Document Detail


Caspase-dependent cell death involved in brain damage after acute subdural hematoma in rats.
MedLine Citation:
PMID:  16890922     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
B Alessandri; T Nishioka; A Heimann; R M Bullock; O Kempski
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2006-08-07
Journal Detail:
Title:  Brain research     Volume:  1111     ISSN:  0006-8993     ISO Abbreviation:  Brain Res.     Publication Date:  2006 Sep 
Date Detail:
Created Date:  2006-09-11     Completed Date:  2006-11-24     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0045503     Medline TA:  Brain Res     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  196-202     Citation Subset:  IM    
Affiliation:
Institute for Neurosurgical Pathophysiology, University of Mainz, Langenbeckstrasse 1, D-55131 Mainz, Germany. beat.alessandri@uni-mainz.de
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MeSH Terms
Descriptor/Qualifier:
Amino Acid Chloromethyl Ketones / 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:
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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