The pathogenesis of pulmonary hypertension is a complex multifactorial process that involves the remodeling arteries. This encompasses concentric medial thickening small arterioles, neomuscularization previously nonmuscular capillary-like vessels, and structural wall changes in larger arterial muscularization characterized by vascular smooth muscle cell hyperplasia hypertrophy. In addition, uncontrolled hypertension, clonal expansion apoptosis-resistant endothelial cells leads to formation plexiform lesions. Based upon large number studies animal models, three major stimuli drive are inflammation, shear stress, hypoxia. Although, precise mechanisms which these impair function structure unknown, reactive oxygen species (ROS)-mediated oxidative damage appears play an important role. ROS highly due their unpaired valence shell electron. Oxidative occurs when production exceeds quenching capacity antioxidant cell. can be produced from complexes membrane (nicotinamide adenine dinucleotide phosphate-oxidase), cellular organelles (peroxisomes mitochondria), cytoplasm (xanthine oxidase). Furthermore, low levels tetrahydrobiopterin (BH4) L-arginine rate limiting cofactor substrate for nitric oxide synthase (eNOS), cause uncoupling eNOS, resulting decreased NO increased production. review will focus on generation systems, scavenger antioxidants, stress associated alterations hypertension. © 2013 American Physiological Society. Compr Physiol 3:1011-1034, 2013.

Language: Английский

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