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  • 1
    ISSN: 1432-0533
    Keywords: Focal cerebral ischemia ; Middle cerebral artery ; Rat ; Reperfusion ; 2,3,5-Triphenyl-tetrazolium chloride
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 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〈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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  • 2
    ISSN: 1432-0533
    Keywords: Focal cerebral ischemia ; Spontaneously hypertensive rat ; Hypertension ; Edema ; 2,3,5-Triphenyltetrazolium chloride
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of induced hypertension instituted after a 2-h delay following middle cerebral artery occlusion (MCAO) on brain edoma formation and histochemical injury was studied. Under isoflurane anesthesia, the MCA of 14 spontaneously hypertensive rats was occluded. In the control group (n=7), the mean arterial pressure (MAP) was not manipulated. In the hypertensive group (n=7), the MAP was elevated by 25–30 mm Hg beginning 2 h after MCAO. Four hours after MCAO, the rats were killed and the brains harvested. The brains were sectioned along coronal planes spanning the distribution of ischemia produced by MCAO. Specific gravity (SG) was determined in the subcortex and in two sites in the cortex (core and periphery of the ischemic territory). The extent of neuronal injury was determined by 2,3,5-triphyenyltetrazolium staining. In the ischemic core, there was no difference in SG in the subcortex and cortex in the two groups. In the periphery of the ischemic territory, SG in the cortex was greater (less edema accumulation) in the hypertensive group (1.041±0.001 vs 1.039±0.001, P 〈 0.05). The area of histochemical injury (as a percent of the cross-sectional area of the hemisphere) was less in the hypertensive group (33±3% vs 21±2%, P 〈 0.05). The data indicate that phenylephrine-induced hypertension instituted 2 h after MCAO does not aggravate edema in the ischemic core, that it improves edema in the periphery of the ischemic territory, and that it reduces the area of histochemical neuronal dysfunction.
    Type of Medium: Electronic Resource
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