IMMERSION AND PERFUSION STAINING WITH 2,3,5-TRIPHENYLTETRAZOLIUM CHLORIDE (TTC) COMPARED TO MITOCHONDRIAL-ENZYMES 6 HOURS AFTER MCA-OCCLUSION IN PRIMATES

Citation
C. Dettmers et al., IMMERSION AND PERFUSION STAINING WITH 2,3,5-TRIPHENYLTETRAZOLIUM CHLORIDE (TTC) COMPARED TO MITOCHONDRIAL-ENZYMES 6 HOURS AFTER MCA-OCCLUSION IN PRIMATES, Neurological research, 16(3), 1994, pp. 205-208
Citations number
20
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
01616412
Volume
16
Issue
3
Year of publication
1994
Pages
205 - 208
Database
ISI
SICI code
0161-6412(1994)16:3<205:IAPSW2>2.0.ZU;2-M
Abstract
2,3,5-triphenyltetrazolium chloride (TTC) is commonly applied in roden ts and cats as a marker of infarcted tissue as early as 20 min after t he onset of focal ischaemia. At this stage it is suggested that it ref lects hypoperfusion rather than failure of respiratory chain. Immersio n of brain slices in TTC solution is preferable in comparison to perfu sion with TTC in order to ensure, that enough TTC enters the post-occl usion tissue. We compared immersion technique versus perfusion techniq ue 6 h after permanent occlusion of the left middle cerebral artery in 18 baboons. In addition, we assessed the function of the respiratory chain enzymes of stained and unstained tissue in three baboons. The im mersion technique revealed an absence of TTC staining limited to subco rtical structures in two animals. In seven experiments TTC indicated i nvolvement of almost the entire MCA territory. The extent of the ischa emic lesion indicated by the perfusion technique was very similar. Tis sue samples from the presumed infarcted areas revealed normal mitochon drial function. We conclude that perfusion and immersion technique do not cause significant different ischaemic delineation 6 h after middle cerebral artery occlusion. TTC staining appears to be a reliable meth od of evaluating volume of infarction in primates. Furthermore, absenc e of TTC staining 6 h after stroke onset is caused by energy or oxygen depletion rather than by mitochondrial injury.