Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the alterations in the stable end products of nitric oxide, i.e., nitrate and nitrite, in the plasma during and after rat focal cerebral ischemia by an automated procedure based on the Griess reaction. At 2 h of middle cerebral artery (MCA) occlusion, plasma nitrate/nitrite levels were significantly higher (53 +/- 8 microM, mean +/- SD, n = 5, p < 0.05) than in rats with sham operation (36 +/- 9 microM, n = 5), and were mildly elevated at 4 h of MCA occlusion (42 +/- 9 microM, n = 5, n.s.). At 30 min of reperfusion after 2 h of MCA occlusion, plasma nitrate/nitrite levels were more markedly elevated (72 +/- 7 microM, n = 5, p < 0.01 vs. sham operation), but were moderately elevated at 2 h of reperfusion after 2 h of MCA occlusion (61 +/- 10 microM, n = 5, p < 0.05). Plasma nitrite levels were not changed during these experimental periods. Administration of 20 mg/kg of NG-nitro-L-arginine methyl ester (L-NAME) significantly decreased plasma nitrate/nitrite as well as nitrite at 30 min of reperfusion after 2 h of MCA occlusion (n = 5), but 2 mg/kg of L-NAME did not (n = 3). The effect of 20 mg/kg of L-NAME on plasma nitric oxide end products was reversed by the simultaneous administration of 200 mg/kg of L-arginine (n = 3), but not D-arginine (n = 3). The present study suggests that the L-arginine-nitric oxide pathway is activated during acute cerebral ischemia and reperfusion.
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PMID:Elevation of plasma nitric oxide end products during focal cerebral ischemia and reperfusion in the rat. 816 91

1. A possible cerebroprotective effect of nicorandil was investigated in a canine model of 5 min global cerebral ischaemia, and compared with protective effects of nitroglycerin and nicardipine. 2. Cerebral ischaemia was produced by occlusion of the left subclavian and the brachiocephalic arteries with preceding ligation of the intercostal arteries. The decrease in baroreflex sensitivity (BRS), measured by phenylephrine-induced reflex bradycardia, was used to assess the cerebroprotective effect. 3. Nicorandil (10 or 30 micrograms kg-1 min-1, i.v.), nitroglycerin (3 micrograms kg-1 min-1, i.v.) or nicardipine (0.3 micrograms kg-1 min-1, i.v.) were infused for 60 min just before ischaemia. Nitroglycerin and nicardipine decreased mean arterial blood pressure to an extent similar to that induced by the lower dose of nicorandil. Blood flow in the dorsal medulla oblongata was increased by nicorandil and nicardipine, but not by nitroglycerin. 4. Nicorandil at both doses and nitroglycerin prevented the post-ischaemic decrease in BRS. In these cases, bilateral vagotomy during the reperfusion period decreased BRS, indicating that the vagal component of BRS was protected from ischaemia. On the other hand, nicardipine failed to exert a cerebroprotective effect. 5. The present study suggests that nicorandil may possess a direct cerebroprotective effect and that its property as a nitrate might, at least in part, be important for the observed cerebral protection.
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PMID:Protection by nicorandil against the dysfunction of the central vagal baroreflex system following transient global cerebral ischaemia in dogs. 840 37

To assess the interaction of nitric oxide (NO) and superoxide during reperfusion after cerebral ischemia, we studied the dose effects of superoxide dismutase (SOD) on the levels of nitrosyl hemoglobin and plasma nitrite + nitrate which were increased at 30 min reperfusion after 2 h middle cerebral artery occlusion in rats. SOD was administered at 10 min before reperfusion. With 1, 5 and 10 mg/Kg of SOD, plasma nitrite + nitrate level was decreased by 25 mg/kg of SOD. The same amount of apo enzyme was without effect. These results suggest effect of superoxide in the NO level released during reperfusion after cerebral ischemia.
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PMID:Effects of superoxide dismutase on nitric oxide production during reperfusion after focal cerebral ischemia is rats. 861 63

We investigated the levels of nitrosyl hemoglobin (HbNO) in rat jugular blood by electron spin resonance (ESR) spectroscopy during and after middle cerebral artery occlusion. The levels of plasma nitric oxide (NO) end products, nitrate plus nitrate, were compared with the levels of HbNO. Small amounts of HbNO were detected in sham-operated rats (n=4) and those subjected to 2 h of occlusion (n=4), whereas nitrite plus nitrate was increased only in the latter (P<0.01; vs.sham). Upon reperfusion after 2 h of occlusion both HbNO and nitrite plus nitrate clearly increased after 15 min (n=4) and 30 min (n=6) reperfusion (P<0.01; vs.occlusion). Administration of superoxide dismutase (5 mg/kg) significantly increased HbNO (P<0.05) but not plasma nitrate plus nitrate (n=5). The increase in HbNO suppressed by administration of NG-nitro-L-arginine methyl ester (20mg/kg; n=4,P<0.01), and this suppression could be reversed by L-arginine (200 mg/kg) (n=4). The present study clearly showed that the L-arginine-NO synthase pathway was activated during reperfusion after focal cerebral ischemia and indicated the involvement of a reaction between NO and superoxide during early reperfusion.
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PMID:Generation of nitric oxide and superoxide during reperfusion after focal cerebral ischemia in rats. 863 53

Nitric oxide (NO.) has been implicated in the process of cerebral ischemia/reperfusion injury. We have examined the production of NO., as reflected by nitrite (NO2-) + nitrate (NO3-) accumulation, from synaptosomes isolated from neonatal or adult rat brain and subjected to a period of glucose and oxygen deprivation. There was a significant increase in the amount of NO2- + NO3- production from adult synaptosomes under these conditions, whereas there was no difference compared to control in the production of NO2- + NO3- from the neonatal synaptosomes. The total antioxidant status of the synaptosomes at these different stages of brain development was found to be the same. These data suggest that the vulnerability of the adult brain to ischemia/reperfusion injury may be associated with the production of NO. from nerve terminals. The ratios of antioxidant capacity to NO. production under such conditions have been shown here to be different between the neonatal and adult nerve terminals. Thus the well documented resistance of neonatal brain to ischemia/reperfusion injury may involve the neonatal nerve terminal being under less oxidative stress than the adult.
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PMID:Nitric oxide and antioxidant status in glucose and oxygen deprived neonatal and adult rat brain synaptosomes. 889 46

We aimed to investigate effect of temperature on the jugular levels of nitric oxide (NO) at reperfusion after focal cerebral ischemia. Both nitrosyl hemoglobin (HbNO) (2.5 +/- 0.4 microM) and plasma nitrite plus nitrate levels (61 +/- 5 microM) in rats under normothermia (approximately 37 degrees C) after 30 min of reperfusion following 2 h of left middle cerebral artery occlusion were significantly high, compared with sham operated rats (1.3 +/- 0.1 microM, 40 +/- 4 microM, respectively). Both HbNO (1.5 +/- 0.3 microM) and nitrite plus nitrate levels (43 +/- 7 microM) under moderate hypothermia (approximately 32 degrees C) were significantly low, compared with normothermic rats. HbNO (2.8 +/- 0.8 microM) and nitrite plus nitrate levels (65 +/- 8 microM) under mild hyperthermia (approximately 39 degrees C) were not significantly high. These results firstly demonstrated that hypothermia suppresses the elevation in intrajugular NO after cerebral ischemia-reperfusion.
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PMID:Hypothermia suppresses nitric oxide elevation during reperfusion after focal cerebral ischemia in rats. 897 45

While nitric oxide (NO) has been implicated as a mediator of glutamate excitotoxicity after cerebral ischemia/reperfusion, melatonin has been reported to inhibit brain NO production by suppressing nitric oxide synthase. The purpose of the present studies was to determine the effect of exogenous melatonin administration on NO-induced changes during brain ischemia/reperfusion. Indicators of cerebral cortical and cerebellar NO production [nitrite/nitrate levels and cyclic guanosine monophosphate (cGMP)] were used to estimate neural changes after transient bilateral carotid artery ligation followed by reperfusion in adult Mongolian gerbils (Meriones unguiculatus). Results show for the first time that melatonin prevents the increases in NO and cGMP production after transient ischemia/reperfusion in frontal cerebral cortex and cerebellum of Mongolian gerbils. The inhibitory effect of melatonin on NO production and its ability to scavenge free radicals and the peroxynitrite anion may be responsible for the protective effect of melatonin on neuronal structures during transient ischemia followed by reperfusion.
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PMID:Melatonin prevents increases in neural nitric oxide and cyclic GMP production after transient brain ischemia and reperfusion in the Mongolian gerbil (Meriones unguiculatus). 937 43

The time-course effects of transient cerebral ischemia on nitric oxide (NO) formation in the rat hippocampus were evaluated by the consecutive determination of oxidative NO metabolites (NO2- and NO3-), using brain microdialysis under the freely moving condition. Bilateral carotid artery occlusion (CAO; 2-vessel occlusion, 2VO; 10 and 20 min) and combined vertebral artery occlusion (4VO; 10 min) produced a transient increase in hippocampal NO2- and NO3- levels, according to the duration and degree of ischemic insults. In addition, 4VO produced a gradual increase in hippocampal NO2- and NO3- levels over a 24 h period after reperfusion, which was abolished by an inducible NO synthase inhibitor, aminoguanidine (10 mg/kg, intraperitoneally). These findings suggest that the dynamic changes in oxidative NO metabolite levels reflect NO production following transient cerebral ischemia, which is possibly mediated in part by an inducible NO synthase, in the rat hippocampus.
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PMID:Consecutive evaluation of nitric oxide production after transient cerebral ischemia in the rat hippocampus using in vivo brain microdialysis. 948 73

A specific and simple method for the direct simultaneous detection of extracellular nitrite (NO2-) and nitrate (NO3-) has been developed, using high-performance liquid chromatography separation with UV and electrochemical detection in series. These stable endproducts of nitric oxide (NO.) were determined in dialysis perfusate obtained through in vivo brain microdialysis during and after experimental photoinduced cerebral ischemia in rats. The chromatographic conditions were optimized with a reversed-phase column (250 x 46 mm) using 10 mM n-octylamine pH 6.0 as a mobile phase. Absorbance was measured at 220 nm for NO3- detection; electrochemical detection was performed at +0.7 V for NO2- evaluation. This assay system holds the advantages of in vivo consecutive measurements, high precision, good reproducibility, technical simplicity, fast response (about 7 min), and wide availability.
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PMID:Nitrite/nitrate balance during photoinduced cerebral ischemia in the rat determined by high-performance liquid chromatography with UV and electrochemical detection. 954 31

Long-term potentiation (LTP) has been widely studied as a form of synaptic plasticity that represents a cellular mechanism of learning and memory. Among numerous processes and molecules that may be involved in LTP formation, a great many of them including neurotrophic and transcription factors have been described as those involved in neural death after ischemic insult. Nitric oxide (NO) is a molecule that is known to also exert double-edged effects on LTP formation. Here we will be describing recent advances with respect to the LTP mechanisms in the hippocampal synapses, a critical brain region for learning and memory function. In another context, we described our study elucidating the changes in hippocampal LTP as a functional response to transient cerebral ischemic insult, from the viewpoint of its relevance to NO production. As indices of NO production, nitrite and nitrate levels were determined by in vivo microdialysis. It was demonstrated that hippocampal LTP deficiency after transient cerebral ischemia was preceded by an increase in hippocampal NO production. Direct or indirect inhibition of an inducible NO synthase restored ischemia-induced LTP deficiency. These findings suggest that NO production, in part via inducible NO synthase, is responsible for LTP deficiency after transient cerebral ischemia in the rat hippocampus.
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PMID:[Transient cerebral ischemia and long-term potentiation in the rat hippocampus]. 955 73


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