{'fraction_non_alphanumeric': 0.01867816091954023, 'fraction_numerical': 0.0035919540229885057, 'mean_word_length': 5.449074074074074, '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}}
Vecuronium and Porcine Malignant Hyperthermia

Vecuronium was studied in eight malignant hyperthermia (MH) susceptible pigs for its potential to either trigger or prevent MH. Two sets of experiments were performed in the same animals: 1-hr total neuromuscular blockade by vecuronium infusion with thiopental anesthesia in the absence of invasiue monitoring and halothane; and 1-hr infusion of vecuronium with thiopental anesthesia with invasive monitoring in the absence of and then, followed by 30-min infusion in the presence of halothane, followed in turn by exposure to halothane alone. One-hour infusion of vecuronium in the absence of halothane and invasive monitoring did not trigger MH in any animal. During the second set of experiments, MH, evidenced by rising rectal temperature, elevated end-tidal PCO2, mixed venous oxygen desaturation, and muscle rigor, occurred in one animal during vecuronium alone, in four animals during vecuronium infusion and simultaneous exposure to halothane, and in three animals during exposure to halothane alone after recovery from vecuronium neuromuscular blockade. In view of the results of control experiments, the development of MH during vecuronium neuromuscular blockade before exposure to halothane was attributed to surgical stress rather than to vecuronium itself. It is concluded that vecuronium is not a trigger to MH in susceptible pigs.