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Cellular dysoxia

Genri Numata, Satoshi Kodera, Hiroyuki Kiriyama, Atsuko Nakayama, Eisuke Amiya, Arihiro Kiyosue, Masaru Hatano, Eiki Takimoto, Masafumi Watanabe, Issei Komuro
Background: Central venous oxygen saturation (ScvO2 ) reflects the balance of oxygen delivery and consumption. Low ScvO2 indicates the presence of inadequate oxygen delivery, while high ScvO2 indicates reduced oxygen consumption and is sometimes associated with a high mortality rate in critically ill patients from dysoxia. Thiamine is an essential cofactor in cellular aerobic metabolism. Thiamine deficiency is more prevalent than was previously thought, and underlies severe conditions in critically ill patients...
2017: Journal of Intensive Care
Christos Lazaridis
Shock is a systemic form of acute circulatory failure leading to cellular dysoxia and death. Such a state of aerobic metabolism failure also underlies neuronal cell death in severe traumatic brain injury. It is becoming increasingly recognized that ischemic hypoxia is not the sole mechanism and that multiple alternate cooperating mechanisms may be responsible for compromising neuronal oxidative metabolism. These different mechanisms can be usefully understood via analysis of the classic subdivisions of tissue hypoxia...
February 2017: Journal of Critical Care
Hoong Sern Lim
Cardiogenic shock remains a highly lethal condition. Conventional therapy including revascularization and mechanical circulatory support aims to improve cardiac output and oxygen delivery, but increasing basic and clinical observations indicate wider circulatory and cellular abnormalities, particularly at the advanced stages of shock. Progressive cardiogenic shock is associated with microcirculatory and cellular abnormalities. Cardiogenic shock is initially characterized by a failure to maintain global oxygen delivery; however, progressive cardiogenic shock is associated with the release of pro-inflammatory cytokines, derangement of the regulation of regional blood flow, microcirculatory abnormalities, and cellular dysoxia...
August 2016: Clinical Cardiology
Hollmann D Aya, Andrea Carsetti, Simone Bazurro, Davide Bastoni, Manu L N G Malbrain, Maurizio Cecconi
Shock is defined as a state in which the circulation is unable to deliver sufficient oxygen to meet the demands of the tissues, resulting in cellular dysoxia and organ failure. In this process, the factors that govern the circulation at a haemodynamic level and oxygen delivery at a microcirculatory level play a major role. This manuscript aims to review the blood flow regulation from macro- and micro-haemodynamic point of view and to discuss new potential therapeutic approaches for cardiovascular instability in patients in cardiovascular shock...
2015: Anaesthesiology Intensive Therapy
Matthew J Rogatzki, Brian S Ferguson, Matthew L Goodwin, L Bruce Gladden
Through much of the history of metabolism, lactate (La(-)) has been considered merely a dead-end waste product during periods of dysoxia. Congruently, the end product of glycolysis has been viewed dichotomously: pyruvate in the presence of adequate oxygenation, La(-) in the absence of adequate oxygenation. In contrast, given the near-equilibrium nature of the lactate dehydrogenase (LDH) reaction and that LDH has a much higher activity than the putative regulatory enzymes of the glycolytic and oxidative pathways, we contend that La(-) is always the end product of glycolysis...
2015: Frontiers in Neuroscience
Abele Donati, Dick Tibboel, Can Ince
Current hemodynamic monitoring of critically ill patients is mainly focused on monitoring of pressure-derived hemodynamic variables related to systemic circulation. Increasingly, oxygen transport pathways and indicators of the presence of tissue dysoxia are now being considered. In addition to the microcirculatory parameters related to oxygen transport to the tissues, it is becoming increasingly clear that it is also important to gather information regarding the functional activity of cellular and even subcellular structures to gain an integrative evaluation of the severity of disease and the response to therapy...
2013: Critical Care: the Official Journal of the Critical Care Forum
Mark Williams, Jean Vannier, Laure Corbari, Jean-Charles Massabuau
BACKGROUND: We examine the physiological and lifestyle adaptations which facilitated the emergence of ostracods as the numerically dominant Phanerozoic bivalve arthropod micro-benthos. METHODOLOGY/PRINCIPAL FINDINGS: The PO(2) of modern normoxic seawater is 21 kPa (air-equilibrated water), a level that would cause cellular damage if found in the tissues of ostracods and much other marine fauna. The PO(2) of most aquatic breathers at the cellular level is much lower, between 1 and 3 kPa...
2011: PloS One
Laurie A Loiacono, David S Shapiro
Organ function is critically linked to the way tissues use available oxygen. In sepsis, tissue-related hypoxic injury is the result of hypoxemia and hypoperfusion and cytokine-mediated mitochondrial dysfunction termed cytopathic hypoxia. Organ dysfunction in sepsis is more likely related to derailment of the metabolic processes of cells to use available oxygen. Cellular dysoxia rather than hypoxia may be the most appropriate way of describing sepsis-related tissue injury. Lactate is a marker of aerobic mitochondrial dysfunction and anaerobic tissue metabolism and in some circumstances is considered the fuel of choice for certain tissues...
April 2010: Critical Care Clinics
Matthieu Legrand, Egbert G Mik, Tanja Johannes, Didier Payen, Can Ince
Ischemia is the most common cause of acute renal failure. Ischemic-induced renal tissue hypoxia is thought to be a major component in the development of acute renal failure in promoting the initial tubular damage. Renal oxygenation originates from a balance between oxygen supply and consumption. Recent investigations have provided new insights into alterations in oxygenation pathways in the ischemic kidney. These findings have identified a central role of microvascular dysfunction related to an imbalance between vasoconstrictors and vasodilators, endothelial damage and endothelium-leukocyte interactions, leading to decreased renal oxygen supply...
July 2008: Molecular Medicine
Miguel López-Lázaro
Hypoxia-inducible factor 1 (HIF-1) activates the transcription of genes involved in diverse aspects of cellular and integrative physiology, including energy metabolism, cell growth, survival, invasion, migration or angiogenesis. The activity of this transcription factor is known to be increased by hypoxia, but also by a growing number of apparently unrelated factors that can activate it even in nonhypoxic conditions. Here I propose a model in which an alteration in oxygen metabolism is the key cellular event involved in HIF-1 activation under hypoxic and nonhypoxic conditions...
May 2006: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
Patrícia M Veiga C Mello, Vinay K Sharma, R Phillip Dellinger
Despite improved understanding of the pathophysiology of shock and significant advances in technology, it remains a serious problem associated with high morbidity and mortality. Early treatment is essential but is hampered by the fact that signs and symptoms of shock appear only after the shock state is well established and the body's compensatory mechanisms have started to fail. Although the causes of shock are varied, the basic abnormality in all varieties is tissue and cellular dysoxia. In this overview we discuss the definition, classification and pathogenesis of shock in light of the recent advances in our understanding of its mechanisms...
December 2004: Seminars in Respiratory and Critical Care Medicine
Daniel Goldman, Ryon M Bateman, Christopher G Ellis
Inherent in the inflammatory response to sepsis is abnormal microvascular perfusion. Maldistribution of capillary red blood cell (RBC) flow in rat skeletal muscle has been characterized by increased 1) stopped-flow capillaries, 2) capillary oxygen extraction, and 3) ratio of fast-flow to normal-flow capillaries. On the basis of experimental data for functional capillary density (FCD), RBC velocity, and hemoglobin O2 saturation during sepsis, a mathematical model was used to calculate tissue O2 consumption (Vo2), tissue Po2 (Pt) profiles, and O2 delivery by fast-flow capillaries, which could not be measured experimentally...
December 2004: American Journal of Physiology. Heart and Circulatory Physiology
L B Gladden
For much of the 20th century, lactate was largely considered a dead-end waste product of glycolysis due to hypoxia, the primary cause of the O2 debt following exercise, a major cause of muscle fatigue, and a key factor in acidosis-induced tissue damage. Since the 1970s, a 'lactate revolution' has occurred. At present, we are in the midst of a lactate shuttle era; the lactate paradigm has shifted. It now appears that increased lactate production and concentration as a result of anoxia or dysoxia are often the exception rather than the rule...
July 1, 2004: Journal of Physiology
Guillermo Gutierrez
A two-compartment mass transport model of tissue CO(2) exchange is developed to examine the relative contributions of blood flow and cellular hypoxia (dysoxia) to increases in tissue and venous blood CO(2) concentration. The model assumes perfectly mixed homogeneous conditions, steady-state equilibrium, and CO(2) production occurring exclusively at the tissues. The behavior of the model is compared with published data derived from an isolated dog hindlimb preparation subjected to either reductions in blood flow (ischemic hypoxia) or decreases in arterial PO(2) (hypoxic hypoxia)...
February 15, 2004: American Journal of Respiratory and Critical Care Medicine
David Brealey, Mervyn Singer
Sepsis is an increasingly common problem, particularly among critically ill patients. Mechanisms by which sepsis induces organ dysfunction have not been elucidated. The coexisting findings (unique to sepsis) of metabolic acidosis yet increased tissue oxygen tensions suggest cellular availability but decreased use of oxygen (tissue dysoxia). Because mitochondria use more than 90% of total body oxygen consumption for adenosine triphosphate (ATP) generation, a bioenergetic abnormality is implied. Cell and animal data have shown that nitric oxide (and its metabolites), produced in considerable excess in patients with sepsis, can affect oxidative phosphorylation by inhibiting several of its component respiratory enzymes...
October 2003: Current Infectious Disease Reports
M Piagnerelli, K Zouaoui Boudjeltia, M Vanhaeverbeek, J-L Vincent
Changes in red blood cell (RBC) function can contribute to alterations in microcirculatory blood flow and cellular dysoxia in sepsis. Decreases in RBC and neutrophil deformability impair the passage of these cells through the microcirculation. While the role of leukocytes has been the focus of many studies in sepsis, the role of erythrocyte rheological alterations in this syndrome has only recently been investigated. RBC rheology can be influenced by many factors, including alterations in intracellular calcium and adenosine triphosphate (ATP) concentrations, the effects of nitric oxide, a decrease in some RBC membrane components such as sialic acid, and an increase in others such as 2,3 diphosphoglycerate...
July 2003: Intensive Care Medicine
Curtis N Sessler, Wes Shepherd
An estimated 750,000 cases of severe sepsis occur annually in the United States, and the mortality rate is about 30%. As a condition that disproportionately affects the elderly and is related to invasive and immunosuppressive healthcare, increases in the frequency of sepsis are anticipated. The complex pathophysiology of sepsis encompasses the interplay of pro- and anti-inflammatory mediators, activated circulating and resident inflammatory cells, disrupted coagulation, endothelial activation and injury, vasodilatation and vascular hyporesponsiveness to vasoactive mediators, cardiac dysfunction, and cellular dysoxia...
October 2002: Current Opinion in Critical Care
A D Farmery, J P Whiteley
A simple mathematical model of electron flow along the mitochondrial respiratory cytochrome assembly and the transfer of electrons to molecular oxygen is presented. First, an expression for the current-voltage relationship for a biological oxygen electrode is derived, and from this the relationship between oxygen consumption rate and oxygen partial pressure is determined. An independent relationship between mitochondrial oxygen partial pressure and oxygen supply rate is then derived. By eliminating oxygen partial pressure from these two expressions, we may obtain a relationship between oxygen supply rate and oxygen consumption rate...
November 21, 2001: Journal of Theoretical Biology
A de Jaeger, F Proulx, T Yandza, M A Dugas, B Boeuf, A Manika, J Lacroix, M Lambert
OBJECTIVE: To characterize global, regional, and end-organ markers of cellular dysoxia during orthotopic liver transplantation and early reperfusion in pigs. DESIGN: Descriptive study. SETTING: University hospital research laboratory. ANIMALS AND INTERVENTIONS: 7 fasted, anesthetized, and mechanically ventilated Yorkshire pigs underwent orthotopic liver transplantation. Oxygen consumption (VO2) and oxygen delivery (DO2) were both calculated using standard formulae...
March 1998: Intensive Care Medicine
P Rhee, L Langdale, C Mock, L M Gentilello
OBJECTIVE: Mitochondrial cytochrome a,a3 redox shifts can be determined by near-infrared wavelength reflection. Since near-infrared wavelengths penetrate skin and bone, a potential exists to noninvasively measure mitochondrial oxidation using this phenomenon. The purpose of this study was to compare conventional parameters of resuscitation with regional measurements of spectroscopically derived cytochrome redox state in a hemorrhagic shock model. DESIGN: Prospective, controlled laboratory investigation...
January 1997: Critical Care Medicine
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