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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Reactive oxygen species (ROS) are constantly produced in human beings under normal circumstances. Antioxidant systems help defend the body against ROS but may be overwhelmed during periods of oxidative stress, which can cause lipid peroxidation, damage to DNA, and cell death. Critical illness, such as sepsis or adult respiratory distress syndrome, can drastically increase the production of ROS and lead to oxidative stress. Sources of oxidative stress during critical illness include activation of the phagocytic cells of the immune system (the respiratory burst), the production of nitric oxide by the vascular endothelium, the release of iron and copper ions and metalloproteins, and the vascular damage caused by ischemia reperfusion. Only indirect measurements of ROS are available, but the presence of oxidative stress in critical illness is supported by clinical studies. In general, serum antioxidant vitamin concentrations seem to decrease and measures of oxidative stress seem to increase in critically ill populations. Oxidative stress has been associated with sepsis, shock, a need for mechanical ventilation, organ dysfunction, acute respiratory distress syndrome, disseminated intravascular coagulation, surgery, and the presence of an acute-phase response. In addition, higher levels of oxidative stress seem to occur in patients with more notable injuries. Dietary supplementation with antioxidant vitamins seems to be the logical answer to decreasing serum antioxidant concentrations, but antioxidants may have adverse effects. The benefit of supplementing antioxidants in critically ill populations has not been shown and requires further study.
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PMID:Oxidative stress in critical care: is antioxidant supplementation beneficial? 973

Despite its initial description as primarily a pulmonary disorder, the acute respiratory distress syndrome (ARDS) has been recognized as one component of a systemic disorder associated with microvascular permeability and widespread organ involvement that often afflicts the gastrointestinal tract. Although a healthy gut is an important defense for the body, its unique vascular anatomy and its predisposition toward ischemia and mucosal hypoxia put the gastrointestinal tract at high risk of injury during the course of the systemic inflammatory response syndrome. Once the mucosa is damaged and host defenses break down translocation of bacteria and bacterial toxins is likely to contribute to the inflammation associated with sepsis and ARDS. Gastric tonometry offers a potentially useful mechanism to monitor regional perfusion and oxidative metabolism in the splanchnic vascular bed. Many studies have shown that tonometry can assist the clinician on prognostic assessment of patients. Several studies also have demonstrated improved patient outcome when therapies aimed to protect the GI tract are aggressively pursued with tonometric guidance.
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PMID:Revving the motor of multiple organ dysfunction syndrome. Gut dysfunction in ARDS and multiorgan failure. 988 96

Consider intensive care for any patient with an intracerebral hemorrhage (ICH) and coma, cardiac ischemia, rhythm disturbances, severe respiratory distress, labile hypertension, or progressive neurologic deficits. Begin treatment with diuretics and prophylaxis of deep venous thrombosis; some patients may also require fluid restriction, hyperventilation, antiepileptic drugs, intracerebral drainage, or surgical evacuation. Common causes of ICH include hypertension; vascular malformations; hemorrhagic infarction; and administration of sympathomimetics, anticoagulants, or fibrinolytics. To predict outcome, consider both the clinical features and radiologic findings at presentation.
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PMID:Treating intracerebral hemorrhage effectively in the ICU. The key steps: provide supportive care and determine the cause. 1015 48

Endothelial cells derived from human umbilical veins represent an established model for endothelial cell research. However, it may be possible that endothelial cell physiology shows topographic differences. Until now, our research concentrated on an ovine ischemia/reperfusion model. Sheep subjected to 3 h of infrarenal aortic clamping followed by 4 h of reperfusion developed secondary lung damage. This damage is related to an infiltration of polymorphonuclear granulocytes into the lung tissue in accordance with an increased pulmonary permeability. To study this phenomenon in vitro, endothelial cells of ovine pulmonary arteries were cultured onto Transwell-membranes. The permeability of a monolayer of the endothelial cells was tested after stimulation with PMA, TNF-alpha, serum of experimental sheep, and serum of control sheep. Different sizes (4, 20, and 70 kDa) of dextran molecules conjugated to FITC were applicated at the top of the monolayer. After 5 h of incubation, fluorescence activity of both the upper and lower chamber was measured. PMA stimulation lead to a permeability of over 80%. Serum of experimental sheep increased permeability with 21.3% (mean of all dextrans). This increase was partially mediated by TNF-alpha (mean increase in permeability 15.4%). Thus, ischemia-reperfusion injury evokes high levels of cytokines. These cytokines may cause a remote increase in pulmonary endothelial permeability, leading to acute respiratory distress syndrome (ARDS) or organ failure.
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PMID:Ischemia-reperfusion directly increases pulmonary endothelial permeability in vitro. 1022 Mar 2

Neutrophils are important professional phagocytic cells that provide the host with a first line of defense against acute bacterial and fungal diseases and recurrent, severe or unusual infections are associated with inherited defects of neutrophil function. Furthermore, abundant evidence links inappropriate neutrophil-mediated tissue damage to the pathogenesis of conditions such as acute respiratory distress syndrome, septicemia with multiorgan failure, ischemia-reperfusion injury and rheumatoid arthritis. Flow cytometry has been increasingly used to evaluate the functional capabilities of neutrophils. In this review, we discuss the use of flow cytometry to assess neutrophil functional responses including calcium mobilization, F-actin assembly, adhesion, aggregation, degranulation, phagocytosis and reactive oxygen species (ROS) production. The use of flow cytometry to identify neutrophil priming is also discussed. The advantage of flow cytometry is that the majority of neutrophil functions can be measured using a small volume of whole blood that reduces artifactual changes in function caused by purification procedures. The advent of numerous new fluorochromes and multiparametric analysis allows the simultaneous measurement of several neutrophil functions in the same population of cells. Flow cytometric analysis provides a rapid screen for abnormalities of neutrophil function and reflects more accurately their behavior in vivo.
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PMID:The use of flow cytometry to measure neutrophil function. 1061 7

Nitric oxide is produced by many cell types in the lung and plays an important physiologic role in the regulation of pulmonary vasomotor tone by several known mechanisms. Nitric oxide stimulates soluble guanylyl cyclase, resulting in increased levels of cyclic GMP in lung smooth muscle cells. The gating of K+ and Ca2+ channels by cyclic GMP binding is thought to play a role in nitric oxide-mediated vasodilation. Nitric oxide may also regulate pulmonary vasodilation by direct activation of K+ channels or by modulating the expression and activity of angiotensin II receptors. Administration of nitric oxide by inhalation has been shown to acutely improve hypoxemia associated with pulmonary hypertension in humans and animals. This is presumably due to its ability to induce pulmonary vasodilation. Inhaled nitric oxide improves oxygenation and reduces the need for extracorporeal membrane oxygenation in term and near-term infants with persistent pulmonary hypertension. However, long-term benefits to these infants have been difficult to demonstrate. In other pathologic conditions, such as prematurity and acute respiratory distress syndrome, short-term benefits have not been shown conclusively to outweigh potential toxicities. For example, high-dose inhaled nitric oxide decreases surfactant function in the lung. Inhaled nitric oxide also acts as a pulmonary irritant, causing priming of lung macrophages and oxidative damage to lung epithelial cells. Conversely, protective effects of nitric oxide have been described in a number of pathological states, including hyperoxic and ischemia/reperfusion injury. Nitric oxide has also been reported to protect against oxidative damage induced by other reactive intermediates, including superoxide anion and hydroxyl radical. The dose and timing of nitric oxide administration needs to be ascertained in clinical trials before recommendations can be made regarding its optimal use in patients.
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PMID:Nitric oxide in the lung: therapeutic and cellular mechanisms of action. 1066 37

Ischemia leads to impaired ATP metabolism, with increased production of purine degradation products, such as hypoxanthine and xanthine, which are useful markers of tissue hypoxia. These extracellular markers of ischemia have been studied extensively in many clinical conditions of oxidative stress, including perinatal asphyxia, acute respiratory distress syndrome, cerebral ischemia, and preeclampsia. The aim of this study was to explore the usefulness of urinary hypoxanthine and xanthine as ischemia markers in acute coronary syndromes. Urinary excretion of hypoxanthine and xanthine was assessed by high-performance liquid chromatography in 30 patients with acute coronary syndromes and in 30 age- and sex-matched controls. Serum and urine uric acid, creatinine, and urea concentrations were also determined. Hypoxanthine excretion was significantly elevated in patients compared with healthy controls (84.37+/-8.63 and 42.70+/-3.97 nmol/mg creatinine, mean+/-SEM, P<0.0001). Urinary xanthine levels were also increased in patients with acute coronary syndromes (100.13+/-12.14 and 34.74+/-4.07 nmol/mg creatinine patients and controls, respectively; P<0.0001). Hypoxanthine and xanthine excretion showed a strong positive correlation in both groups. Significant negative correlations between urinary hypoxanthine and uric acid and xanthine and uric acid were observed in the patients, but not in controls. In conclusion, increased levels of ATP degradation products hypoxanthine and xanthine are observed in various hypoxic clinical conditions. This study suggests that these parameters may be useful markers of ischemia in patients with acute coronary syndromes.
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PMID:Urinary hypoxanthine and xanthine levels in acute coronary syndromes. 1078 78

The authors examined the differential effects of neonatal respiratory distress syndrome (RDS)--a condition associated with elevated risk for neonatal hypoxia-ischemia--on the cognitive development of the two sexes. The authors also attempted to establish whether the severity of respiratory distress is linked to cognitive outcome. Findings revealed an appreciable female advantage in cognitive recovery from RDS, yet the association between severity of RDS and outcome did not reach conventional statistical significance level. The sex effect on intelligence test performance was significantly greater for nonverbal subtests than for verbal ones. These results augment earlier findings of sex differences in cognitive recovery from perinatal intracranial hemorrhage. The current investigation also extends these results to a population of children at neonatal hypoxic risk for whom early brain injury was excluded on the basis of neonatal cranial ultrasound findings.
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PMID:Neonatal hypoxic risk in preterm birth infants: the influence of sex and severity of respiratory distress on cognitive recovery. 1149 96

Dysregulated polymorphonuclear leukocyte (PMN) apoptosis and PMN-mediated organ damage have been associated with several medical conditions such as systemic inflammatory response syndrome (SIRS), acute respiratory distress syndrome (ARDS), and ischemia/reperfusion injury. IL-1beta and IL-8 are two cytokines that are elevated under similar conditions. Therefore, we hypothesized that PMN exposed to these cytokines would secrete factors that could affect PMN apoptosis in a cell contact-independent manner. We have previously shown that media conditioned by IL-1beta-stimulated PMN (CM-IL1beta) for 2 h suppressed spontaneous PMN apoptosis. Data presented here demonstrate that media conditioned by IL-8-stimulated PMN (CM-IL8) also have the ability to suppress spontaneous, as well as FasL- and TNF-alpha-induced apoptosis. In contrast, CM-IL1beta was able to suppress FasL-induced, but not TNF-alpha-induced, apoptosis. To elucidate the mechanisms these media use to elicit their effects, we examined the expression and function of several apoptosis-related proteins. Experimental results demonstrate that both CM-IL1beta and CM-IL8 have the ability to delay caspase activation, but have no effect on the expression of their upstream activator, Fas, or its ligand, FasL. Examination of several Bcl-2 family members revealed a selective regulation by each media: CM-IL1beta up-regulated Bcl-X(L), while CM-IL8 down-regulated Bak expression. Additionally, CM-IL1beta, but not CM-IL8, promoted the activation of NF-kappaB, which has anti-apoptotic activity. Together, we can conclude that IL-1beta- and IL-8-stimulated PMN have the ability to suppress PMN apoptosis in a paracrine manner, and that the extent and mechanism of suppression is specific for each.
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PMID:Paracrine suppression of apoptosis by cytokine-stimulated neutrophils involves divergent regulation of NF-kappaB, Bcl-X(L), and Bak. 1179 69

Reactive oxygen species are reactive, partly reduced derivatives of molecular oxygen. Important reactive oxygen species in biological systems include superoxide radical anion, hydrogen peroxide, and hydroxyl radical. Peroxynitrite, is another important species in biological systems. A variety of enzymatic and non-enzymatic processes can generate reactive oxygen species in mammalian cells. An extensive body of experimental evidence from studies using animal models supports the view that reactive oxygen species are important in the pathogenesis of ischemia-reperfusion syndromes, sepsis, acute respiratory distress syndrome, and multiple organ dysfunction syndrome. This view is further supported by data from clinical studies that correlate biochemical evidence of reactive oxygen species-mediated stress with the development of acute respiratory distress syndrome or sepsis in patients. Ethyl pyruvate, a simple derivative of pyruvic acid, has been shown to be efficacious in several animal models of critical illness, and warrants further evaluation in this regard.
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PMID:Reactive oxygen species as mediators of organ dysfunction caused by sepsis, acute respiratory distress syndrome, or hemorrhagic shock: potential benefits of resuscitation with Ringer's ethyl pyruvate solution. 1184 84


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