| Caspase-dependent cell death involved in brain damage after acute subdural hematoma in rats. | |
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MedLine Citation:
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PMID: 16890922 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Traumatic brain injury is associated with acute subdural hematoma (ASDH) that worsens outcome. Although early removal of blood can reduce mortality, patients still die or remain disabled after surgery and additional treatments are needed. The blood mass and extravasated blood induce pathomechanisms such as high intracranial pressure (ICP), ischemia, apoptosis and inflammation which lead to acute as well as delayed cell death. Only little is known about the basis of delayed cell death in this type of injury. Thus, the purpose of the study was to investigate to which extent caspase-dependent intracellular processes are involved in the lesion development after ASDH in rats. A volume of 300microL blood was infused into the subdural space under monitoring of ICP and tissue oxygen concentration. To asses delayed cell death mechanisms, DNA fragmentation was measured 1, 2, 4 and 7 days after ASDH by TUNEL staining, and the effect of the pan-caspase inhibitor zVADfmk on lesion volume was assessed 7 days post-ASDH. A peak of TUNEL-positive cells was found in the injured cortex at day 2 after blood infusion (53.4+/-11.6 cells/mm(2)). zVADfmk (160ng), applied by intracerebroventricular injection before ASDH, reduced lesion volume significantly by more than 50% (vehicle: 23.79+/-7.62mm(3); zVADfmk: 9.06+/-4.08). The data show for the first time that apoptotic processes are evident following ASDH and that caspase-dependent mechanisms play a crucial role in the lesion development caused by the blood effect on brain tissue. |
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Authors:
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B Alessandri; T Nishioka; A Heimann; R M Bullock; O Kempski |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2006-08-07 |
Journal Detail:
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Title: Brain research Volume: 1111 ISSN: 0006-8993 ISO Abbreviation: Brain Res. Publication Date: 2006 Sep |
Date Detail:
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Created Date: 2006-09-11 Completed Date: 2006-11-24 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0045503 Medline TA: Brain Res Country: Netherlands |
Other Details:
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Languages: eng Pagination: 196-202 Citation Subset: IM |
Affiliation:
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Institute for Neurosurgical Pathophysiology, University of Mainz, Langenbeckstrasse 1, D-55131 Mainz, Germany. beat.alessandri@uni-mainz.de |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Amino Acid Chloromethyl Ketones
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pharmacology,
therapeutic use Animals Apoptosis / drug effects, physiology* Blood / metabolism* Brain Infarction / drug therapy, enzymology*, etiology* Brain Injuries / complications, physiopathology Brain Ischemia / etiology, physiopathology Caspases / metabolism* Disease Models, Animal Enzyme Inhibitors / pharmacology, therapeutic use Hematoma, Subdural, Acute / complications*, physiopathology In Situ Nick-End Labeling Intracranial Hypertension / etiology, physiopathology Male Neuroprotective Agents / pharmacology, therapeutic use Rats Rats, Sprague-Dawley Signal Transduction / drug effects, physiology Treatment Outcome |
| Chemical | |
Reg. No./Substance:
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0/Amino Acid Chloromethyl Ketones; 0/Enzyme Inhibitors; 0/Neuroprotective Agents; 0/benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone; EC 3.4.22.-/Caspases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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