Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cytomegalovirus infection is a benign disease in immunocompetent patients. In-vitro and in-vivo studies show that cytomegalovirus may cause arterial and venous thrombosis through different mechanisms. We describe two cases of acute cytomegalovirus infection complicated by portal and mesenteric vein thrombosis leading to intestinal ischemia. Both patients carried the heterozygous prothrombin G20210A mutation. The presence of this unusual complication should be searched for in patients with acute cytomegalovirus infection and abdominal symptoms in order to start early anticoagulation. The necessity for full thrombophilic screening is also pointed out.
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PMID:Acute portal and mesenteric thrombosis: unusual presentation of cytomegalovirus infection. 1653 19

The effect of ischemic preconditioning (IPC) in orthotopic liver transplantation (OLT) has not yet been clarified. We performed a pilot study to evaluate the effects of IPC in OLT by comparing the outcomes of recipients of grafts from deceased donors randomly assigned to receive (IPC+ group, n = 23) or not (IPC- group, n = 24) IPC (10-min ischemia + 15-min reperfusion). In 10 cases in the IPC+ group and in 12 in the IPC- group, the expression of inducible nitric oxide synthase (iNOS), neutrophil infiltration, and hepatocellular apoptosis were tested by immunohistochemistry in prereperfusion and postreperfusion biopsies. Median aspartate aminotransferase (AST) levels were lower in the IPC+ group vs. the IPC- group on postoperative days 1 and 2 (398 vs. 1,234 U/L, P = 0.002; and 283 vs. 685 U/L, P = 0.009). Alanine aminotransferases were lower in the IPC+ vs. the IPC- group on postoperative days 1, 2, and 3 (333 vs. 934 U/L, P = 0.016; 492 vs. 1,040 U/L, P = 0.008; and 386 vs. 735 U/L, P = 0.022). Bilirubin levels and prothrombin activity throughout the first 3 postoperative weeks, incidence of graft nonfunction and graft and patient survival rates were similar between groups. Prereperfusion and postreperfusion immunohistochemical parameters did not differ between groups. iNOS was higher postreperfusion vs. prereperfusion in the IPC- group (P = 0.008). Neutrophil infiltration was higher postreperfusion vs. prereperfusion in both groups (IPC+, P = 0.007; IPC-, P = 0.003). Prereperfusion and postreperfusion apoptosis was minimal in both groups. In conclusion, IPC reduced ischemia/reperfusion injury through a decrease of hepatocellular necrosis, but it showed no clinical benefits.
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PMID:Effect of ischemic preconditioning in whole liver transplantation from deceased donors. A pilot study. 1655 38

Drug-eluting stents (DESs) deliver biphasic (early and late) elution of anti-inflammatory compounds. We therefore hypothesized that DESs would be associated with early reductions in inflammatory biomarker release after percutaneous coronary intervention (PCI). A total of 741 patients with non-ST-elevation acute coronary syndrome underwent PCI in the Randomized Trial to Evaluate the Relative PROTECTion against Post-PCI Microvascular Dysfunction and Post-PCI Ischemia among Anti-Platelet and Anti-Thrombotic Agents (PROTECT) Thrombolysis In Myocardial Infarction 30 study of eptifibatide and reduced-dose antithrombin compared with bivalirudin. Serial biomarkers C-reactive protein, troponin, creatine kinase-MB, soluble CD40 ligand, interleukin-6, prothrombin fragment F1.2, and RANTES (regulated on activation, normal T-cell expressed and secreted) were assessed through 24 hours after PCI. DES use was at the investigator's discretion. Patients treated with DESs (n = 665) versus bare metal stents (n = 139) were more likely to have patent arteries before PCI (92.0% vs 86.6%, p = 0.04), Thrombolysis In Myocardial Infarction myocardial perfusion grade 3 (57.9% vs 47.7%, p = 0.033), and the left anterior descending artery as the culprit artery (38.5% vs 18.3%, p <0.001). The increase in C-reactive protein and troponin was lower among patients undergoing DES implantation (median 2.1 vs 3.5 mg/L for C-reactive protein, median 0.11 vs 0.41 ng/ml for troponin), even after adjustment for randomized treatment, clopidogrel before treatment, diabetes mellitus status, epicardial patency, left anterior descending artery location, and myocardial perfusion (p = 0.036 and p = 0.039, respectively). Interleukin-6 was lower with DESs on univariate analysis but not multivariate analysis. Creatine kinase-MB, soluble sCD40 ligand, prothrombin fragment F1.2, and RANTES did not differ by DES use. In conclusion, patients undergoing DES implantation achieved more reductions in periprocedural markers of inflammation and necrosis than patients receiving bare metal stents among those with non-ST-elevation acute coronary syndrome.
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PMID:Comparison of effects of bare metal versus drug-eluting stent implantation on biomarker levels following percutaneous coronary intervention for non-ST-elevation acute coronary syndrome. 1705 55

The purpose of the present study was to assess the therapeutic effect of hypothermic retrograde jugular vein flush (HRJVF) on heatstroke. HRJVF was accomplished by infusion of 4 degrees C isotonic sodium chloride solution via the external jugular vein (1.7 mL/100 g of body weight over 5 min). Immediately after the onset of heatstroke, anesthetized rats were divided into 2 major groups and given the following: 36 degrees C or 4 degrees C isotonic sodium chloride solution, i.v. They were exposed to ambient temperature of 43 degrees C to induce heatstroke. Another group of rats was exposed to room temperature (24 degrees C) and used as normothermic controls. When the 36 degrees C saline-treated rats underwent heat exposure, their survival time values were found to be 23 to 28 min. Immediately after the onset of heatstroke, resuscitation with an i.v. dose of 4 degrees C saline significantly improved survival during heatstroke (208-252 min). All heat-stressed animals displayed systemic inflammation and activated coagulation, evidenced by increased tumor necrosis factor alpha, prothrombin time, activated partial thromboplastin time, and d-dimer, and decreased platelet count and protein C. Biochemical markers evidenced cellular ischemia and injury/dysfunction: plasma levels of blood urea nitrogen, creatinine, glutamic oxaloacetic transaminase, glutamic pyruvic transaminase, and alkaline phosphatase; and striatal levels of glycerol, glutamate, and lactate/pyruvate; dihydroxy benzoic acid, lipid peroxidation, oxidized-form glutathione reduced-form glutathione, dopamine, and serotonin were all elevated during heatstroke. Core and brain temperatures and intracranial pressure were also increased during heatstroke. In contrast, the values of mean arterial pressure, cerebral perfusion pressure, and striatal levels of local blood flow, partial pressure of oxygen, superoxide dismutase, catalase, glutathione peroxidase, and glutathions reductase activities were all significantly lower during heatstroke. The circulatory dysfunction, systemic inflammation, hypercoagulable state, and cerebral oxidative stress, ischemia, and damage during heatstroke were all significantly suppressed by HRJVF. These findings demonstrate that brain cooling caused by HRJVF therapy may resuscitate persons who had a stroke by attenuating cerebral oxidative stress, systemic inflammation, activated coagulation, and tissue ischemia/injury during heatstroke.
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PMID:Brain cooling causes attenuation of cerebral oxidative stress, systemic inflammation, activated coagulation, and tissue ischemia/injury during heatstroke. 1687 31

The present study was performed to assess the prophylactic effect of platonin, a cyanine photosensitizing dye and an inhibitor of proinflammatory cytokines, in an animal model of heatstroke. Anesthetized rats were immediately divided into 2 major groups after the start of heat stress and administered either isotonic sodium chloride solution (dose, 1 mL/kg of body weight i.v.) or platonin (dose, 12.5-50 microg/mL per kilogram of body weight i.v.). They were exposed to ambient temperature of 43 degrees C to induce heatstroke. Another group of rats were exposed to room temperature (26 degrees C) and used as normothermic controls. Their physiological and biochemical parameters were continuously monitored. When the isotonic sodium chloride solution-pretreated rats underwent heat stress, their survival time values were found to be from 20 to 24 min. Pretreatment with intravenous doses of platonin (12.5-50 microg/mL per kilogram of body weight) immediately after the start of heat exposure significantly improved survival time during heatstroke (duration, 63-185 min). As compared with normothermic controls, all vehicle-pretreated heatstroke animals displayed higher levels of creatinine, serum urea nitrogen, alkaline phosphatase, aspartate aminotransferase, alanine aminotransferase, tumor necrosis factor alpha, prothrombin time, activated partial thromboplastin time and D-dimer in the plasma, cellular ischemia and injury markers in striatum, and intracranial pressure. In contrast, all vehicle-pretreated heatstroke animals had lower levels of mean arterial pressure, cerebral perfusion pressure, cerebral blood flow, brain Po2, and platelet count and protein C in the plasma. Immediately after the start of heat exposure, the previous administration of platonin significantly improved survival time by reducing the systemic inflammation, hypercoagulable state, and tissue ischemia and damage during heatstroke. The results demonstrate that platonin is effective for attenuation of heatstroke reactions.
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PMID:Platonin, a cyanine photosensitizing dye, is effective for attenuation of heatstroke in rats. 1711 36

The authors report a case of fatal stroke due to thrombosis of a cerebral arteriovenous malformation (AVM) in a young patient. The patient presented with a progressive severe headache that had lasted for a few days, followed by a rapid deterioration in the level of consciousness. Computed tomography and magnetic resonance imaging were immediately performed, and the images showed a large area of venous ischemia in the left hemisphere as well as a left temporal pial AVM. An emergency decompressive craniectomy was unsuccessful in preventing deterioration in the patient's condition. An autopsy examination revealed a thrombosed AVM leading to a wide area of venous ischemia and massive brain swelling. Thrombophilia investigations identified a heterozygous mutation at position 20209 of the prothrombin gene, a recently reported rare prothrombotic defect. Acute neurological decline after spontaneous thrombosis of an intracranial AVM is rare, and an association with the prothrombin defect in this patient is likely.
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PMID:Fatal spontaneous thrombosis of a cerebral arteriovenous malformation in a young patient with a rare heterozygous prothrombin gene mutation. Case report. 1733 May 43

Hyperbaric oxygen has been found to be beneficial in treating heatstroke animals. We attempted to further assess the possible mechanism of therapeutic protection offered by hyperbaric oxygen in experimental heatstroke. Anesthetized rats, immediately after the onset of heatstroke, were randomized into the following groups and given: a) hyperbaric oxygen (100% O(2) at 253 kPa for 1 h); or b) normal air. They were exposed to 43 degrees C temperature to induce heatstroke. When the untreated rats underwent heat stress, their survival time values were found to be 20-24 min. Resuscitation with hyperbaric oxygen increased the survival time to new values of 152-176 min. All untreated heatstroke rats displayed cerebrovascular dysfunction (evidenced by hypotension, intracranial hypertension, and cerebral hypoperfusion, hypoxia, and ischemia), hypercoagulable state (evidenced by increased levels of activated partial thromboplastin time, prothrombin time, and D-dimer, but decreased values of platelet count and protein C in plasma), and tissue ischemia/injury (evidenced by increased levels of creatinine, serum urea nitrogen, aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase in plasma, and dihydrobenzoic acid, lipid peroxidation, and oxidized-form glutathione/reduced-form of glutathione ratio in hypothalamus). The cerebrovascular dysfunctions, hypercoagulable state, tissue ischemia/injury, and brain oxidative stress that occurred during heatstroke were all suppressed by hyperbaric oxygen therapy. The current results indicate that hyperbaric oxygen therapy may resuscitate rats that had a heatstroke by decreasing multiple organ dysfunction and brain oxidative stress.
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PMID:Hyperbaric oxygen improves survival in heatstroke rats by reducing multiorgan dysfunction and brain oxidative stress. 1750 57

Ischemia/reperfusion (IR) injury in transplanted livers contributes to organ dysfunction and failure and is characterized in part by loss of NO bioavailability. Inhalation of NO is nontoxic and at high concentrations (80 ppm) inhibits IR injury in extrapulmonary tissues. In this prospective, blinded, placebo-controlled study, we evaluated the hypothesis that administration of inhaled NO (iNO; 80 ppm) to patients undergoing orthotopic liver transplantation inhibits hepatic IR injury, resulting in improved liver function. Patients were randomized to receive either placebo or iNO (n = 10 per group) during the operative period only. When results were adjusted for cold ischemia time and sex, iNO significantly decreased hospital length of stay, and evaluation of serum transaminases (alanine transaminase, aspartate aminotransferase) and coagulation times (prothrombin time, partial thromboplastin time) indicated that iNO improved the rate at which liver function was restored after transplantation. iNO did not significantly affect changes in inflammatory markers in liver tissue 1 hour after reperfusion but significantly lowered hepatocyte apoptosis. Evaluation of circulating NO metabolites indicated that the most likely candidate transducer of extrapulmonary effects of iNO was nitrite. In summary, this study supports the clinical use of iNO as an extrapulmonary therapeutic to improve organ function following transplantation.
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PMID:Inhaled NO accelerates restoration of liver function in adults following orthotopic liver transplantation. 1822 Feb 94

Pro-inflammatory mediators, such as nitric oxide (NO), prostaglandin E(2) (PGE(2)), and several cytokines (tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and IL-6) are responsible for central nervous system (CNS) injuries that include ischemia, Alzheimer's disease, and neural death. Inhibition of these pro-inflammatory mediators would be an effective therapy to reduce the progression of neurodegenerative diseases. In this study, we examined the anti-inflammatory effects of a human prothrombin fragment-2-derived peptide, NSA9 (NSAVQLVEN), on the production of pro-inflammatory mediators in lipopolysaccharide (LPS)-activated brain microglia. NSA9 significantly inhibited the release of NO, PGE(2), and pro-inflammatory cytokines in a dose-dependent manner. Furthermore, NSA9 reduced the expression of inducible NO synthase (iNOS) and cyclooxygenase (COX)-2 mRNA and protein, which control the production of NO and PGE(2), respectively. Moreover, NSA9 suppressed the LPS-induced nuclear translocation and activation of nuclear factor-kappaB (NF-kappaB). These results suggest that NSA9 strongly inhibits the pro-inflammatory responses of microglia through the modulation of NF-kappaB activity.
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PMID:Anti-inflammatory effect of a human prothrombin fragment-2-derived peptide, NSA9, in EOC2 microglia. 1826 78

Acute rhabdomyolysis is a syndrome characterized by the lesion of skeletal muscle resulting in subsequent release of intracellular contents into the circulatory system, which can cause potentially lethal complications. These contents include myoglobin, creatine phosphokinase, potassium, aldolase, lactate dehydrogenase and glutamic-oxaloacetic transaminase. There are numerous causes that can lead to acute rhabdomyolysis and many of patients present with multiple causes. The most common potentially lethal complication of rhabdomyoloysis is acute renal failure. In this article we present a case of a patient that developed clinical signs of acute rhabdomyolysis after consumption of heroin and alcohol. After approximately nine hours of alcohol and heroin induced coma he had acute compartment syndrome of the right arm, and clinical and laboratory signs of acute rhabdomyolysis with acute renal failure as a complication of rhabdomyolysis. Acute rhabdomyolysis developed in the patient as the result of acute compartment syndrome, with direct toxic activity of alcohol and diamorphine. During the period of coma, due to lying in particular position over a long period of time, pressure upon the certain part of the body caused muscle compression and capillary occlusion in fascial compartments, which led to ischemia. Upon pressure relief and beginning of tissue recovery, post ischemic compartment syndrome occurred with subsequent rhabdomyolysis. Getting out of coma the patient started to complain of severe pain in the right arm, which clinically worsened on passive stretching of the limb, with the loss of sensation and weakness. Laboratory findings showed high levels of creatine phosphokinase as the most sensitive marker of muscular damage. The peak of creatine phosphokinase level can be predictive for the development of acute renal failure because myoglobin level may return to normal within 6 hours after muscle injury. The peak of creatine phosphokinase (186.080 U/L; normal range 0-177) was recorded at 12 hours of admission. Other pertinent laboratory results such as urea, creatinine, prothrombin time, alanine aminotransferase and aspartate aminotransferase were also changed significantly. The peak of potassium level before dialysis was 6.8 mmol/L. Emergency fasciotomy of the anterior and posterior compartment syndrome was performed by a team of physicians after clinical examination. The second look debridement was performed at 48 and 72 hours. The plastic surgical procedure was performed 4 weeks later. On admission the patient also had oliguria with dark brown pigment in his urine. Arterial blood gases revealed metabolic and respiratory acidosis. The patient was hypovolemic and IV rehydratation with crystalloids, sodium bicarbonate and mannitol started immediately upon admission. Despite therapy his urine output decreased. Hemodialysis was initiated at serum potassium level of 6.8 mm/L and continued until his urine output returned to normal in three weeks. The patient was discharged from the hospital after six weeks, with normal urine output, without functional abnormality in his upper right limb. Acute rhabdomyolysis should be considered as a possibility in any patient with prolonged imobilization while in coma as well as in any intoxicated patient. Of course, creatine phosphokinase is the most sensitive indicator of muscle injury and the degree of creatine phosphokinase elevation correlates with the amount of muscle injury and disease severity. Other laboratory findings can help identify common complications of rhabdomyolysis such as acute renal failure, metabolic derangements and disseminated intravascular coagulopathy.
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PMID:[Acute rhabdomyolysis: a case report and literature review]. 1884 54


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