{'fraction_non_alphanumeric': 0.040271966527196654, 'fraction_numerical': 0.024581589958158997, 'mean_word_length': 4.047493403693931, 'pattern_counts': {'":': 0, '<': 1, '<?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}}
Nitric oxide production in normal, endotoxemic and critically ill colic horses.

Total serum nitrate/nitrite concentration (SNN in µM L−1), an indirect measure of nitric oxide (NO), has been reported to be increased during critical illness in people and dogs. The relationship of NO to critical illness in horses is unknown. The purpose of this study was to quantify and compare SNN in normal, endotoxin treated, and horses with naturally acquired colic requiring surgical intervention. 
 
 
 
Sixteen healthy adult mares were randomly administered either endotoxin (E.coli 055 B5, 0.2 µg kg−1 in 1 L 0.9% NaCl; Group 1; ENDO, n = 8) or 1 L 0.9% NaCl (Group 2: SAL, n = 8) IV over 15 minutes. Clinical symptoms of colic were evident within 45 minutes post infusion in ENDO horses. Group 3 were horses with naturally occurring colic requiring emergency surgical intervention (COLIC, n = 17). Jugular venous samples were collected for SNN analysis prior to infusion (t = 0 hours) and 4 hours postinfusion (t = 4 hours) in ENDO and SAL and prior to anesthetic induction in COLIC horses. SNN is reported as median values in µM L−1. Data were log transformed if necessary to fit a normal distribution. Analysis of variance was used to compare SNN among groups. Significance was based on a p-value of < 0.05. 
 
 
 
COLIC had significantly higher SNN (12.78 µm L−1) as compared to ENDO (3.6 µm L−1) and SAL (5.7 µm L−1). SNN was increased significantly at t = 4 hours as compared to t = 0 hours in both ENDO and SAL with no significant difference between groups at t = 0 or in the magnitude of change from t = 0. 
 
 
 
We conclude that SNN was significantly increased in horses with surgical colic as compared to endotoxin and saline treated horses. A higher dose of endotoxin may be needed in an equine model to induce NO response. NO production in horses may relate to the severity and duration of critical illness.