{'fraction_non_alphanumeric': 0.01335113484646195, 'fraction_numerical': 0.0, 'mean_word_length': 5.410256410256411, '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 effect of ancrod on perfusion of myocutaneous flaps.

Ancrod is a defibrinogenating enzyme that also stimulates production of prostacyclin and, thereby, acts indirectly as a vasodilator and inhibitor of platelet aggregation. The actions of ancrod have provided the rationale for successful clinical use in the treatment of peripheral vascular disease and venous thrombosis. A porcine panniculus carnosus myocutaneous flap model was utilized to study the effects of ancrod on flap perfusion and viability. Ancrod treatment appeared to increase perfusion at one distal flap site, as measured by dermofluorometry. A small but not statistically significant increase in percent of viable flap surface area was also observed in ancrod-treated piglets.