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

Paraplegia remains to be one of the most dangerous complications following thoracoabdominal aortic surgery with an incidence of 0.5 to 40%. Therefore, intraoperative monitoring of spinal cord function is very important when choosing the appropriate surgical technique. Early detection of spinal cord injury continues to be a crucial problem, moreover, the currently applied electrophysiological methods appear to be inaccurate. The aim of the study was to detect prospective spinal cord injury intraoperatively by monitoring the biochemical parameters of the cerebrospinal fluid (CSF). The authors studied the reversible aerobic/anaerobic metabolic changes by monitoring CSF lactate levels, moreover S-100 protein and neuron-specific enolase (NSE) concentrations--specific for neuroglia and neuronal injury, respectively. One of the important methods to prevent paraplegia is the intraoperative CSF drainage, which may improve spinal cord perfusion. Between 1996-1998 51 patients underwent reconstructive thoracic or thoracoabdominal aortic aneurysm operation. The continuously drained CSF was collected in 10 ml fractions during the preparation, whereas during aortic cross-clamping and de-clamping 10 minute fractions were used. All CSF samples were immediately analysed intraoperatively for pH, pCO2, HCO3, potassium and lactate levels, S-100 protein and NSE were analysed by immunoluminescence. CSF lactate levels increased slightly during aortic clamping and a moderate, but non-significant increase was found in the hyperemic phase (reperfusion) in patients without spinal cord ischemia. Spinal cord injury was detected in 7 cases. These patients exhibited a significant CSF-lactate increase (control vs aortic cross-clamping: 1.9 vs 5.3 mmol/l), moreover CSF-lactate remained elevated throughout the whole operation. Paraplegia did not occur, Tarlov 2 paraparesis developed in four cases and three patients displayed cerebral damage. Intraoperative CSF--especially CSF-lactate--monitoring may help the operating team to detect early anaerobic changes of the metabolism the spinal cord.
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PMID:[New method for the intraoperative biochemical monitoring of cerebrospinal fluid in surgery of thoracoabdominal aortic aneurysms]. 1093 38

We investigated effects of extracellular ATP on intracellular chloride activities ([Cl-]i) and possible contribution of the Cl--HCO3- exchange to this increase in [Cl-]i in isolated guinea pig ventricular muscles. The [Cl-]i and intracellular pH (pHi) were recorded in quiescent ventricular muscles using double-barreled ion-selective microelectrode techniques. MgATP at a concentration higher than 0.1 mM, induced an increase in [Cl-]i, and this increase in [Cl-]i was dependent on the concentration of ATP but not on the concentration of magnesium ions present in the perfusion solution. NaADP, but not NaAMP, at a concentration of 0.5 mM induced a similar increase in [Cl-]i as that induced by MgATP. However, the NaADP-induced increase in [Cl-]i was transient and gradually returned to the control level even though NaADP was continuously present. Furthermore, ATP also triggered a transient acidification of pHi, and both increases in [Cl-]i and intracellular H+ induced by ATP were prevented when preparations were pretreated with stilbene derivatives, SITS and DIDS, or perfused with a Cl--free solution. Our findings showed that the increased extracellular ATP concentrations might trigger an increase in [Cl-]i in ventricular muscles. In light of previous studies showing that cardiac ischemia induced increases in extracellular nucleotide concentrations and [Cl-]i in ventricular muscles, we propose that ischemia-induced accumulation of ATP concentration in the extracellular space may be an important factor to trigger increment of [Cl-]i during ischemic conditions.
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PMID:Enhancement of intracellular Cl- concentrations induced by extracellular ATP in guinea pig ventricular muscle. 1120 17

Carbon dioxide interacts both with reactive nitrogen species and reactive oxygen species. In the presence of superoxide, NO reacts to form peroxynitrite that reacts with CO2 to give nitrosoperoxycarbonate. This compound rearranges to nitrocarbonate which is prone to further reactions. In an aqueous environment, the most probable reaction is hydrolysis producing carbonate and nitrate. Thus the net effect of CO2 is scavenging of peroxynitrite and prevention of nitration and oxidative damage. However, in a nonpolar environment of membranes, nitrocarbonate undergoes other reactions leading to nitration of proteins and oxidative damage. When NO reacts with oxygen in the absence of superoxide, a nitrating species N2O3 is formed. CO2 interacts with N2O3 to produce a nitrosyl compound that, under physiological pH, is hydrolyzed to nitrous and carbonic acid. In this way, CO2 also prevents nitration reactions. CO2 protects superoxide dismutase against oxidative damage induced by hydrogen peroxide. However, in this reaction carbonate radicals are formed which can propagate the oxidative damage. It was found that hypercapnia in vivo protects against the damaging effects of ischemia or hypoxia. Several mechanisms have been suggested to explain the protective role of CO2 in vivo. The most significant appears to be stabilization of the iron-transferrin complex which prevents the involvement of iron ions in the initiation of free radical reactions.
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PMID:The role of carbon dioxide in free radical reactions of the organism. 1244 30

We investigated the effects of simulated ischemia on intracellular Cl- concentration ([Cl-]i) in guinea pig ventricular myocardial cells and possible role of the [Cl-]i on the ischemia/reperfusion-induced arrhythmias in perfused rat hearts. Our results provided direct evidence that the [Cl-]i in ventricular muscle was increased under ischemic conditions, which suggested that activation of the Cl-(-)HCO3- exchanger by ischemia would partially contribute to the elevation of [Cl-]i. Application of stilbene derivatives or lowering Cl- concentration in perfusion solution delayed the onset of ischemia-induced deterioration in action potentials, pHi, [Cl-]i, and suppressed the incidence of ischemia/reperfusion-induced arrhythmias. The conclusion was made to emphasize the important role of intracellular Cl- homeostasis in cardiac physiology and pathogenesis of myocardial ischemia/reperfusion injury.
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PMID:[The relationship between intracellular chloride concentration and ischemia reperfusion-induced arrhythmias in myocardial cells]. 1290 2

It is likely that brain tissue acidosis during ischemia is associated with neuronal injury. The authors measured brain extracellular H+, PCO2 and HCO3- concentrations during an ischemic event produced by temporary occlusion of the middle or anterior cerebral arterial distributions, with a 10-minute recovery period. Patients who were to undergo craniotomy for cerebrovascular surgery were recruited for the study. A probe that measures PCO2, pH, and temperature was inserted into tissue at risk for ischemia during temporary arterial occlusion. As a control for this treatment, PaCO2 was increased 10 mm Hg in five patients over a 10-minute period. Under baseline conditions, there was no difference in arterial blood pressure, blood gas levels, or brain temperature between patients who underwent temporary arterial occlusion or those in whom hypercapnia was induced. In patients in whom hypercapnia was induced, H+, PCO2, and HCO3- concentrations increased and all values returned to baseline levels within 10 minutes. In 10 patients who underwent a median 9-minute arterial occlusion, transient ischemia was seen with an increase in tissue H+ and PCO2 levels of 100% and 60%, respectively, and a 20% decrease in HCO3- levels. After a 10-minute postischemic recovery, only PCO2 had returned to baseline levels. These results are consistent with a rapid equilibration of lactic acidosis across the cell membrane during ischemia which decreases HCO3- concentration. After ischemia, extracellular acidosis may be prolonged because of the extrusion of H+ from the cell by membrane ion exchange.
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PMID:Brain tissue acid-base changes during ischemia. 1509 3

A significant number of moribund and dead lobsters Homarus americanus were reported to New York state authorities by lobster fishers in Long Island Sound (LIS) during the summer of 2002. Morbid lobsters were characterised by an orange discolouration of the abdomen, lethargy, an excess of epibionts and poor post-capture survival. On necropsy, severe extensive multifocal or diffuse mineralised granulomatous inflammation of the gills and antennal glands was the most striking pathology. In the gills, granulomas often occluded the lumen of filaments, resulting in congestion, ischemia and coagulative necrosis of gill tissues. In the antennal glands, granulomas were concentrated along the border between the coelomosac and labyrinth. No significant pathogens were recovered from diseased individuals. In prechronic individuals, however, it was evident that granulomas were focused around calcium carbonate (aragonite) crystals. This disease may result from anomalously high sea-bottom temperatures in LIS (approximately 23 degrees C) during the summer of 2002 and associated disruptions of the calcium chemistry of lobsters in favour of deposition of minerals in soft tissues. The ultimate cause of death of affected lobsters is probably respiratory failure due to reduced effective surface area of the gills, exacerbated by hypermetabolic temperatures and an abundance of epibionts.
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PMID:Excretory calcinosis: a new fatal disease of wild American lobsters Homarus americanus. 1510 45

The aim of the study was to investigate the protective effect of aprotinin in a rat hind limb ischemia/reperfusion (I/R) model. A well-known antioxidant, alpha-tocopherol, was also tested for comparison. Ischemia was induced for 4 h by vascular clamping of the iliac arteries of 24 Sprague-Dawley rats, followed by 1 h of reperfusion. Muscle injury was evaluated in three groups: a saline group, an alpha-tocopherol group and an aprotinin group. Blood pH, pO2, pCO2, HCO3, creatine kinase (CPK), lactate dehyrogenase (LDH) and thiobarbituric acid reactive substances (TBARS) as well as muscle TBARS were measured at the end of the reperfusion. Muscle tissue samples were taken for histological examination. alpha-Tocopherol and aprotinin groups showed a significant amelioration of plasma CPK (p=0.002, p=0.002), LDH (p=0.004, p=0.004) and muscle tissue TBARS (p=0.001, p=0.001) compared with the control. Plasma TBARS were significantly lower in the aprotinin group compared with the control (p=0.017). Also, tissue TBARS was significantly lower in the aprotinin group than the alpha-tocopherol group (p<0.001). Neutrophil infiltration was less prominent in the alpha-tocopherol and aprotinin groups compared to the control (p=0.006, p=0.001). These results suggest that aprotinin, a potent anti-inflammatory drug, is more useful than alpha-tocopherol, a powerful antioxidant, for attenuating muscle injury after I/R.
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PMID:Aprotinin ameliorates ischemia/reperfusion injury in a rat hind limb model. 1560 95

Lithium carbonate used in the long-term treatment of manic-depressive illness has been reported to lead to progressive renal impairment in rats and humans. Caffeic acid phenethyl ester (CAPE), a component of honeybee propolis, protects tissues from reactive oxygene species mediated oxidative stress in ischemia-reperfusion and toxic injuries. The beneficial effect CAPE on lithium-induced nephrotoxicity has not been reported yet. The purpose of this study was to examine a possible renoprotective effect of CAPE against lithium-induced nephrotoxicity in a rat model. Twenty-two adult male rats were randomly divided into three experimental groups, as follows: control group, lithium-treated group (Li), and lithium plus CAPE-treated group (Li+CAPE). Li were treated intraperitoneally (i.p.) with 25 mg/kg Li2CO3 solution in 0.9% NaCl twice daily for 4 weeks. CAPE was co-administered i.p. with a dose of 10 microM/kg/day for 4 weeks. Serum Li, blood urea nitrogen and plasma creatinine, urinary N-acetyl-beta-D-glucosaminidase (NAG, a marker of renal tubular injury), and malondialdehyde (MDA, an index of lipid peroxidation), were used as markers of oxidative stress-induced renal impairment in Li-treated rats. Superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities were studied to evaluate the changes of antioxidant status in renal tissue. Serum Li levels were found high in the Li and Li+CAPE groups. In Li-administrated rats, urinary NAG and renal MDA levels were increased according to control and Li+CAPE groups (p < 0.05). CAPE caused a significant reduction in the levels of these parameters. Likewise, renal SOD, CAT and GSH-Px activities were decreased in Li-administrated animals; CAPE caused a significant increase in the activities of these antioxidant enzymes. In conclusion, CAPE treatment has a protective effect against Li-induced renal tubular damage and oxidative stress in a rat model.
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PMID:Lithium-induced renal toxicity in rats: protection by a novel antioxidant caffeic acid phenethyl ester. 1613 21

Chloride (Cl-) efflux induces depolarization and contraction of vascular smooth muscle cells. In the basilar arteries from the New Zealand white rabbits, the role of Cl- flux in serotonin-induced contraction was demonstrated by (i) inhibition of Na+-K+-2Cl- co-transporter (NKCC1) to decreased Cl- influx with bumetanide; (ii) a disabled Cl-/HCO3- exchanger with bicarbonate free HEPES solution; (iii) blockade of Cl- channels using 5-nitro-2-(3-phenylpropylamino) benzoic acid (NPPB) and indanyloxyacetic acid 94, R-(+)-methylindazone (R-(+)-IAA-94); and (iv) substitution of extracellular Cl- with methanesulfonate acid (113 mmol/L; Cl-, 10 mmol/L). In addition, the expression of NKCC1 in brain tissues after neonatal hypoxia-ischemia was examined at mRNA and protein levels using RT-PCR and Western blotting techniques. NKCC1 mRNA and protein expressions were increased at 24 and 48 h and returned to normal levels at 72 h after hypoxia insult when compared with the control littermates. In conclusion, Cl- efflux regulates cerebral circulation and the up-regulation of NKCC1 after neonatal hypoxia-ischemia may contribute to brain injury.
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PMID:Role of Cl- in cerebral vascular tone and expression of Na+-K+-2Cl- co-transporter after neonatal hypoxia-ischemia. 1633 78

The objectives of this study were to compare the protective effects of ascorbic acid and iloprost on lung injury caused by ischemia reperfusion (I/R) of the lower extremities of rats. Wistar albino rats (n = 34) were divided into five groups. In the I/R group (n = 6), the aorta was cross-clamped for 3 hr, followed by 1 hr of reperfusion. In the vitamin C group (n = 8), animals were pretreated with 100 mg/kg ascorbic acid via the left jugular vein before aortic cross-clamping. In the iloprost group (n = 8), animals were pretreated with 20 ng/(kg x min) iloprost by constant intravenous infusion via the left jugular venous cannula. In the sham group (n = 6), the abdomen was left open at the same period and a juguler venous line was established. In the control group (n = 6), lungs were removed and blood samples taken immediately after sternotomy. No treatment was given in this group. After both lungs were removed, biochemical parameters were measured and histopathological evaluation was made. Although the arterial blood pO2 and HCO3 levels were statistically significantly high in both the vitamin C and iloprost groups compared to the I/R group, plasma malondialdehyde (MDA) levels were significantly low. Meanwhile, the MDA levels in the lung tissue were significantly low in the vitamin C group compared to the I/R group. The MDA level in the lung tissue in the iloprost group was also low compared to the I/R group, but it was not statistically significant. The lungs of the I/R group displayed intense interstitial leukocytic infiltration in histopathological examination compared to the other groups. Pretreatment of animals with iloprost and vitamin C significantly decreased the pulmonary injury characterized by decreased plasma leukocyte sequestration. The results suggest that both vitamin C and iloprost are useful agents for attenuating the lung injury caused by increased oxidative stress and neutrophil accumulation after a period of I/R of the lower extremities.
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PMID:Ascorbic acid (vitamin C) and iloprost attenuate the lung injury caused by ischemia/reperfusion of the lower extremities of rats. 1637 48


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