Literature DB >> 1697139

A reversible component of cerebral injury as identified by the histochemical stain 2,3,5-triphenyltetrazolium chloride (TTC).

D J Cole1, J C Drummond, E A Ghazal, H M Shapiro.   

Abstract

The extent of histochemical change following middle cerebral artery occlusion was quantitatively determined in three groups of Sprague-Dawley rats with 2,3,5-triphenyltetrazolium chloride (a marker of mitochondrial oxidative enzyme function). In group I (n = 7) occlusion was maintained for 3 h, with immediate sacrifice. In group II (n = 7) occlusion was maintained for 5 h, with immediate sacrifice. In group III (n = 7) occlusion was maintained for 3 h, followed by a 2-h period of reperfusion prior to sacrifice. The area of injury was significantly larger (P less than 0.05) in the 5-h occlusion group [15 +/- 4% (mean +/- SD)] compared to the 3-h occlusion group (9 +/- 2%); indicating a time-dependent worsening of the histochemical detection of injury. However, the area of injury was significantly less in the reperfusion group (5 +/- 2%) compared to the group that was evaluated after 3 h of occlusion without reperfusion (9 +/- 2%); indicating that some component of the injury revealed by 2,3,5-triphenyltetrazolium chloride is potentially reversible. These data suggest that contrary to previous understanding, the histochemical abnormality revealed by 2,3,5-triphenyltetrazolium chloride is reversible in some circumstances and does not necessarily represent inevitable infarction.

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Year:  1990        PMID: 1697139     DOI: 10.1007/bf00308918

Source DB:  PubMed          Journal:  Acta Neuropathol        ISSN: 0001-6322            Impact factor:   17.088


  20 in total

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Authors:  F B Meyer; T M Sundt; T Yanagihara; R E Anderson
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Review 4.  Cell damage in the brain: a speculative synthesis.

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7.  The temporal evolution of hypoglycemic brain damage. I. Light- and electron-microscopic findings in the rat cerebral cortex.

Authors:  R N Auer; H Kalimo; Y Olsson; B K Siesjö
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8.  Rat middle cerebral artery occlusion: evaluation of the model and development of a neurologic examination.

Authors:  J B Bederson; L H Pitts; M Tsuji; M C Nishimura; R L Davis; H Bartkowski
Journal:  Stroke       Date:  1986 May-Jun       Impact factor: 7.914

9.  Blood-brain barrier disruption and exacerbation of ischemic brain edema after restoration of blood flow in experimental focal cerebral ischemia.

Authors:  T Kuroiwa; M Shibutani; R Okeda
Journal:  Acta Neuropathol       Date:  1988       Impact factor: 17.088

10.  Evaluation of 2,3,5-triphenyltetrazolium chloride as a stain for detection and quantification of experimental cerebral infarction in rats.

Authors:  J B Bederson; L H Pitts; S M Germano; M C Nishimura; R L Davis; H M Bartkowski
Journal:  Stroke       Date:  1986 Nov-Dec       Impact factor: 7.914

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  7 in total

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3.  Delayed institution of hypertension during focal cerebral ischemia: effect on brain edema.

Authors:  P M Patel; J C Drummond; D J Cole; R Giamela; J Steinauer
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4.  A comparison of the area of histochemical dysfunction after focal cerebral ischaemia during anaesthesia with isoflurane and halothane in the rat.

Authors:  T S Ruta; J C Drummond; D J Cole
Journal:  Can J Anaesth       Date:  1991-01       Impact factor: 5.063

5.  Refinement of embolic stroke model in rats: Effect of post-embolization anesthesia duration on arterial blood pressure, cerebral edema and mortality.

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6.  A Comparative Study of Variables Influencing Ischemic Injury in the Longa and Koizumi Methods of Intraluminal Filament Middle Cerebral Artery Occlusion in Mice.

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7.  Identification of ischemic regions in a rat model of stroke.

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  7 in total

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