engleski

Brain damage secondary to hemorrhagic traumatic shock in baboons

In a baboon model of hemorrhagic-traumatic schock with full instrumentation and observation up to 72 hours, we have tested the hypothesis that lipid peroxidation with generation of reactive aldehydes such as 4-hydroxynonenal (HNE) might contribute to brain damage. We have performed an immunohistochemical analysis of the distribution of HNE in the brain. For the immuno-histochemical detection of HNE adducts, immuno-peroxidase technique was used on standard paraffin sections. Monoclonal antibodies from the clone "HNE Ig4" were used. The antibody is specific for the HNE-histidine epitope in HNE-protein (peptide) conjugates. On the coronar section of the brain, ventricular tissue was reduced in size due to the evident brain edema. On the horizontal section through the brain stem and cerebellum acute hemorrhagic infarction was noticed, but damaged tissue did not show HNE presence. On the other hand, soft membranes, as well as subarachnoidal and cerebral blood vessels, showed marked immunopositive reaction to HNE. Pioglial border as well as astrocytes and neurons around the blood vessels showed strong immunohistochemical reaction. From these studies we conclude that: 1. Oxidative stress and thus generated "second toxic messenger of free radicals", aldehyde 4-hydroxynonenal (HNE) may play a role in cascade of events determining the brain damage induced by hemorrhagic schock. 2. HNE present in the brain tissue seems to be of vascular origin and could play a role in function of the blood brain barrier and regulation of of the cerebral blood flow. 3. Due to that, HNE could be of relevance for determination of the outcome of the brain hemorrhagic-traumatic schock.

oxidative stress; HNE; brain; shock; hemorrhagic injury; baboons

nije evidentirano