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

Chronic hypoxia (CH) leads to the deterioration of myocardial functions with impaired calcium handling in the sarcoplasmic reticulum (SR), which may be mediated by oxidative stress. We hypothesized that administration of antioxidant melatonin would protect against cardiac and ischemia-reperfusion (I/R) injury by ameliorating SR calcium handling. Adult Sprague-Dawley rats that had received a daily injection of melatonin or vehicle were exposed to 10% oxygen for 4 wk. The heart of each rat was then dissected and perfused using a Langendorff apparatus. The ratio of heart-to-body weight, ventricular hypertrophy and hematocrit were increased in the hypoxic rats compared with the normoxic controls. Malondialdehyde levels were also increased in the heart of hypoxic rats and were lowered by the treatment of melatonin. The hearts were subjected to left coronary artery ischemia (30 min) followed by 120-min reperfusion. Lactate dehydrogenase leakage before ischemia, during I/R and infarct size of the isolated perfused hearts were significantly elevated in the vehicle-treated hypoxic rats but not in the melatonin-treated rats. Spectroflurometric studies showed that resting calcium levels and I/R-induced calcium overload in the cardiomyocytes were more significantly altered in the hypoxic rats than the normoxic controls. Also, the hypoxic group had decreased levels of the SR calcium content and reduced amplitude and decay time of electrically induced calcium transients, indicating impaired contractility and SR calcium re-uptake. Moreover, there were reductions in protein expression of calcium handling proteins, markedly shown at the level of SR-Ca(2+) ATPase (SERCA) in the heart of hypoxic rats. Melatonin treatment significantly mitigated the calcium handling in the hypoxic rats by preserving SERCA expression. The results suggest that melatonin is cardioprotective against CH-induced myocardial injury by improving calcium handling in the SR of cardiomyocytes via an antioxidant mechanism.
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PMID:Melatonin ameliorates calcium homeostasis in myocardial and ischemia-reperfusion injury in chronically hypoxic rats. 1848 39

Recent studies have indicated that hydrogen sulfide (H(2)S) is capable of modulating many physiological processes, which prompted us to investigate the potential of H(2)S as a lung protective agent. To explore changes in the generation of endogenous H(2)S and the role of H(2)S in the pathogenesis of pulmonary ischemia-reperfusion (I/R) injury in rats, we built an isolated rat lung I/R model. Lungs were subjected to 45 min ischemia followed by reperfusion (45 min) and were pretreated with H(2)S (50 micromol/l or 100 micromol/l) or an irreversible inhibitor of cystathionine-gamma-lyase (CSE), propargylglycine (PPG; 2 mmol/l). We examined indices of lung injury: lung histological change, perfusion flow rate, ratio of lung wet weight to dry weight (w/d), and lung compliance. H(2)S content and CSE protein expression in lung tissues were measured. Malondialdehyde (MDA) content, activities of superoxide dismutase (SOD) and catalase (CAT), and restraint of superoxide anion (O(2)(-)) production in lung tissues were measured to reflect oxidative stress. In the current study, we demonstrated that H(2)S content and CSE activity in lungs after I/R were significantly higher than those in the control group. Preperfusion with H(2)S attenuated the lung I/R injury while preperfusion with PPG aggravated the lung I/R injury. H(2)S preperfusion reduced I/R-induced MDA production and potentiated SOD and CAT activities and the restraint of O(2)(-) production in the lungs under I/R, which attenuated lung oxidative injury. These findings suggest that endogenous CSE/H(2)S pathway might be involved in the pathogenesis of lung I/R injury and that administration of H(2)S might be of clinical benefit in lung I/R injury.
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PMID:Hydrogen sulfide protects rat lung from ischemia-reperfusion injury. 1848 39

We examined the effect of vitamin C on muscle injury distal to the tourniquet which was applied for 4 hours with 10- and 20-minute reperfusion intervals after 2 hours of tourniquet. Sixty-four Sprague-Dawley rats were allocated to 4 randomized groups. After 2 hours tourniquet, 10- and 20-minutes of reperfusion were allowed to half of each group respectively. Afterward an additional 2 hours compression was applied. Except the control group the animals received vitamin C intravenously, before the first tourniquet in Group I, at the reperfusion interval in Group II, and at both times in Group III. Malondialdehyde levels were measured in blood and the tibialis anterior muscle. The muscle was histopathologically examined. The data was evaluated statistically. The effects of timing and the dose of vitamin C on ischemia reperfusion injury remain controversial and there was no statistical difference between 10- and 20-minute reperfusion intervals. But the blood malondialdehyde levels showed that vitamin C has a positive effect on the muscle injury caused by ischemia-reperfusion.
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PMID:The effect of vitamin C on ischemia reperfusion injury because of prolonged tourniquet application with reperfusion intervals. 1915 33

Recent studies have documented that remote organs are affected by ischemic injury to the kidney. Here we studied whether the liver also suffers damage during induction of renal ischemia-reperfusion in rats and compared this to bilateral nephrectomy. Hepatic levels of tumor necrosis factor-alpha increased significantly after 6 and 24 h of renal ischemia or nephrectomy. Malondialdehyde, an index of lipid peroxidation, increased while total glutathione was decreased in the liver in both the renal ischemia and nephrectomy groups, suggesting activation of oxidative stress. Expression of liver spermine-spermidine acetyl transferase, an enzyme upregulated in early phases of hepatic injury was significantly increased 6 h after either kidney ischemia or nephrectomy. Apoptosis was increased in hepatocytes 24 h after nephrectomy. We also found histological evidence of hepatocyte injury following both ischemia and bilateral nephrectomy. Infusion of reduced glutathione, before the induction of renal ischemia, significantly improved liver architecture and was associated with a reduction in hepatic malondialdehyde and serum alanine transaminase levels. Our study shows that acute kidney ischemia or renal failure activates oxidative stress and promotes inflammation, apoptosis, and tissue damage in hepatocytes.
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PMID:Ischemic and non-ischemic acute kidney injury cause hepatic damage. 1917 57

The aim of this prospective case-control study was to determine the change in serum maternal ischemia-modified albumin (IMA) during normal pregnancies. A total of 117 pregnant (first trimester (n=24), second trimester (n=34), and third trimester (n=35)) and non-pregnant healthy women (n=23) were included. Maternal serum IMA, Malondialdehyde (MDA), and albumin levels were measured. Compared with non-pregnant women, the cross-sectional mean IMA levels in pregnant women were significantly increased, while the mean serum MDA and albumin levels were significantly decreased throughout pregnancy. Furthermore, a significant negative correlation between serum IMA and albumin levels (r=-0.354, p<0.001) was found, and there was a weak positive correlation between serum albumin and MDA levels (r=0.334, p<0.001). Serum IMA, which has recently been developed as a clinical marker of ongoing myocardial ischemia, appears to be elevated in normal pregnancy. This may be due to the physiologic oxidative stress state of pregnancy.
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PMID:The novel ischemia marker 'ischemia-modified albumin' is increased in normal pregnancies. 1923 58

Ischemia and reperfusion (I/R) injury is characterized by significant oxidative stress, characteristic changes in the antioxidant system and organ injury leading to significant morbidity and mortality. This study was designed to assess the possible protective effect of montelukast, a selective antagonist of cysteinyl leukotriene receptor 1 (CysLT1), on hepatic I/R injury in rats. Wistar albino rats through clamping hepatic artery, portal vein, and bile duct, were subjected to 45 min of hepatic ischemia followed by 60 min reperfusion period. Montelukast (10 mg/kg; i.p.) was administered 15 min prior to ischemia and immediately before reperfusion period. At the end of the reperfusion period, the rats were killed by decapitation. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH) activity, and proinflammatory cytokines (TNF-alpha and IL-1beta) were determined in blood samples. Malondialdehyde (MDA), and glutathione (GSH) levels and myeloperoxidase (MPO) and Na+, K+-ATPase activities were determined in the liver tissue samples while formation of reactive oxygen species was monitored by using chemiluminescence (CL) technique with luminol and lucigenin probes. Tissues were also analyzed histologically. Serum ALT, AST, and LDH activities were elevated in the I/R group, while this increase was significantly decreased by montelukast treatment. Hepatic GSH levels and Na+, K+-ATPase activity, significantly depressed by I/R, were elevated back to control levels in montelukast-treated I/R group. Furthermore, increases in tissue luminol and lucigenin CL, MDA levels, and MPO activity due to I/R injury were reduced back to control levels with montelukast treatment. Since montelukast administration alleviated the I/R-induced liver injury and improved the hepatic structure and function, it seems likely that montelukast with its anti-inflammatory and antioxidant properties may be of potential therapeutic value in protecting the liver against oxidative injury due to ischemia-reperfusion.
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PMID:Protective potential of montelukast against hepatic ischemia/reperfusion injury in rats. 1951 88

The possible protective effect of betulinic acid on renal ischemia/reperfusion (I/R) injury was studied. Wistar Albino rats were unilaterally nephrectomized and subjected to 45 min of renal pedicle occlusion followed by 6 h of reperfusion. Betulinic acid (250 mg/kg, i.p.) or saline was administered at 30 min prior to ischemia and immediately before the reperfusion. Creatinine, blood urea nitrogen (BUN), lactate dehydrogenase (LDH) and TNF-alpha as well as the oxidative burst of neutrophil and leukocyte apoptosis were assayed in blood samples. Malondialdehyde (MDA), glutathione (GSH) levels, Na(+), K(+)-ATPase and myeloperoxidase (MPO) activities were determined in kidney tissue which was also analysed microscopically. I/R caused significant increases in blood creatinine, BUN, LDH and TNF-alpha. In the kidney samples of the I/R group, MDA levels and MPO activity were increased significantly, however, GSH levels and Na(+), K(+)-ATPase activity were decreased. Betulinic acid ameliorated the oxidative burst response to both formyl-methionyl-leucyl-phenylalanine (fMLP) and phorbol 12-myristate 13-acetate (PMA) stimuli, normalized the apoptotic response and most of the biochemical indices as well as histopathological alterations induced by I/R. In conclusion, these data suggest that betulinic acid attenuates I/R-induced oxidant responses, improved microscopic damage and renal function by regulating the apoptotic function of leukocytes and inhibiting neutrophil infiltration.
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PMID:Betulinic acid protects against ischemia/reperfusion-induced renal damage and inhibits leukocyte apoptosis. 1961 40

The fact that a considerable amount of clinical conditions suffering from ischemia-reperfusion injury (IRI) occur under general anesthesia has triggered researchers to focus on the effects of anesthetic drugs on IRI. Hence, the aim of this study was to compare the use of different anesthetic drugs in a skeletal IRI model. Tourniquet IRI method was performed and two experimental groups were established as sham-control and IRI group. Rats in each group were anesthetized either with thiopental, ketamine, propofol or etomidate. Malondialdehyde, superoxide dismutase, catalase, and glutathione peroxidase were measured in skeletal muscle via a spectrophotometer. Zinc, iron, copper, and selenium were evaluated by atomic absorption spectrophotometer. In rats anesthetized with thiopental (40 mg/kg, i.p.), malondialdehyde values in IRI group were higher and glutathion peroxidase levels were lower compared to sham-control group. However, superoxide dismutase and catalase activities were identical. On the other hand, while the level of zinc in IRI group attenuated, no differences in iron and copper values were determined. Rats anesthetized with ketamine (60 mg/kg), propofol (100 mg/kg), or etomidate (20 mg/kg) did not show increased malondialdehyde levels in comparison with control levels. While the drugs did not cause a distinction in the levels of superoxide dismutase, catalase, glutathion peroxidase, iron, and copper, zinc was in a lower level in IRI group compared to sham-control. In conclusion, ketamine, propofol, and etomidate, with anesthetic doses, denoted efficacious effects on IRI; hence the drugs might be preferred in certain operations with the risk of IRI.
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PMID:The comparison of the effects of anesthetic doses of ketamine, propofol, and etomidate on ischemia-reperfusion injury in skeletal muscle. 1967 50

We recently reported that excessive superoxide anion radical (O(2)(-)) was generated in the jugular vein during reperfusion in rats with forebrain ischemia/reperfusion using a novel electrochemical sensor and excessive O(2)(-) generation was associated with oxidative stress, early inflammation, and endothelial injury. However, the source of O(2)(-) was still unclear. Therefore, we used allopurinol, a potent inhibitor of xanthine oxidase (XO), to clarify the source of O(2)(-) generated in rats with forebrain ischemia/reperfusion. The increased O(2)(-) current and the quantified partial value of electricity (Q), which was calculated by the integration of the current, were significantly attenuated after reperfusion by pretreatment with allopurinol. Malondialdehyde (MDA) in the brain and plasma, high-mobility group box 1 (HMGB1) in plasma, and intercellular adhesion molecule-1 (ICAM-1) in the brain and plasma were significantly attenuated in rats pretreated with allopurinol with dose-dependency in comparison to those in control rats. There were significant correlations between total Q and MDA, HMGB, or ICAM-1 in the brain and plasma. Allopurinol pretreatment suppressed O(2)(-) generation in the brain-perfused blood in the jugular vein, and oxidative stress, early inflammation, and endothelial injury in the acute phase of forebrain ischemia/reperfusion. Thus, XO is one of the major sources of O(2)(-)- in blood after reperfusion in rats with forebrain ischemia/reperfusion.
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PMID:Xanthine oxidase is one of the major sources of superoxide anion radicals in blood after reperfusion in rats with forebrain ischemia/reperfusion. 1978 28

The present study investigated the protective effect of zinc aspartate, in connection with reactive oxygen species and nitric oxide, on long-term ischemia-reperfusion injury (IRI) in rat skeletal muscle. Following ketamine anesthesia, 24 rats were randomly assigned to four groups: groups 1 and 2, each without tourniquet application, received no drug and zinc, respectively; groups 3 and 4, each subjected to tourniquet-induced IRI (3 + 24 h), received no drug and zinc, respectively. IRI was achieved by the application of an elastic rubber band in the left hind limb of the anesthetized rats. Gastrocnemius muscle samples were obtained for biochemical measurements. Malondialdehyde levels were lower in group 2 and higher in group 3 than those seen in group 1. However, zinc aspartate (group 4) totally reversed malondialdehyde levels to control levels. Superoxide dismutase activity was increased in group 2 compared with group 1; however, there was no difference between groups 1 and 3, and Zn injection (group 4) increased superoxide dismutase activity. While catalase values were similar in groups 1 and 2, significant increments were observed in 3 and 4. A similar enhancement in glutathione levels were observed in groups 2 and 4 compared with group 1. Nitric oxide levels were lower in group 2 than 1, and no difference between groups 1 and 3 was demonstrated. In conclusion, zinc seems to be an effective treatment option against IRI.
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PMID:Protective effect of zinc aspartate on long-term ischemia-reperfusion injury in rat skeletal muscle. 1993 81


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