{'fraction_non_alphanumeric': 0.05658263305322129, 'fraction_numerical': 0.012324929971988795, 'mean_word_length': 5.2229965156794425, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
[The effects of the receptor antagonist of glutamic acid on the brain tissue of severely scalded rats].

OBJECTIVE
To explore the influence of glutamic acid on burned rat brain tissue and the effects of the receptor antagonist of glutamic acid.


METHODS
Rats inflicted with 30% TBSA III degree scalding injury were taken as the model. The water content, K(+), Na(+), Ca(2+), Mg(2+), nitric oxide metabolites (NO(2)(-)/NO(3)(minus sign))concentrations of scalded rat brain were determined at 2, 6, 12 and 24 postburn hours (PBH). Morphological and histochemical studies of the brain tissue were carried out with LM and EM.


RESULTS
The water content, Na(+), Ca(2+)and NO(2)(minus sign)/NO(3)(minus sign) concentrations of the brain tissue after scalding injury were higher than those in control group. But intracerebral ATP enzyme decreased postburn. It was found by EM examination that there existed swelling of capillary endothelium, nerve cells and some intracytoplasmic mitochondria. There appeared pinosome on capillary wall. After the administration of receptor antagonist of glutamic acid, D-2-amino-group-7-phosphoenanthate (D-AP7), the brain water content, Na(+), Ca(2+)and NO(2)(-)/NO(3)(-) concentrations in brain tissue, and the capillary wall pinosome decreased, and the swelling of nerve cells ameliorated.


CONCLUSION
There might be postburn increased cerebral microvascular permeability, ischemic injury of cerebral tissue cells and the development of brain edema. The postburn alterations in the morphology and metabolism of brain tissue were correlated with the over secretion of glutamic acid. And the excitatory toxic effects of glutamic acid were mediated by its receptor. The receptor antagonist of glutamic acid D-AP7 might ameliorate postburn cerebral injury.