Rat locomotor and feeding behavior varies on a diurnal basis; at night the animals actively forage and eat, whereas during the day they are more inactive and somnolent. At night, cardiac output is higher, presumably for enhanced perfusion of the active muscles to support increased metabolism and for enhanced perfusion of the digestive organs to support increased digestion and nutrient absorption. Conversely, it is hypothesized that during the daytime, blood flow to these two tissues is relatively low. The purpose of this study was to test these hypotheses by measuring cardiac output and the distribution of cardiac output in rats at various times in the diurnal cycle (8:00 A.M., 4:00 P.M., and 8:00 P.M.). The radiolabeled microsphere technique was used to measure cardiac output and distribution of blood flow to the tissues. Distribution of the total cardiac output was accounted for by complete dissection, weighing, and counting of organs and carcass. Cardiac output at 8:00 P.M. (136 +/- 9 ml/min) was elevated 13% (P less than 0.05) over that at 4:00 P.M. The proportion of the cardiac output distributed to the skeletal muscles (4:00 P.M.: 25%; 8:00 P.M.: 27%) and to the digestive tract (4:00 P.M.: 14%; 8:00 P.M.: 14%) did not change between the two time periods. Thus total muscle blood flow increased (P less than 0.05) from 31 +/- 2 at 4:00 P.M. to 36 +/- 4 ml/min at 8:00 P.M.; the only digestive organ to show a significant increase in blood flow from 4:00 P.M. to 8:00 P.M. was the stomach (133 +/- 17 to 166 +/- 19 ml/min, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

The toxicity of Aspergillus ochraceus contaminated wheat and various chemical forms of ochratoxin A (OA) were compared by feeding diets containing A. ochraceus contaminated wheat (3.0 micrograms OA/g diet) and 3.0 micrograms/g of purified OA in the K salt, Na salt, or organic acid form to broiler chicks from hatching to 4 weeks of age. All OA diets caused listlessness, emaciation, dehydration, and occasional diarrhea. Cumulative mortalities were 0, 13, 17, and 10% for the control, contaminated wheat, OA Na salt, OA K salt, and OA acid, respectively. Necropsies at the end of the experiment revealed pale friable livers, enlarged pale kidneys, and enlarged gall bladders in all OA treatments. Body weights and gain were significantly depressed throughout the experiment, and cumulative feed conversion ratios were significantly increased by all forms of OA. Relative kidney and liver weights were also significantly increased by all forms of OA. Serum analysis revealed significant decreases in total protein, albumin, globulin, cholesterol, and phosphorus concentrations and significant increases in uric acid concentrations in chicks fed all forms of OA. Determinations of median lethal dose (LD50) were conducted by dosing day-old chicks and recording mortality for 10 days. LD50 values were 4.41, 3.95, and 2.69 mg/kg for OA acid, Na salt, and K salt, respectively. These results indicated that the K salt of OA was more toxic than the Na salt in acute oral dosing. During the feeding study, results also suggested that chemical form of OA affected its toxicity, but after feeding 3.0 micrograms/g OA for 4 weeks, no significant differences in toxicity were caused by the various chemical forms of OA or the A. ochraceus contaminated diet.

The toxicity to broiler chicks of Chaetomium contaminated corn and various chemical forms of oosporein were compared by feeding diets containing 60% Chaetomium contaminated corn (300 micrograms oosporein/g diet), and 300 or 150 micrograms/g of purified oosporein in either the K salt, Na salt, or organic acid form from hatching to 3 weeks of age. The Chaetomium contaminated corn diet caused 100% mortality during the first week of feeding. Necropsies revealed extensive visceral and articular gout, enlarged pale kidneys, dehydration, proventricular enlargement with mucosal necrosis, and a dark green discoloration of the gizzard lining. When the mortality percentages of the two experiments conducted were considered collectively, the K and Na salts of oosporein caused significantly higher mortality than the organic acid form of oosporein. The K salt caused the most severe lesions and the organic acid caused the least severe lesions. No mortality occurred at the 150 micrograms/g K salt or 150 micrograms/g organic acid levels. Relative kidney weights were increased by all forms of oosporein at 300 micrograms/g, but at 150 micrograms/g only the K salt caused an increase in kidney weight. The LD50 values, based on mortality from 1 to 10 days, were 5.77, 5.00, and 4.56 mg/kg for oosporein acid, oosporein Na salt, and oosporein K salt, respectively. These results suggest that the salts of oosporein (particularly the K salt) are more toxic than the organic acid, and the natural occurrence of oosporein in a salt form could contribute to the increased toxicity of the Chaetomium contaminated corn.

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Two populations of broiler chickens [Athens-Canadian (AC) and a commercial stock] were selected for resistance to aflatoxicosis by dosing chickens in each population with a single oral dose of aflatoxin, which resulted in 40 to 70% mortality. Chickens that did not receive aflatoxin served as the nonselected control groups. Birds surviving the aflatoxin challenge were used as breeders for subsequent generations. Rapid progress was made in the AC population for resistance to aflatoxin, but only moderate progress for this trait was attained in the commercial broiler stock. After five generations of selection in the AC population, LD50 values of 9.42 and 17.05 milligrams aflatoxin per kilogram body weight (BW) were determined for the nonselected and selected lines, respectively. After four generations of selection in the commercial broiler population, LD50 values of 6.05 and 8.02 mg aflatoxin/kg BW were determined for the nonselected and selected lines, respectively. These data demonstrate that genetic progress can be made in chickens, but the amount of progress for resistance to aflatoxin may be influenced by the population.