{'fraction_non_alphanumeric': 0.03551136363636364, 'fraction_numerical': 0.020596590909090908, 'mean_word_length': 5.021367521367521, '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}}
Low density lipoproteins of male donors decrease prostacyclin (PGI2) and enhance thromboxane (TXA2) release from rat aortas perfused under pulsatile pressure.

The influence of low density lipoproteins (LDL)-cholesterol (1.69 +/- 0.08 mg/ml) and of high density lipoproteins (HDL)-cholesterol (0.62 +/- 0.09 mg/ml), respectively, on the levels of 6-oxo-PGF1 alpha and TXB2 in the perfusates of rat aortas perfused under pulsatile pressure was studied. After passage through the aortas the concentration of LDL-cholesterol was significantly decreased in the perfusates, whereas the HDL-cholesterol level was unchanged. In comparison to controls, perfused with lipoprotein free solution, the concentration of 6-oxo-PGF1 alpha was significantly decreased more than 50% by LDL and the TXB2 level was enhanced significantly by approximately 50%. This results in a significant rise of the TXB2/6-oxo-PGF1 alpha ratio in the perfusates. HDL did not significantly change the ratio of these eicosanoids in the perfusates. These results suggest that this concentration of LDL enhanced the formation of the proaggregatory TXA2 and decreased the formation of the antiaggregatory PGI2 in rat aortas perfused under pulsatile pressure. The proaggregatory action of an elevated level of LDL during the development of atherosclerosis in men may be also mediated by changes in the metabolism of eicosanoids of the vessel wall.