{'fraction_non_alphanumeric': 0.028287461773700305, 'fraction_numerical': 0.012996941896024464, 'mean_word_length': 4.716157205240175, '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}}
[Distribution and significance of endothelin-1 and endothelin receptor a mRNA in liver after endotoxemia].

OBJECTIVE
To study the distribution and significance of endothelin-1 (ET-1) and endothelin receptor A (ETAR) mRNA in liver after endotoxemia using situ hybridization.


METHODS
30 rats were randomized into control and endotoxin groups. The endotoxin group was injected with endotoxin at a dose of 10 mg/kg body wt. Hybridization of ET-1 and ETAR mRNA of the hepatic tissue was proceeded at 3, 6, 12 and 24 hours after endotoxin administration.


RESULTS
By in situ hybridization, the cell expression of ET-1 mRNA was hepatic sinusoids, the endothelial cells of portal vein, and Kupffer cell and the cell expression of ETAR mRNA was the small artery smooth muscle cells of hepatic lobule and the hepatic sinusoidal lining cells. The accumulation of grain was observed in many cells of the liver. The number of accumulating grain increased in unit scope.


CONCLUSION
ET-1 is synthesized by the hepatic sinusoids, hepatic vascular endothelial cells, and Kupffer cells, ETAR may be located on the hepatic vascular smooth muscle cells and Ito cells (fat-storing cells) around sinusoid. Endotoxin may, on transcription and translation level, lead to the increase of ET-1 and ETAR in synthesis and release.