A study was conducted to examine sources of variation introduced into a phagocytosis assay as a result of the isolation of neutrophils from bovine blood, including variation attributable to isolation of neutrophils from blood, variation between duplicate determinations of percentage phagocytosis, and the variation in the ability of neutrophils isolated from blood (over repeated collections from the jugular vein) to phagocytose. For the phagocytosis assay, jugular venous blood from each of 4 cows was divided into 2 equal portions. The neutrophils were isolated by lysis of red blood cells with 0.2% sodium chloride. The neutrophils (2 X 10(7)) were incubated in duplicate with 32P-labeled Staphylococcus aureus ([32P]SA; 2 X 10(8)) inskimmed milk samples (2.5% final concentration) prepared from 4 cows. This process was repeated thrice on neutrophils isolated from 4 cows at 2-week intervals. The proportions of variation in percentage of 32P-labeled S aureus phagocytosed between duplicate neutrophil isolations and between duplicate assay determinations were 0 and 1%. Differences among skimmed milk sources and among runs, using blood neutrophils taken at different times from the same donor cow, accounted for 62 and 36% of the total variation. The results indicated that variation arising from blood neutrophil isolation introduced into a phagocytosis assay within a single-day trial is of no concern. The large variation among skimmed milk sample sources indicated differences among cows in the ability of their milk to support phagocytosis. The variation in neutrophil isolations over time for any cow was considered too large to allow for evaluation of physiologic and environmental effects on phagocytosis of neutrophils isolated from blood.

Eight adult cats were inoculated IV (n = 6) or SC (n = 2) with Ehrlichia risticii-infected P388Dl (continuous murine macrophage) cells or with E risticii released from P388D1 cells. Three additional cats were inoculated with organism-free P388D1 cultured monocytes, and 1 cat, which served as a medium control, was inoculated with balanced salt solution. Clinical signs of illness were observed in the IV inoculated cats from which E risticii was isolated. One cat developed intermittent diarrhea between postinoculation days (PID) 8 and 18, and the other cat developed lymphadenopathy, acute depression, and anorexia between PID 20 and 24. Ehrlichia risticii was isolated in cultures from 2 of 6 IV inoculated cats on PID 6, 10, and 17. Both cats were inoculated with E risticii released from the P388D1 cells. Ehrlichia risticii was not isolated from SC inoculated cats or from control cats. All 8 cats inoculated with E risticii seroconverted between PID 10 and 23. A pony inoculated with E risticii isolated from 1 of the inoculated cats developed clinical signs of equine monocytic ehrlichiosis including fever, anorexia, depression, and mild colic. Ehrlichia risticii was isolated from the blood of this pony on PID 7, 9, 11, and 16.

In healthy adult goats, closure of the esophageal groove was induced by thirst, IV administered vasopressin, and intracarotid administration of hypertonic NaCl solutions. The efficiency of stimulation was tested directly by visual inspection of the course taken by orally administered solutions through a ruminal or abomasal fistula, palpation of the lips of the esophageal groove through a ruminal fistula, and indirectly by following the glucose dynamics in the blood after oral administration of glucose solution. Esophageal groove closure was observed during drinking after a 48-hour period of water deprivation. Intracarotid administration of 1.5 ml of a saturated solution or 10.5 ml of a 1.5% solution of NaCl also stimulated groove closure; however, groove closure stimulated by administration of vasopressin is the most satisfactory procedure for passing compounds of therapeutic importance directly from the cardiac orifice to the abomasum.

In vitro effects of a mixture of Escherichia coli heat-stable enterotoxins (STa and STb) on isolated jejunum of 3-week-old male pigs were studied, using everted intestinal sac techniques. Heat-stable enterotoxins increased chloride secretion and chloride absorption in everted intestinal sacs. The increase of secretory flux was greater than that for absorptive flux. Vasoactive intestinal peptide (6 x 10-9M) increased chloride secretion, but had no effect on chloride absorption. Neither vasoactive intestinal peptide nor pilocarpine (10-5M) had additive effect to ST. Secretory effects of ST were not blocked by atropine 2 x 10-5M), clonidine (10-6M), or morphine (4.2 X 10-6M).