Effect of unilateral common carotid artery occlusion on levels of prostaglandins D2, F2 alpha and 6-keto-prostaglandin F1 alpha in gerbil brain.

Gaudet, Robert; Levine, Lawrence

doi:10.1161/01.str.11.6.648

“…Since Furlow et al (11) have initially shown that AA can produce cerebral ischemia, several AA metabolites have been implicated to be important factors in the de velopment of cerebral ischemia or infarction (2,10,19,20). AA-induced cerebral infarction is concomitant with the attenuation of EEG amplitude in the rat (20).…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of KW-3635, a Thromboxane A2 Antagonist, on Arachidonic Acid-Induced Transient Cerebral Ischemia in Dogs.

Satoh

¹

,

Kobayashi

²

,

Higo

³

et al. 1994

Jpn.J.Pharmacol

4

0

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ABSTRACT-We investigated the effect of KW-3635, a selective thromboxane (TX) A2-receptor antagonist, on the arachidonic acid (AA)-induced transient cerebral ischemia in anesthetized dogs. Intracarotid-arterial injection of AA (0.25-1 mg/kg) produced a transient and reversible decrease in electroencephalographic (EEG) activity. The reduction of EEG power was inhibited by the intravenous injection of KW-3635 or aspirin, a cyclooxygenase inhibitor. Local cortical perfusion (LCP) measured by a laser-doppler flow meter was also reduced concomitantly with the reduction of EEG power. Although KW-3635 at 1 and 3 mg/kg (i.v.) did not affect the maximum reduction of LCP, the duration of the reduction period of LCP was significantly shortened by KW-3635. On the other hand, aspirin at 1 and 3 mg/kg (i.v.) inhibited both the maximum and the delay of LCP reduction. The intravenous administration of KW-3635 or aspirin caused dose-dependent inhibition of ex vivo platelet aggregation stimulated by AA (150 pM) at the doses that im prove the EEG activity. These data suggest that TXA2 is one of the important factors in the AA-induced transient reduction of EEG activity in anesthetized dogs. The TXA2-receptor antagonist may be useful for protection against the ischemic brain damage following transient ischemic attack.

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“…In kindling from amygdala and many other regions, morphology and molecular biological alteration were found mainly in hippocampus. This included neuron loss 1 -3 -8 " 11 , mossy fiber sprouting 8 ' 10 , modification of neurotransmitter receptors 13 ' 16 , and induction of gene expression 17 " 21 , suggesting that hippocampus plays a very important role in kindling. Also hippocampus sclerosis is the main pathological founding in human MLTE.…”

Section: The Rapid Hippocampal Kindling Model Of Traumatic Head Injurymentioning

confidence: 99%

Neural Responses to Injury--Prevention, Protection, and Repair: Neurochemical Protection of the Brain, Neural Plasticity and Repair

Bazán¹

1998

PsycEXTRA Dataset

0

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Public reporting burden for this collection of information is estimated to average 1 hour per response, including tha time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing the collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden, to Washington Headquarters Services, Directorate for Information Operations and Reports, 1215 Jefferson Davis Highway, Suite 1204, Arlington, VA 22202-4302, and to the Office of Management and Budget, Paperwork Reduction Project (07040188), Washington, DC 20503. AGENCY USE ONLY (Leave blank}2. REPORT DATE October 1998 REPORT TYPE AND DATES COVERED Final (20 Sep 93-19 Sep 98) TITLE AND SUBTITLENeural Responses to Injury: Prevention, Protection, and FUNDING NUMBERS DAMD17-93-V-3013 PERFORMING ORGANIZATION NAME(S) AND ADDRESS(ES)Louisiana FOREWORDOpinions, interpretations, conclusions and recommendations are those of the authors and are not necessarily endorsed by the U.S. Army.( ) Where copyrighted material is quoted, permission has been obtained to use such material.( ) Where material from documents designated for limited distribution is quoted, permission has been obtained to use the material.( ) Citations of commercial organizations and trade names in this report do not constitute an official Department of Army endorsement or approval of the products or services of these organizations.(v/) In conducting research using animals, the investigator(s) adhered to the "Guide for the Care and Use of Laboratory Animals," prepared by the Committee on Care and use of Laboratory Animals of the Institute of Laboratory Resources, National Research Council (NIH Publication No. 86-23, Revised 1985).(S) For the protection of human subjects, the investigator(s) adhered to policies of applicable Federal Law 45 CFR 46.( ) In conducting research utilizing recombinant DNA technology, the investigator(s) adhered to current guidelines promulgated by the National Institutes of Health.( ) In the conduct of research utilizing recombinant DNA, the investigator(s) adhered to the NIH guidelines for Research Involving Recombinant DNA Molecules.( ) In the conduct of research involving hazardous organisms, the investigator(s) adhered to the CDC-NIH Guide for Biosafety in Microbiological and Biomedical Laboratories.Investigator Signature ANIMAL USE SEPTEMBER 20,1997 THROUGH SEPTEMBER 19,1998 DAMD17-93-V-3013The experimental animals used during this period for the project, Neural Responses to Injury: Prevention, Protection, and Repair, Subproject: Neurochemical Protection of the Brain, Neural Plasticity and Repair, are as follows: SpeciesNumber Allowed Number Used LSUIACUC# The development of chronic epilepsy is a very serious complication of head injury, neurodegenerative diseases, brain tumors, and exposure to neurotoxic agents. Head injury is often associated with loss of short-term memory, indicating trauma to t...

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“…In kindling from amygdala and many other regions, morphology and molecular biological alteration were found mainly in hippocampus. This included neuron loss 1 -3 -8 " 11 , mossy fiber sprouting 8 ' 10 , modification of neurotransmitter receptors 13 ' 16 , and induction of gene expression 17 " 21 , suggesting that hippocampus plays a very important role in kindling. Also hippocampus sclerosis is the main pathological founding in human MLTE.…”

Section: The Rapid Hippocampal Kindling Model Of Traumatic Head Injurymentioning

confidence: 99%

“…It has been clearly established that kindling can induce neuron loss and mossy fiber sprouting 1 ' 3 ' 8 " 11 , but it is still controversial whether kindling epileptogenesis requires neuron loss ' ' ' or mossy fiber sprouting ' ' . It is well known that gene expression is required in neuronal apoptosis and neurite growth, so is almost certain that regulation of gene expression is involved in kindling-induced neuronal death and neurite reorganization.…”

Section: The Requirement Of Gene Expression Regulation In Kindlingmentioning

confidence: 99%

Neural Responses to Injury: Prevention, Protection, and Repair. Neurochemical Protection of the Brain, Neural Plasticity and Repair

Bazán¹

1998

0

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Public reporting burden for this collection of information is estimated to average 1 hour per response, including tha time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing the collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden, to Washington Headquarters Services, Directorate for Information Operations and Reports, 1215 Jefferson Davis Highway, Suite 1204, Arlington, VA 22202-4302, and to the Office of Management and Budget, Paperwork Reduction Project (07040188), Washington, DC 20503. AGENCY USE ONLY (Leave blank}2. REPORT DATE October 1998 REPORT TYPE AND DATES COVERED Final (20 Sep 93-19 Sep 98) TITLE AND SUBTITLENeural Responses to Injury: Prevention, Protection, and FUNDING NUMBERS DAMD17-93-V-3013 PERFORMING ORGANIZATION NAME(S) AND ADDRESS(ES)Louisiana FOREWORDOpinions, interpretations, conclusions and recommendations are those of the authors and are not necessarily endorsed by the U.S. Army.( ) Where copyrighted material is quoted, permission has been obtained to use such material.( ) Where material from documents designated for limited distribution is quoted, permission has been obtained to use the material.( ) Citations of commercial organizations and trade names in this report do not constitute an official Department of Army endorsement or approval of the products or services of these organizations.(v/) In conducting research using animals, the investigator(s) adhered to the "Guide for the Care and Use of Laboratory Animals," prepared by the Committee on Care and use of Laboratory Animals of the Institute of Laboratory Resources, National Research Council (NIH Publication No. 86-23, Revised 1985).(S) For the protection of human subjects, the investigator(s) adhered to policies of applicable Federal Law 45 CFR 46.( ) In conducting research utilizing recombinant DNA technology, the investigator(s) adhered to current guidelines promulgated by the National Institutes of Health.( ) In the conduct of research utilizing recombinant DNA, the investigator(s) adhered to the NIH guidelines for Research Involving Recombinant DNA Molecules.( ) In the conduct of research involving hazardous organisms, the investigator(s) adhered to the CDC-NIH Guide for Biosafety in Microbiological and Biomedical Laboratories.Investigator Signature ANIMAL USE SEPTEMBER 20,1997 THROUGH SEPTEMBER 19,1998 DAMD17-93-V-3013The experimental animals used during this period for the project, Neural Responses to Injury: Prevention, Protection, and Repair, Subproject: Neurochemical Protection of the Brain, Neural Plasticity and Repair, are as follows: SpeciesNumber Allowed Number Used LSUIACUC# The development of chronic epilepsy is a very serious complication of head injury, neurodegenerative diseases, brain tumors, and exposure to neurotoxic agents. Head injury is often associated with loss of short-term memory, indicating trauma to t...

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Effect of unilateral common carotid artery occlusion on levels of prostaglandins D2, F2 alpha and 6-keto-prostaglandin F1 alpha in gerbil brain.

Cited by 55 publications

References 35 publications

Protective Effects of KW-3635, a Thromboxane A2 Antagonist, on Arachidonic Acid-Induced Transient Cerebral Ischemia in Dogs.

Protective Effects of KW-3635, a Thromboxane A2 Antagonist, on Arachidonic Acid-Induced Transient Cerebral Ischemia in Dogs.

Neural Responses to Injury--Prevention, Protection, and Repair: Neurochemical Protection of the Brain, Neural Plasticity and Repair

Neural Responses to Injury: Prevention, Protection, and Repair. Neurochemical Protection of the Brain, Neural Plasticity and Repair

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