{'fraction_non_alphanumeric': 0.03996925441967717, 'fraction_numerical': 0.009223674096848577, 'mean_word_length': 4.786666666666667, 'pattern_counts': {'":': 0, '<': 2, '<?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}}
Resuscitation of ischemia/reperfusion with hyperalimentation increases intestinal PGI2 synthase (PS) content and PGI2 release.

Normal rat splanchnic blood flow and eicosanoid synthesis were compared to sham (Sham) and hemorrhage/reperfusion (SK + R) animals treated with 5 days of total parenteral nutrition (TPN). After in vivo measurement of superior mesenteric artery (SMA) blood flow, the splanchnic bed was perfused in vitro and venous effluent assayed for eicosanoid release by EIA. Aortic, SMA, ileal muscularis/serosa, and mucosa homogenates were analyzed for cyclooxygenase (COX) and prostacyclin synthase (PS) content by Western blot and for COX activity by radiochromatography. SK + R + TPN decreased SMA blood flow 33% and increased splanchnic PGI2 release twofold (p < .05) compared with the Sham +TPN and normal groups. groups SK + R + TPN did not alter COX activity in any of the tissues but Western blot analysis showed a twofold increase in COX and PS content in ileum muscularis/serosa (p < .05). These data show that SK + R + TPN induced a decrease in SMA blood flow and a compensatory increase in release of splanchnic PGI2. The mechanism for increased splanchnic PGI2 release after SK + R + TPN was an increase in PS and COX content (not activity) in the ileal muscularis/serosa.