688 research outputs found
The key role of nitric oxide in hypoxia: hypoxic vasodilation and energy supply-demand matching
Full text linkSignificance: a mismatch between energy supply and demand induces tissue hypoxia with the potential to cause cell death and organ failure. Whenever arterial oxygen concentration is reduced, increases in blood flow - 'hypoxic vasodilation' - occur in an attempt to restore oxygen supply. Nitric oxide is a major signalling and effector molecule mediating the body's response to hypoxia, given its unique characteristics of vasodilation (improving blood flow and oxygen supply) and modulation of energetic metabolism (reducing oxygen consumption and promoting utilization of alternative pathways). Recent advances: this review covers the role of oxygen in metabolism and responses to hypoxia, the hemodynamic and metabolic effects of nitric oxide, and mechanisms underlying the involvement of nitric oxide in hypoxic vasodilation. Recent insights into nitric oxide metabolism will be discussed, including the role for dietary intake of nitrate, endogenous nitrite reductases, and release of nitric oxide from storage pools. The processes through which nitric oxide levels are elevated during hypoxia are presented, namely (i) increased synthesis from nitric oxide synthases, increased reduction of nitrite to nitric oxide by heme- or pterin-based enzymes and increased release from nitric oxide stores, and (ii) reduced deactivation by mitochondrial cytochrome c oxidase. Critical issues: several reviews covered modulation of energetic metabolism by nitric oxide, while here we highlight the crucial role NO plays in achieving cardiocirculatory homeostasis during acute hypoxia through both vasodilation and metabolic suppression Future directions: we identify a key position for nitric oxide in the body's adaptation to an acute energy supply-demand mismatc
Risk assessment with gene expression markers in sepsis development (code repository)
No full text<p>Code repository for the research article "Risk assessment with gene expression markers in sepsis development".</p>
<p>Authors: Albert Garcia-Lopez, Sascha Schäuble, Tongta Sae-Ong, Bastian Seelbinder, Michael Bauer, Evangelos J Giamarellos-Bourboulis, Mervyn Singer, Roman Lukaszewski, Gianni Panagiotou</p>
Reversal of life-threatening, drug-related potassium-channel syndrome by glibenclamide
No full textWe describe three critically ill patients who received drugs with K(ATP) channel-opening properties and subsequently developed severe life-threatening complications, including hyperkalaemia and cardiovascular disturbances. Administration of the sulfonylurea-receptor inhibitor glibenclamide promptly reversed these abnormalities. Over the past 3 years, we have seen this syndrome and response in five patients taking nicorandil, ciclosporin, or isoflurane, which suggests that this disorder arises more frequently than is currently realised
Pulmonary mechanical dysfunction in the critically ill
No full textModern ventilators employed in intensive care units (ICUs) display in real time and breath by breath flow (V̇), volume (V), and pressure (Paw) curves, both as a function of time and as a loop. Data obtained from curve analysis can help the physician to understand the interactions between the patient and the ventilator. The right interpretation of information provided from modern ventilators allows real time monitoring of the actual needs of the patient, ensuring a custom ventilatory support and reducing the risk of complications that can increase the mortality and prolong the ICU length of stay. In patients undergoing mechanical ventilation, measurements of respiratory mechanics can be performed at the bedside in dynamic (no flow interruption) or static (occlusion techniques) conditions. From these, it’s also possible to derive the values of pulmonary compliance and airway resistance
Exploring alternative routes for oxygen administration
Full text linkBACKGROUND: Hypoxemia may compromise cell metabolism and organ function. Supplemental oxygen (O2) at high concentrations may prove ineffective, and issues relating to hyperoxia, barotrauma, mechanical ventilation, and extracorporeal oxygenation are well documented. Old reports suggest the potential safety and efficacy of alternative routes for O2 administration, such as intravenous or intestinal. We re-explored these routes in rat models of hypoxemia. METHODS: Hypoxemia was induced in spontaneously breathing, anesthetized rats by breathing a hypoxic gas mix (FiO2 0.1). Pilot studies infusing pure O2 gas caused early death, likely due to pulmonary embolism. Instead, rats (n = 6/group) were given intravenous O2 via a continuous infusion of pre-oxygenated Hartmann's solution (10 ml/kg/h) for 3 h with normal Ringer's lactate used in control animals. In separate experiments (n = 8/group), bowel intraluminal oxygenation was assessed with pure O2 administered through a cannula placed into the jejunal lumen at a dose of a 15 ml/kg bolus followed by a continuous infusion of 50 ml/kg/h; no treatment was given to controls. Echocardiography, arterial blood gas analysis, mean arterial pressure, muscle and liver tPO2, muscle microvascular perfused vessel density, and urine output were measured. RESULTS: Administration of oxygenated Hartmann's solution (PO2 of solution at end-experiment = 87.5 ± 1.7 kPa) was safe but did not increase either systemic or tissue oxygenation. Similarly, the administration of bowel O2 was safe but did not improve neither systemic nor liver oxygenation. CONCLUSIONS: In this rat model of hypoxemia, the intravenous infusion of gaseous O2 was unfeasible as it induced early mortality. Although safe, both intravenous infusion of oxygenated Hartmann's solution and bowel O2 administration were unable to improve arterial or tissue oxygenation
Correspondence between Mervyn M. Dymally and Vernon Jordan, December 1967
No full textCorrespondence between Mervyn M. Dymally about Vernon Jordan increasing voter awareness in Los Angeles. Enclosed is a grant proposal from the Urban Affairs Foundation
Aspects of stuckness in Mervyn Peakes's fiction / Alice Mills
Full text link"This thesis argues that stuckness is a central trope in all of Mervyn Peake's extended works of fiction and that most of Peake's characters become stuck at critical points in their lives."Doctor of Philosoph
Ormond: or the secret witness. By the author of Wieland, Arthur Mervyn, &c. &c.
No full text[2],338,[2]p. ; 12⁰.The author of Wieland, Arthur Mervyn, &c. &c. = Charles Brockden Brown.Dedication signed: S. C.With a half-title and a final advertisement leaf.Reproduction of original from the British Library.Blakey, p.196English Short Title Catalog, ESTCT131855.Electronic data. Farmington Hills, Mich. : Thomson Gale, 2003. Page image (PNG). Digitized image of the microfilm version produced in Woodbridge, CT by Research Publications, 1982-2002 (later known as Primary Source Microfilm, an imprint of the Gale Group)
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