{'fraction_non_alphanumeric': 0.06484069312465064, 'fraction_numerical': 0.041922861934041364, 'mean_word_length': 4.682539682539683, '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}}
Effect of hypertonic sodium chloride (7.5%) on uncontrolled hemorrhage in rats and its interaction with different anesthetic procedures.

Small volumes (4-6 ml/kg) of hypertonic NaCl (7.5%, HS) have been shown to correct the hemodynamic alterations caused by severe blood loss, but it has been claimed that its use is detrimental to rats undergoing uncontrolled arterial bleeding. The interaction between uncontrolled hemorrhage and HS was reexamined in experiments performed on male Wistar rats anesthetized with neurolidol-ketamine (NK), pentobarbital (P), chloralose (C), or urethane (U), (n = 20 in each group), half of them treated with HS (4 ml/kg IV) 15 min after start of bleeding. Uncontrolled hemorrhage was induced by cutting the tail at 12% (T12%) or 50% (T50%) from its tip. NK induced large blood loss (T50%, 32.6 ml/kg; T12%, 16.2 ml/kg) and hypotension (T50%, 70 mmHg drop, T12%; 25 mmHg). Mortality was 3/10 (T50%) and 2/10 (T12%). HS produced a significant transient recovery of mean arterial pressure (MAP) and increased blood loss to 38.9 and 21.8 ml/kg for T50% and T12% respectively, but mortality was not significantly different (T50%, 5/10; T12%, 3/10). The other three anesthetics with a T50% cut produced mild blood loss and slight hypotension, unaffected by HS. Only three of 60 rats died under these anesthetics (two HS, one untreated). In a supplementary P-anesthetized group (P-MIMIC), blood was forcibly removed from a large artery to mimic the loss observed in the NK-T50% group. Hypotension and death rates in P-MIMIC (four HS, one control) were comparable to those observed in NK-T50%. It is concluded that the effects of NK are probably due to its powerful vasodilator effect, apparently sufficient to impede the normal vasoconstrictor response to shock.