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Pathophysiology of Acute Cerebral Hemorrhage Injury

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DOI: 10.38007/Proceedings.0000445

Author(s)

Tingting Meng, Ya’Ni Hou, Xiaojia Hu and Huaifen Ma

Corresponding Author

Tingting Meng

Abstract

The purpose of this paper is to explore the pathophysiological theory of acute cerebral hemorrhage. First of all, the early pathophysiological changes of hemorrhage, the further study of primary injury and secondary injury in the acute stage of cerebral hemorrhage were analyzed. The adult male SD rats were divided into four groups to establish cerebral hemorrhage model. The experimental results showed that the level of LC3 and Beclin. 1 protein in the right basal ganglia was not affected by hyperglycemia without ICH. Compared with the control group, the ratio of LC3-II / lc3-i and the level of Beclin. 1 protein in the brain tissue around hematoma increased 24 hours after ICH (20.13 ± 2.44% vs.0.56 ± 0.48%, P < 0.01; 107.69 ± 12.80% vs.65.42 ± 21.84%, P < 0.01). Compared with the group with normal blood glucose, acute hyperglycemia could reduce the LC3-II / lc3-i ratio and Beclin. 1 protein level (0.57 ± 0.48% vs.20.13 ± 2.44%, P < 0.01; 43.49 ± 13.88% vs.107.69 ± 12.80%, P < 0.05). After intracerebral hemorrhage, there were obvious neurological deficit symptoms and brain edema, and the autophagy level of the tissue around the hematoma increased.

Keywords

Acute cerebral hemorrhage; Brain histopathology; Nerve function; Pathophysiology