Effect of aerosolized albuterol sulfate on resting energy expenditure determined by use of open-flow indirect calorimetry in horses with recurrent airway obstruction

OBJECTIVE: To evaluate effects of sedation on stability of resistance of the respiratory system (RRS) and measures of resting energy expenditure (REE) by use of open-flow indirect calorimetry (IC) and treatment with aerosolized albuterol on REE in horses with recurrent airway obstruction (RAO). ANIMALS: 9 clinically normal horses and 8 horses with RAO. PROCEDURE: In phase 1, RRS was measured by using forced oscillometry (FOT) in 5 clinically normal horses before and after sedation with xylazine. In phase 2, REE was measured in 4 clinically normal horses between 20 and 25 minutes and again 35 to 40 minutes after sedation with xylazine. In phase 3, IC was performed between 20 and 25 minutes and FOT was performed between 30 and 35 minutes after xylazine administration in 8 horses with RAO; after administration of 450 microg of albuterol, IC and FOT were repeated. RESULTS: In phase 1, RRS values were significantly lower 5 and 10 minutes after sedation. In phase 2, diminishing sedation did not significantly affect REE. In phase 3, there was a significant decrease in mean RRS (1.15 +/- 0.25 vs 0.84 +/- 0.14 cm H20/L/s) and REE (30.68 +/- 17.89 vs 27.46 = 16.54 kcal/kg/d) after albuterol administration. CONCLUSIONS AND CLINICAL RELEVANCE: FOT and IC are useful in obtaining repeatable measurements of RRS and REE, respectively, in sedated horses. Concurrent bronchodilation and decreased REE after albuterol administration suggest that increased work of breathing as a result of airway obstruction may contribute to increased energy demands in horses with RAO.     

Sleep time following anesthesia in mouse lines selected for resistance or susceptibility to fescue toxicosis

In previous work, a mouse line selected for resistance (R) to fescue toxicosis had higher activities of two hepatic Phase II detoxification enzymes than a mouse line selected for fescue toxicosis susceptibility (S). The primary objective of the present study was to determine whether those same lines also differed in hepatic Phase I enzyme activity, estimated from sleep time (ST) following sodium pentobarbital anesthesia. Additional objectives were to determine whether ST differences between lines were modulated by endophyte-infected fescue in the diet (with or without an enzyme inducer) and whether ST of individual mice was correlated with the effect of a toxin-containing diet on the postweaning growth of those mice. In Exp. I, 24 males from each line were randomly assigned to each of five diets: control (commercial rodent food meal); E+ (50% endophyte-infected fescue seed, 50% control); E+P (the E+ diet supplemented with 1,000 ppm phenobarbital); E- (50% endophyte-free fescue seed, 50% control); and E-P (the E- diet supplemented with 1,000 ppm phenobarbital). After 4 wk on these diets, ST was measured on all the mice. A second ST was recorded on each mouse by randomly sampling one-fourth of the population after 1, 2, 3, or 4 wk on a pelleted rodent food diet. Regardless of diet, R mice had shorter first and second ST than S mice (P < 0.01), suggesting higher hepatic Phase I microsomal enzyme activity. Mice on both phenobarbital-supplemented diets had shorter first ST than mice whose diets did not include that microsomal enzyme inducer (P < 0.01). In Exp. II, ST was measured on male and female R and S mice (n = 280) after they had been fed the E- diet for 2 wk, then the E+ diet for 2 wk, and then a pelleted rodent food diet for 2 wk. Growth response to the E+ diet was the percentage of reduction in gain on the E+ diet compared to gain on the E- diet the previous 2 wk. As in Exp. I, S mice slept longer than R mice (P < 0.01). The residual correlation between ST and gain reduction associated with the E+ diet equaled 0.04. Thus, an animal's apparent Phase I enzyme activity did not predict its growth rate depression on the toxin-containing diet. Based on these and previous studies, divergent selection for toxicosis response in mice was successful partially by causing divergence in activities of hepatic Phase I and II detoxification enzymes.