Immunohistochemical Investigation of Cerebral Ischemia in Gerbils

Yanagihara, Takehiko; Yoshimine, Toshiki; Morimoto, Kazuyoshi; Yamamoto, Kazumi; Homburger, Henry A.

doi:10.1097/00005072-198503000-00009

Cited by 102 publications

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“…This appears to correspond to the columnar pattern of increased tissue nicotinamide adenine dinucleotide (reduced form) fluorescence in incomplete cerebral ischemia 23 and was probably caused by residual blood flow in the small arteries descending perpendicularly from the leptomeninges after carotid occlusion. 1 In the thalamus, local CBF declined gradually. A steep CBF gradient was also present in the thalamus between the midline structure (anatomic sites 26 and 27) and the adjacent region (anatomic site 25) after 15 minutes of ischemia and may explain the development of immunohistochemical lesions in the paramedian structure (anatomic site 25) after 30 minutes of ischemia.…”

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confidence: 99%

“…While CBF measurement, particularly by quantitative autoradiography, has served well in demonstrating residual blood flow in ischemic brains, its contribution in elucidating the pathophysiologic mechanism of selective tissue vulnerability during progressive cerebral ischemia is relatively limited, partly because of the lack of a sensitive morphologic method for detecting early ischemic damage. Recently, we observed immunohistochemistry to be very sensitive in detecting ischemic damage after cervical or intracranial arterial occlusion in gerbils, 1 - 5 and we have developed a method to evaluate the correlation between degree of ischemia and evolution of ischemic damage by combining quantitative autoradiography and immunohistochemical techniques. 6 We report our observations on cerebral ischemia after unilateral common carotid artery (CCA) occlusion for 5-30 minutes in gerbils arterial blood from the tail artery for blood gas analysis, 30 /tCi of 4-iodo[7V-methyl- 14 C]antipyrine (Amersham, Arlington Heights, 111.)…”

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Cerebral blood flow and neuronal damage during progressive cerebral ischemia in gerbils.

Matsumoto

Hatakeyama

Morimoto

et al. 1990

Stroke

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A combined autoradiographic and immunohistochemical method was used to correlate the extent of focal cerebral ischemia and morphologic ischemic damage following unilateral carotid occlusion in 16 gerbils for 5-30 minutes. Immunohistochemical lesions detectable by the reaction for microtubule-associated proteins 1 and 2 were visible in the subiculum-CAl and CA2 regions of the hippocampus and layer III/TV of the cerebral cortex after 5 minutes of ischemia (n=4). Local blood flow was promptly reduced but still heterogeneous after 10 minutes of ischemia (n=4); local blood flow in immunohistochemical lesions was <5 ml/100 g/min except in highly vulnerable regions, where flow values of 5-15 ml/100 g/min were observed. After 15 minutes of ischemia (n=4) local blood flow in less vulnerable regions including the thalamus and caudoputamen also declined to <5 ml/100 g/min, and immunohistochemical lesions became visible in those regions after 30 minutes of ischemia (n=4). On the other hand, many brain regions tolerated local blood flow of <5 ml/100 g/min without ischemic damage. The present study demonstrates that selective tissue vulnerability during progressive cerebral ischemia depends on the degree of hypoperfusion and on factors inherent to neurons in various brain regions.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Cerebral blood flow and neuronal damage during progressive cerebral ischemia in gerbils.

Matsumoto

Hatakeyama

Morimoto

et al. 1990

Stroke

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“…Disappearance of the immunohistochemical reac tion for tubulin in ischemic brain tissue following unilateral carotid occlusion in gerbils has been re ported by Yanagihara et al (1985). It is unclear from their study whether the observed loss of im munostaining reflected actual leakage of tubulin or microtubules from ischemic neural tissue, a change in antigenicity, or a loss of disassembled tubulin subunits during tissue processing.…”

Section: Discussionmentioning

confidence: 99%

Protein Synthesis in Postischemic Rat Brain: A Two-Dimensional Electrophoretic Analysis

Kiessling

Dienel

Jacewicz

et al. 1986

J Cereb Blood Flow Metab

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Summary: This study examined the pattern of protein synthesis in the neocortex, caudate-putamen, and the hippocampus following transient forebrain ischemia in rats, The animal model of temporary ischemia used in this study causes permanent damage to vulnerable neu rons with a time course of injury that varies fr om hours (caudate nucleus) to days (hippocampus), To examine the spectrum of proteins synthesized in these regions at 3 and 18 h after recirculation, cerebral proteins were pulse-la beled in vivo by an intravenous injection of [ 3 sSJmethio nine. Newly synthesized (3sS-labeled) and constitutive (unlabeled) proteins were analyzed by two-dimensional gel electrophoresis and fluorography, In all three brain regions, specific proteins underwent preferential syn thesis (Mr �27,000, �65,000, �70,000, � I 10,000), while others showed decreased synthesis (neuron-specific eno lase, 0.-and l3-tubulin). There was an early (3 h post isch emia) induction of the Mr � 70,000 mammalian "stress"Tr ansient cerebral ischemia is associated with prolonged severe inhibition of brain protein syn thesis. Gradual recovery occurs long after energy metabolites have been restored and other metabolic processes normalized (Kleihues et aI. , 1975; Cooper et aI., 1977; Dienel et aI., 1980; Nowak et aI., 1985). Although the prolonged impairment of amino acid incorporation does not seem to reduce the total amount of brain protein or the activities of enzymes with low turnover rates, postischemic re- Schlesinger et al. (1982)]. In the present study newly synthesized ( 3 sS-labeled) proteins including stress proteins and constitutive (unlabeled) brain proteins were analyzed by two-dimensional gel electrophoresis and fluorography following the in vivo administration of [ 3 SS]methionine in control and postischemic animals. During transient ischemia (30 min) produced by occlusion of the four major arteries supplying the brain, all forebrain regions are severely ischemic but subsequently differ in the extent and rate of progression of neuronal cell death (Pulsinelli et aI., POSTlSCHEMIC PROTEIN SYNTHESIS IN RAT BRAIN 6431982a,b). Following restoration of cerebral blood flow, ischemic cell death progresses for several hours (in the caudate-putamen) to days (in the hip pocampus and neocortex). The majority of CAl py ramidal neurons and striatal small-to medium-sized neurons die, whereas injury to CA 3 pyramidal or neocortical neurons is relatively mild or absent. This phenomenon of selective and "delayed neu ronal cell death" (Kirino, 1982; Pulsinelli et aI. , 1982a) suggests that neurons remain viable throughout the ischemic period or even hours thereafter, but that certain sUbpopulations subse quently succumb owing to ischemia-induced meta bolic derangements of as-yet unidentified nature. The objective of this investigation was to assess whether regional differences in the spectrum of proteins synthesized by postischemic brain tissue exist and possibly predict the success or failure to recover from a potentially lethal insult. METHODS Ani...

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“…There have been some uncertainties of the descriptions of hippocampal subregions and cortical layers in our previous publications. 8 - 10 The most vulnerable hippocampal subregion appears to be just medial to the CA1 region, and we will use the term "subiculum-CAl region" in this article. Cortical layers III and IV are difficult to distinguish in immunohistochemical preparations, and we will use the term "layer HI/IV" to designate the most vulnerable layer in the cerebral cortex.…”

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Immunohistochemical investigation of ischemic and postischemic damage after bilateral carotid occlusion in gerbils.

Hatakeyama

Matsumoto

Brengman

et al. 1988

Stroke

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We investigated progression and recovery of neuronal damage during and after global cerebral ischemia in gerbils after bilateral occlusion of the common carotid arteries, using the immunohistochemical method (reaction for tubulin and creatine kinase BB-isoenzyme). The earliest, but reversible, ischemic lesions occurred after 3 minutes' ischemia in the subiculum-CA1 and CA2 regions of the hippocampus. The lesions became irreversible after 4 minutes' ischemia. The ischemic and postischemic lesions in the cerebral cortex, thalamus, and caudoputamen were partially or completely reversible if the ischemic period was 5 minutes, whereas delayed degeneration occurred in the pyramidal cells of the medial CAl region after reperfusion for 48 hours (delayed neuronal death). After 10 minutes' ischemia and subsequent reperfusion, delayed neuronal death extended from the medial to the lateral CAl region; the ischemic and postischemic lesions in the cerebral cortex, thalamus, and caudoputamen also expanded during reperfusion. Our investigation demonstrates that selective vulnerability existed in global cerebral ischemia as in incomplete or regional ischemia and suggests that neurons in many areas of the brain possessed the potential for recovery, progressive deterioration, and even delayed neuronal death depending on the severity and duration of cerebral ischemia. (Stroke 1988;19:1526-1534)

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Immunohistochemical Investigation of Cerebral Ischemia in Gerbils

Cited by 102 publications

References 0 publications

Cerebral blood flow and neuronal damage during progressive cerebral ischemia in gerbils.

Cerebral blood flow and neuronal damage during progressive cerebral ischemia in gerbils.

Protein Synthesis in Postischemic Rat Brain: A Two-Dimensional Electrophoretic Analysis

Immunohistochemical investigation of ischemic and postischemic damage after bilateral carotid occlusion in gerbils.

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