Consecutive evaluation of nitric oxide production after transient cerebral ischemia in the rat hippocampus using in vivo brain microdialysis

Togashi, Hiroko; Mori, Kiyoshi; Ueno, Kenichi; Matsumoto, Machiko; Suda, Noriyuki; Saito, Hideya; Yoshioka, Mitsuhiro

doi:10.1016/s0304-3940(97)00918-x

Cited by 80 publications

(32 citation statements)

References 14 publications

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“…This model is frequently used in exploring the mechanisms of delayed cell death and ischemic tolerance in the hippocampus, striatum, and cerebral cortex (3, 5, 6 layer), which are vulnerable to ischemia (21 -23). We previously demonstrated that selective cell death, impaired long-term potentiation (LTP) formation, and increasing NO production in the hippocampal CA1 region were observed in 4VO rats (24,25). Therefore, this model could be useful in the evaluation of the cerebroprotective effect on transient ischemia.…”

Section: Liposome-encapsulated Hemoglobin Ameliorates Impairment Of Fmentioning

confidence: 99%

Liposome-Encapsulated Hemoglobin Ameliorates Impairment of Fear Memory and Hippocampal Dysfunction After Cerebral Ischemia in Rats

et al. 2010

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Abstract. Liposome-encapsulated hemoglobin (LEH) has been developed as a blood substitute. In spite of its size (1/30 -1/40 of erythrocytes), LEH has an oxygen-carrying capacity comparable to erythrocytes. Thus, LEH is expected to carry oxygen into vital organs via collateral routes during ischemia induced by vascular embolism. In the present study, we examined the therapeutic effects of LEH on behavioral impairments in rats after four-vessel occlusion (4VO) for 30 min. In the open-field test, locomotor activity in 4VO rats did not alter 7 days after ischemia. However, in the contextual fear conditioning (CFC) test, the freezing rate was significantly decreased in 4VO rats, although no behavioral changes in the Y-maze test and elevated plus-maze test were observed. Phosphorylation of the cyclic AMP response element-binding protein (CREB) in the hippocampal CA1 region after the CFC test was attenuated. These 4VO-induced impairments were significantly alleviated by the administration of LEH (5 ml/kg, i.v.) during occlusion. Moreover, LEH did not alter hippocampal blood flow and tissue oxygen pressure during 4VO, but it did suppress hyperoxia after ischemia-reperfusion. These findings suggest that LEH, an artificial oxygen carrier, could be a novel therapeutic agent for brain dysfunction after acute cerebral ischemia.

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Section: Liposome-encapsulated Hemoglobin Ameliorates Impairment Of Fmentioning

confidence: 99%

Liposome-Encapsulated Hemoglobin Ameliorates Impairment of Fear Memory and Hippocampal Dysfunction After Cerebral Ischemia in Rats

et al. 2010

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“…After 2 h of stabilization, the dialysates from the striatum were collected at 10-min intervals. The NO concentrations in the dialysates were measured with the Eicom ENO-20 NO analysis system (Eicom, Kyoto) (19). After histological verification of the probe's path, all the data obtained were included in our results.…”

Section: Extracellular No Monitoringmentioning

confidence: 99%

Shengmai San, a Chinese Herbal Medicine Protects Against Rat Heat Stroke by Reducing Inflammatory Cytokines and Nitric Oxide Formation

Wang¹,

Chang²,

Liou³

et al. 2005

J Pharmacol Sci

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Abstract. The aim of the present study was to ascertain whether the possible occurrence of overproduction of inducible nitric oxide synthase (iNOS)-dependent nitric oxide (NO) in the brain and inflammatory cytokines in the peripheral blood exhibited during heat stroke can be reduced by prior administration of Shengmai San, a Chinese herbal medicine. Aminoguanidine, an iNOS inhibitor, was evaluated at the same time as a reference (positive control). Urethaneanesthetized rats were exposed to heat stress (ambient temperature of 43°C) to induce heat stroke. Control rats were exposed to 24°C. Mean arterial pressure and cerebral blood flow after the onset of heat stroke were all significantly lower than in control rats. However, cerebral iNOS immunoreactivity and NO levels were all greater after the onset of heat stroke. The serum levels of interleukin-1β, interleukin-6, and tumor necrosis factor-α were all increased after the onset of heat stroke. Shengmai San (1.2 g / ml per rat) or aminoguanidine (30 µmol / ml per rat) was administered orally, daily, and consecutively for 7 days before the initiation of heat stress; and this significantly attenuated the heat stress-induced arterial hypotension, cerebral ischemia, and increased levels of brain iNOS-dependent NO production and serum cytokines formation. Shengmai San shared with the aminoguanidine almost the same efficacy in reducing iNOSdependent NO and cytokines overproduction during heat stroke. These results suggest that Shengmai San or aminoguanidine protects against heat stroke-induced arterial hypotension and cerebral ischemia by inhibition of iNOS-dependent NO overproduction in the brain and excessive accumulation of several inflammatory cytokines in the peripheral blood stream.

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“…After 6 h of stabilization, the dialysates from the hypothalamus were collected at 20-min intervals. The NO x -concentrations in the dialysates were measured with the Eicom ENO-20 NO x -analysis system (Eicom, Kyoto) (14). In the Eicom ENO-20 NO x -analysis system, after the NO 2 -and NO 3 -in the sample have been separated by the column, the NO 2 -reacts in the acidic solution with the primary aromatic amine to produce an azo compound.…”

Section: Extracellular No Monitoringmentioning

confidence: 99%

Aminoguanidine Protects Against Intracranial Hypertension and Cerebral Ischemic Injury in Experimental Heatstroke

et al. 2004

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Abstract. The aim of the present study was to ascertain whether aminoguanidine attenuated intracranial hypertension and cerebral ischemic injury in experimental heatstroke. Urethaneanesthetized rats were exposed to heat stress (ambient temperature of 43°C) to induce heatstroke. Control rats were exposed to 24°C. Mean arterial pressure, cerebral perfusion pressure, and cerebral blood flow after the onset of heatstroke were all significantly lower than in control rats. However, colonic temperature, intracranial pressure, heart rate, cerebral inducible nitric oxide synthase (iNOS)-dependent NO, and neuronal damage score were greater after the onset of heatstroke. Aminoguanidine (30 mmol / kg, i.v.; 30 min before the start of heat exposure) pretreatment significantly attenuated the heatstroke-induced hyperthermia, arterial hypotension, intracranial hypertension, cerebral ischemia and neuronal damage, and increased iNOS-dependent NO formation in the brain. The extracellular concentrations of ischemic (e.g., glutamate and lactate / pyruvate ratio) and damage (e.g., glycerol) markers in the hypothalamus were also increased after the onset of heatstroke. Aminoguanidine pretreatment significantly attenuated the increase in hypothalamic ischemia and damage markers associated with heatstroke. Delaying onset of aminoguanidine administration (i.e., 0 or 30 min after the start of heat exposure) reduced the preventive efficiency on heatstroke-induced hyperthermia, arterial hypotension, intracranial hypertension, cerebral ischemia, and increased iNOS-dependent NO formation in brain. These results suggest that aminoguanidine protects against heatstroke-induced intracranial hypertension and cerebral ischemic injury by inhibition of cerebral iNOS-dependent NO production.

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Consecutive evaluation of nitric oxide production after transient cerebral ischemia in the rat hippocampus using in vivo brain microdialysis

Cited by 80 publications

References 14 publications

Liposome-Encapsulated Hemoglobin Ameliorates Impairment of Fear Memory and Hippocampal Dysfunction After Cerebral Ischemia in Rats

Liposome-Encapsulated Hemoglobin Ameliorates Impairment of Fear Memory and Hippocampal Dysfunction After Cerebral Ischemia in Rats

Shengmai San, a Chinese Herbal Medicine Protects Against Rat Heat Stroke by Reducing Inflammatory Cytokines and Nitric Oxide Formation

Aminoguanidine Protects Against Intracranial Hypertension and Cerebral Ischemic Injury in Experimental Heatstroke

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