Six healthy, adult horses, with normal (mean +/- SEM) baseline serum concentrations of total triiodothyronine (T3, 1.02 +/- 0.16 nmol/L), free T3 (FT3, 2.05 +/- 0.33 pmol/L), total thyroxine (T4, 19.87 +/- 1.74 nmol/L), free T4 (FT4, 11.55 +/- 0.70 pmol/L), total reverse T3 (rT3, 0.68 +/- 0.06 nmol/L), and cortisol (152.75 +/- 17.50 nmol/L), were judged to be euthyroid on the basis of response to a standardized thyroid-stimulating hormone response test. Serum concentrations of T3, FT3, T4, FT4, rT3, and cortisol were determined immediately before and every 24 hours during a 4-day period of food deprivation, when water was available ad libitum. Similar variables were measured 72 hours after refeeding. Decreases (to percentage of baseline, prefood deprivation value) in circulating T3 (42%), T4 (38%), FT3 (30%), and FT4 (24%) concentrations were maximal after 2, 4, 2, and 4 days of food deprivation, respectively (P < 0.05). Increases (compared with baseline, prefood deprivation value) in rT3 (31%) and cortisol (41%) concentrations were maximal after 1 and 2 days of food deprivation, respectively (P < 0.05). Refeeding resulted in increase in serum T4 and FT4, and decrease in rT3 and cortisol concentrations toward baseline values, after 72 hours (P < 0.05). Refeeding did not effect a return of T3 or FT3 concentration to baseline values after 72 hours (P < 0.05). Food deprivation appears to cause changes in serum concentrations of T3, FT3, T4, FT4, rT3, and cortisol in horses that are similar to those in human beings. This effect of food deprivation should be considered when results of serum thyroid hormone and cortisol assays are interpreted in the face of clinical disease. These results further emphasize the invalidity of making a clinical diagnosis of hypothyroidism on the basis of baseline, serum thyroid hormone concentrations in horses, especially if the horses have been anorectic or inappetent.

Estradiol was administered to 3 steers (0.12 mg/kg of body weight/d for 14 consecutive days), followed by 2 days of nonfeeding (starvation). During estradiol administration, liver nuclear estrogen receptor and serum apolipoprotein B-100 (apoB-100), as well as serum triglycerides concentrations were increased, compared with values before administration. Starvation, together with interruption of estradiol administration, resulted in rapid decreases of the receptor, serum apoB-100, and serum triglycerides concentrations, and increase of nonesterified fatty acids concentration. Of the 3 steers, 2 had higher liver triglyceride content, compared with values before treatment. In the control group (3 steers that received vehicle alone, then starved similarly), these concentrations, except for serum nonesterified fatty acids and triglycerides concentrations after starvation, were not changed. In another experiment, serum apoB-100 concentration in dairy cows was significantly (P < 0.05) lower at parturition than values before and after parturition. These results indicate that estradiol may be involved in development of fatty liver in cattle.

Serum lipoprotein concentrations, routine serum biochemical values, and morphologic changes of the liver were evaluated in cats undergoing weight loss. Food was withheld from 6 obese and 6 control cats for 3 days (days 0 to 2), followed by feeding 50% of previous food intake for 26 days (days 3 to 28). Percutaneous liver biopsy specimens were obtained from all cats on days 0, 7, 14, and 28. Blood samples for serum biochemical analysis and lipoprotein profiles were obtained on days 0, 3, 7, 14, and 28. All cats lost weight throughout the study, and none developed signs of chemical illness, including those of idiopathic hepatic lipidosis syndrome. Serum total cholesterol concentrations decreased initially in all cats, but rapidly returned to normal after day 3 in obese cats, suggesting altered cholesterol metabolism during dietary restriction. Low-density lipoprotein concentrations decreased throughout the study in control cats, but were unchanged in obese cats. Examination of liver biopsy specimens from each cat revealed minimal lipid accumulation in all specimens, although some specimens contained hydropic degeneration.

The bioavailability and pharmacokinetics of ibuprofen, a nonsteroidal antiinflammatory drug, was studied in healthy Shetland ponies. Ibuprofen was administered IV, as a suspension, and as a solid solution oral paste to ponies from which food was withheld. The suspension paste was also administered to ponies that received hay and water ad libitum. Both formulations had an absolute bioavailability of about 80%. Bioavailability was not influenced by feeding.

Two hundred eighty-eight crossbred feeder pigs were used in 2 trials to determine the effects of feed and/or water deprivation at an auction market, and the effects of restricting the intake of the receiving diet on their serum chemical profile. The study also was designed to assess the value of the serum chemical profile as a diagnostic data base for stress disorders in feeder pigs. Performance data indicated that feeder pigs provided water only at the auction facilities lost significantly more weight than did those provided feed and water. Feeder pigs deprived of both feed and water were not significantly different in body weight from either group. Several serum chemical values (creatinine, triglycerides, cholesterol, blood urea nitrogen, and lactate dehydrogenase) were significantly influenced by feed deprivation, but not by feed and water deprivation. However, only the serum creatinine values were significantly different after the 24-hour post-transport period. There were no significant differences in pig weight or serum chemical values 84 days after pigs had arrived at the finishing unit. The serum chemical profile, widely used in human medicine, appears not to provide a reliable marker for identification of short-term nutritional deprivation, nor for transport stress in feeder pigs.

A D-xylose absorption test was conducted on 4 healthy mares deprived of food for 12, 36, 72, and 96 hours before the test, with a 13- to 15-day adjustment period between each test. Maximal plasma concentrations after 72 and 96 hours of food deprivation were approximately 36% lower than those obtained after the 12- and 36-hour periods (P = 0.0001). Absorption curves were flatter and the decrease in plasma concentration was slower after the 72- and 96-hour periods of food deprivation. The rate of D-xylose absorption (P = 0.0108) and the initial rate of urinary excretion (P = 0.0117) were slower at 72 and 96 hours. Gastric emptying appeared to be progressively delayed with food deprivation, as evident by the delay in peak D-xylose excretion in urine (P = 0.0268). Areas under the plasma concentration-time curves and quantitites of D-xylose excreted in urine were similar for all periods of food deprivation, evidence that the same amounts of D-xylose were absorbed, despite changes in the plasma curve. A 15-hour collection period was sufficient to recover all D-xylose excreted in the urine, and during all periods 9.8 +/- 0.6% (mean +/- SEM) of the oral dose was eliminated in the urine.

Concentrations of amino acids in plasma and whole blood in response to 10 hours of food deprivation were determined in healthy 2-day-old foals (n = 8) and were compared with control values in foals of the same age (n = 8) allowed free access to suckle. In addition, response of concentrations of amino acids in plasma to 15 minutes of free-access suckling was determined at the end of the 10-hour period in both groups. Response of 13 amino acids in plasma of food-deprived foals was significantly (P < 0.05) different, compared with that in control foals. Concentrations of 3 amino acids (alanine, glycine, and phenylalanine) in plasma increased significantly (P < 0.05), whereas concentrations of 7 amino acids (asparagine, citrulline, histidine, ornithine, proline, tryptophan, and tyrosine) in plasma decreased significantly (P < 0.05) during food deprivation. Response of concentrations of 2 amino acids (glycine and histidine) in whole blood was significantly (P < 0.05) different from that in plasma of food-deprived vs control foals. Refeeding of food-deprived foals resulted in significantly (P < 0.05) different responses for concentrations of all but 2 amino acids (cystine and taurine) in plasma, compared with responses in controls. Changes in concentrations of amino acids in plasma and whole blood of foals in response to food deprivation are similar to those in foals with septicemia and in children with grade 1 or 2 kwashiorkor. The significantly different response of food-deprived foals to refeeding may be attributable to increased protein intake or altered physiologic state.

Intragastric pH monitoring was investigated in ponies. In cadaver stomachs, close contact with the mucosa led to high pH readings if nonweighted electrodes were used. However, pH recorded by weighted electrodes was markedly less affected by mucosal contact (P < 0.001). The latter were used for subsequent trials. In vivo, high correlations were found between pH recorded by weighted electrodes with or without a wire guard to prevent mucosal contact (correlation, r = 0.866; P < 0.001). Readings from each correlated well with those from simultaneous gastric aspirates (r = 0.774 and r = 0.807, respectively; P < 0.001 for both correlations). Plain electrodes recorded more highly variable (temporally heterogeneous) pH than did guarded electrodes. In vitro, trials using equine gastric fluid indicated that this resulted from greater responsiveness of the plain electrode. In vivo, episodes of nearly neutral pH were a common feature, and high pH correlated with intensely yellow-green, neutral fluid in the stomach (rank correlation, p = 0.626; P < 0.01). Concentration of bile acids did not correlate with pH or color score (p = -0.158 and p = 0.076, respectively). Causes of the episodes could include salivary influx, duodenogastric reflux, and variable gastric acid secretion. Pentagastrin infusion (0.6 micrograms/kg of body weight/ h) reduced intragastric pH (P = 0.018), but episodes of neutrality still occurred. Experiments in fed ponies indicated possible existence of a stable pH gradient, from neutral dorsally to heterogeneous and more acidic ventrally. Care was required in the rational choice of summary variables for expression of monitored pH data. Of the frequency distributions of 3 summary variables assessed in this study (mean, median, and percentage of data > pH 4), only that of the mean approached normality. Thus, use of the mean may allow analysis by parametric statistical methods. Intragastric pH monitoring was found to be a useful technique. Episodes of increased pH were often identified. These may represent episodic duodenogastric reflux.

Twelve nonlactating dairy cows, free of signs of liver disease and with normal serum activities of liver-derived enzymes and normal liver biopsy tissue, were examined over a 72-hour period for serum total bile acid concentrations. The cattle were fed hay twice daily, and blood samples were obtained every hour for 24 hours, every other hour for 24 hours, then every hour for 24 hours. After 3 weeks, the study was repeated on 6 of the cattle, thus providing data for eighteen 72-hour periods. Serum bile acid concentration varied greatly over the 72 hours, with the range being from one third to 3 times the median. There were variations by as much as 60 micromol/L from 1 hour to the next. After another 3 weeks, 8 of the cattle were deprived of hay for 48 hours and then fed hay morning and afternoon of the third (last) day of the study. There was no significant reduction in bile acid concentration after withholding the hay, but the variability was reduced (P = 0.02) during the last 20 hours of the haydeprivation period. In 3 ancillary studies, serum bile acid concentrations were examined over a 48-hour period in 2 cows in early lactation, 3 cows in midlactation, and two 6-month-old heifers. The cows were fed hay and grain twice daily, and the heifers were fed only hay twice daily. In comparison with values for the 12 nonlactating cows fed hay twice daily, mean serum bile acid concentration in the recently freshened cows was significantly (P < 0.002) higher (62.9 vs 22.0 micromol/L). The cows in midlactation had hourly fluctuations as great as 65 micromol/L. Values for the heifers varied less than values in older cattle.

To evaluate underlying causes of calcium oxalate urolithiasis, 24-hour excretion of urine metabolites was measured in 6 Miniature Schnauzers that formed calcium oxalate (CaOx) uroliths during periods when they were fed a standard diet and during periods when food was withheld. Serum concentrations of parathyroid hormone and 1,25-dihydroxyvitamin D also were evaluated. Serum calcium concentrations were normal in all 6 affected Miniature Schnauzers; however, during diet consumption, mean 24-hour urinary excretion of calcium was significantly (P = 0.025) higher than calcium excretion when food was withheld. In 1 dog, urinary calcium excretion was lower during the period of food consumption, compared with the period when food was withheld. Compared with clinically normal Beagles, Miniature Schnauzers that formed CaOx uroliths excreted significantly greater quantities of calcium when food was consumed (P = 0.0004) and when food was withheld (P = 0.001). Miniature Schnauzers that formed CaOx uroliths excreted significantly less oxalate than clinically normal Beagles during fed (P = 0.028) and nonfed (P = 0.004) conditions. Affected Miniature Schnauzers also excreted abnormally high quantities of uric acid. Excretion of citrate was not different between Miniature Schnauzers with CaOx urolithiasis and clinically normal Beagles. In 5 of 6 Miniature Schnauzers with CaOx urolithiasis, concentrations of serum parathyroid hormone were similar to values from age- and gender-matched Miniature Schnauzers without uroliths. The concentration of serum parathyroid hormone in 1 dog was > 4 times the mean concentration of clinically normal Miniature Schnauzers. Mean serum concentrations of 1,25-dihydroxyvitamin D in Miniature Schnauzers with calcium oxalate urolithiasis were similar to concentrations of clinically normal Miniature Schnauzers.