Forebrain ischemia induced by temporary bilateral common carotid occlusion in normotensive rats

Iwasaki, Yuzo; Ito, Seikow; Suzuki, Michiyasu; Nagahori, Takeshi; Yamamoto, Toshiyuki; Konno, Hidehiko

doi:10.1016/0022-510x(89)90098-1

Cited by 82 publications

(45 citation statements)

References 16 publications

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“…Since the original work by Pulsinelli et al [8], reports have been published on delayed neuronal death in the cerebral cortex following transient ischemia of the brain, using transient occlusion of the bilateral common carotid arteries alone or by additional permanent closure of the bilateral vertebral arteries [16,17]. The decrease in cortical CBF during transient ischemia produced by such transient occlusion of the bilateral arteries has been measured by Pulsinelli et al [18], Suzuki et al [19], and Kuroiwa et al [20], and in these studies CBF was reduced to 3-12% of the resting control flow.…”

Section: Discussionmentioning

confidence: 99%

Effects of Stimulating the Nucleus Basalis of Meynert on Blood Flow and Delayed Neuronal Death Following Transient Ischemia in the Rat Cerebral Cortex.

Hotta

Uchida²,

Kagitani³

2002

JJP

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In Alzheimer's disease accompanying dementia, the degeneration of cells in the basal forebrain is quite striking [1,2]. Cholinergic neurons originating in the nucleus basalis of Meynert (NBM) and in the septal complex of the basal forebrain project to the cerebral cortex and hippocampus. Therefore there is a possible link between the cholinergic system and the cognitive mechanism. It was recently demonstrated that the cholinergic system had vasodilative action in the cerebral cortex and hippocampus (see reviews by Sato and Sato [3,4]). These vasodilative responses are independent of both systemic blood pressure and regional cerebral metabolism. The physiological relevance of these responses, however, has not been completely understood. Neurons in the cerebral cortex and hippocampus are degenerative in Alzheimer's disease [5,6], and they are also quite vulnerable to ischemia. The late death of neurons following transient ischemia, Japanese Journal of Physiology, 52, 383-393, 2002 Key words: cerebral cortex, transient ischemia, regional cerebral blood flow, delayed neuronal death, nucleus basalis of Meynert.Abstract: An increase in cortical cerebral blood flow (CBF), independent of metabolic vasodilation, via the activation of cholinergic neurons originating in the nucleus basalis of Meynert (NBM) in the basal forebrain and projecting to the widespread cortices was recently demonstrated. In the present study, we aimed to clarify whether the increase in CBF following a stimulation of the NBM can improve delayed death of the cortical neurons following transient ischemia in rats. CBF was measured with a laser Doppler flowmeter, and the delayed neuronal death of the cerebral cortex produced by intermittent (every 5 s) occlusions of the unilateral common carotid artery for 60 min was measured histologically in the cortical hemisphere at 3 different coronal levels (6 m thickness). In control rats without occlusion there were 6,000-8,000 intact neurons and 9-19 damaged neurons in the cortical hemisphere at each coronal level. During the occlusions, CBF ipsilateral to the occluded artery decreased by 13-32% of the preocclusion level. Five days after the occlusions, the numbers of damaged neurons were increased to 75-181. Repetitive electrical stimulation was delivered to the NBM, ipsilateral to the occluded artery, starting 5 min before the occlusions and finishing around the end of them. The increase in CBF induced by NBM stimulation prevented the occlusion-induced decrease in CBF in all 3 of the cortices. The delayed death of the cortical neurons previously observed after the occlusions was scarcely observable in all the cortices when NBM was stimulated. The present results suggest that NBM-originating vasodilative activation can protect the ischemia-induced delayed death of cortical neurons by preventing a blood flow decrease in widespread cortices.

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Section: Discussionmentioning

confidence: 99%

Effects of Stimulating the Nucleus Basalis of Meynert on Blood Flow and Delayed Neuronal Death Following Transient Ischemia in the Rat Cerebral Cortex.

Hotta

Uchida²,

Kagitani³

2002

JJP

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“…Fixation was then achieved with formaldehyde 10% solution with 0.1 M phosphate buffer. Brains were removed as a whole by wide craniectomy and were placed in formaldehyde 10% solution with 0.1 M phosphate buffer as previously described (Iwasaki et al, 1989;Ozdemir et al, 2013).…”

Section: Induction Of Transient Focal Cerebral Ischemiamentioning

confidence: 99%

Neuroprotective effect of ziprasidone: Preliminary results compared to haloperidol

Çınar¹,

Karaoğlan²,

Mıdı³

et al. 2014

jecm

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Article HistoryReceived 21 / 02 / 2014 Accepted 10 / 05 / 2014Typical and atypical antipsychotic drugs are widely used to treat psychosis. The present study investigated whether ziprasidone, an atypical antipsychotic drug, has a neuroprotective effect on hippocampal neurons in rats with experimentallyinduced transient cerebral ischemia comparatively with haloperidol which is a typical antipsychotic. Transient cerebral ischemia was induced by 10-minute occlusion of bilateral carotis communis arteries. The rats were divided into four groups: Shamoperated control group (Group I), ischemia control group (Group II), haloperidol-treated group (Group III) and ziprasidone-treated group (Group IV). Following 10-minute ischemia, Group III received 1mg/kg haloperidol intramuscularly and Group IV received 2.5 mg/kg ziprasidone intraperitoneally. The animals were sacrificed on the seventh day following induced ischemia to determine the number of intact neurons at hippocampus and dentate gyrus to demonstrate the effects of ischemia and efficacy of the treatments administered. Surviving cell numbers were found in the sham operated group; 198, in the ischemia control group; 80, in the haloperidol-treated group; 185, in ziprasidonetreated group; 189. The groups showed significant difference in the comparison of the surviving cell numbers. However, the number of surviving cells did not significantly different between the ziprasidone and haloperidol-treated group. Previous studies with the ischemia model have demonstrated protective effects of haloperidol on hippocampal region. The findings of the present study show that ziprasidone, which is an atypical antipsychotic drug, may produce neuroprotective effects as potent as haloperidol, which is a typical antipsychotic drug.

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“…In four of 72 rats subjected to two 15-min occlusions with a 15-min interval, the femoral artery was catheterized to monitor the blood pressure and arterial gases as described previously (Iwasaki et al 1989). The rats were allowed free access to food and water before and after surgery.…”

Section: Induction Of Ischemiamentioning

confidence: 99%

“…Six coronal slices were prepared from each brain and embedded in paraffin. Hematoxylin-eosin staining or immunostaining for autologous albumin were performed as described previously (Iwasaki et al 1989). …”

Section: Histological Examinationmentioning

confidence: 99%

“…Although occlusion of the unilateral carotid artery little disturbs the cerebral blood flow and metabolism in the rat (Garcia 1984), permanent ligation of the bilateral common carotid artery has been shown to induce severe ischemic damage in the rat brain (Payan et al 1965;Ogata et al 1976). Moreover, we recently found that temporary occlusion of the bilateral common carotid artery could also induce a variety of ischemic lesions in the rat brain (Iwasaki et al 1989).With this simple method, we compared the brain damage induced by repeti- …”

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confidence: 99%

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Ischemic Brain Damage Induced by Repeated Brief Occlusions of Bilateral Common Carotid Artery in Rats.

Nagahori

Nishijima

Endo

et al. 1994

Tohoku J. Exp. Med.

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School of Medicine, Sendai 980 NAGAHORI, T., NISHIJIMA, M., ENDO, S., TAKAKU, A. and IWASAKI, Y. Ischemic Brain Damage Induced by Repeated Brief Occlusions of Bilateral Common Carotid Artery in Rats. Tohoku J. Exp. Med., 1994, 172 (3), 253-262 Two temporary occlusions of the bilateral common carotid artery for 15 min with an interval of 15 min induced severe brain tissue damage in normotensive Wistar rats. Although no lesions were seen after a single 15-min occlusion, severe ischemic lesions were found in 68% (49/72) of the rats subjected to two consecutive occlusions for 15 min with an interval of 15 min, and the incidence was significantly higher than that in the rats subjected to a single 30-min occlusion (32%, 6/19) or two 15-min occlusions with an interval of 30 min (11%,1/9). The local cerebral blood flow (1CBF) in the caudoputamen, however, was decreased by only 40-60% of pre-occlusion level during occlusions. These results suggest that intermittent incomplete disruption of CBF with short intervals could be more hazardous than a continuous interruption of the same duration. brain ischemic; cerebral blood flow; free fatty acids Various complex methods have been advanced to induce experimental ischemia in the rat brain which is rich in collateral circulations (Pulsinelli and Brierley 1979;Laas et al. 1983;Mendelow et al. 1984;Kameyama et al. 1985;Chen et al. 1986). Although occlusion of the unilateral carotid artery little disturbs the cerebral blood flow and metabolism in the rat (Garcia 1984), permanent ligation of the bilateral common carotid artery has been shown to induce severe ischemic damage in the rat brain (Payan et al. 1965;Ogata et al. 1976). Moreover, we recently found that temporary occlusion of the bilateral common carotid artery could also induce a variety of ischemic lesions in the rat brain (Iwasaki et al. 1989).With this simple method, we compared the brain damage induced by repeti-

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Forebrain ischemia induced by temporary bilateral common carotid occlusion in normotensive rats

Cited by 82 publications

References 16 publications

Effects of Stimulating the Nucleus Basalis of Meynert on Blood Flow and Delayed Neuronal Death Following Transient Ischemia in the Rat Cerebral Cortex.

Effects of Stimulating the Nucleus Basalis of Meynert on Blood Flow and Delayed Neuronal Death Following Transient Ischemia in the Rat Cerebral Cortex.

Neuroprotective effect of ziprasidone: Preliminary results compared to haloperidol

Ischemic Brain Damage Induced by Repeated Brief Occlusions of Bilateral Common Carotid Artery in Rats.

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