Perihematoma damage at different time points in experimental intracerebral hemorrhage

Abstract

The damage degree of neurons in perilesion at different time points was observed in order to explore the optimal operation occasion. Piglet lobar hematomas were produced by pressure-controlled infusions of 2.5 mL autonomous blood into the right frontal hemispheric white matter over 15 min, and the metabolic changes were ambulatorily detected with MRS at 3rd, 12th, 24th and 48th h after hematoma induction. Brain tissues of perihematoma were also obtained at different time points. The transcription level of Bax gene was detected by in situ hybridization and apoptosis by TUNEL technique, and the pathologic change of neurons was observed under an electron microscope. The results showed that the number of Bax positive cells reached the peak at 24 h (79.00±4.243/5 fields). There was no significant difference in A values between 3 h and 6 h, 12 h (P>0.05), but there significant difference between 24 h and 3 h, 6 h, 12 h (P<0.05). The number of apoptotic cells reached the peak at 24 h (P<0.001), and there was no significant difference between 3 h and 6 h (P=0.999). The area of the apoptotic cells showed no significant difference between 3 h and 6 h or among 3 h, 6 h and 6 h (P>0.05). Lac peak mainly occurred at 24 h and 48 h, while on the healthy side, no Lac peak was detectable. The ratio of NAA/Cr presented a descent tendency, but there was no significant difference among the groups before 12 h (P>0.05), there was very significant difference between 3, 6 and 24, 48 h (P<0.01). Under electronic microscopy, the neuronal damage surrounding hematoma in 3 to 6 h was milder than in 24 h to 48 h. It was concluded that the secondary apoptosis, damage and metabolic disturbance of the neurons surrounding hematoma was milder in 3–6 h in acute intracerebral hemorrhage, while obviously aggravated in 24–48 h. An effective intervention is needed to reduce secondary damage as soon as possible.

Keywords

intracerebral hemorrhage / secondary damage / time point / MRS / apoptosis

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