Smooth muscle strips from the midcervical portion of the trachea and bronchial smooth muscle strips from third-generation airways of horses were placed in tissue baths, and isometric contractile force was measured. Active force was measured in response to electrical stimulation and exogenous acetylcholine. Square-wave electrical stimuli were applied at various voltages (10, 12, 15, 18, 20, 25 V), frequencies (3, 5, 10, 15, 20, 25, 30 Hz), and pulse durations (0.2, 0.5, 1.0, 1.5, 2.0 ms). Isometric contractile force increased as voltage, frequency, and pulse duration increased. Maximal contractile response to electrical stimulation was obtained at 18 V, 25 Hz, and 0.5 ms. Atropine (10-6M) or tetrodotoxin (3 X 10-6M) blocked the contraction, indicating that the contractile response was attributable to the release of neurotransmitter from cholinergic nerves. Cumulative concentration-response curves to acetylcholine (10-9M through 10-4M) were determined. Isometric contractile force increased as acetylcholine concentration increased. There was a significant (P less than 0.05) difference in the 50% effective dose for acetylcholine in tracheal smooth muscle and bronchial smooth muscle. The mean (+/- SD) contractile response to maximal electrical stimulus was 89% (+/- 7.4%) of that in response to 10-4M acetylcholine in tracheal smooth muscle and was 68% (+/- 10.4%) of the response to 10-4M acetylcholine in bronchial smooth muscle.

Animals recovered from viral diseases represent an important model to study the host cellular and humoral immune responses to the etiologic agents. This is particularly important for African swine fever virus (ASFV) infections in which antibodies have little or no virus-neutralizing effect. Pigs surviving experimental infection with the naturally occurring low-virulent, nonhemadsorbing ASFV/NH/P68 (NHV) isolate did, however, exhibit virus-specific T-cell activities, as measured by a variety of assays. A strong virus-induced, antigen-specific blastogenic response was observed only with blood mononuclear cells (BMC) from ASF-recovered swine, whereas cells from recovered and naive swine responded similarly to the mitogens concanavalin A and phytohemagglutinin. The ASFV-induced blastogenesis was dependent on virus dose and on the presence of adherent cells. Blood mononuclear cells cultured with antigenically related hemadsorbing ASFV isolates of different virulence characteristics, the highly virulent L60 isolate and moderately virulent DRII isolate, exhibited a similar magnitude of blastogenesis to cells infected with the low-virulent NHV isolate. Virus-infected cells proved to be an efficient inducer of interleukin-2 (IL-2) activity to cells from recovered swine, but not from naive swine, whereas T-cell-specific lectins induced production of similar amounts of IL-2 activity from cells of naive and recovered swine. Correlated with the appearance of virus-induced IL-2 activity in the culture supernatant was the induction of promiscuous killing in cells exposed to prolonged (7 days) virus stimulation. This lymphokine-activated killing could be induced experimentally early in the virus stimulatory process (3 days) by the addition of exogenous lymphokines to the cultures. It was concluded that swine inoculated with low-virulent ASFV isolates are a useful model for identifying and characterizing ASFV immune mechanisms in vitro. Furthermore, this ASFV model implicates lymphokines as inducers of nonspecific cell-mediated immunity; in fact, lymphokine-activated killer type responses may contribute to recovery from this viral infection. More important, ASFV-specific blastogenic and cytotoxic T-cells are prime candidates for the cells inducing and/or conferring protective immunity against challenge ASFV infection.

A study on erythrocyte distribution was performed on 10 healthy, nonstressed adult white Pekin ducks. Results indicated 2 populations of erythrocytes, with average mean corpuscular volumes of 128.37 fl/cell and 308.50 fl/cell. Variations in erythrogram patterns were evident over time, when comparing specimens from different ducks or the same duck. There were 5 patterns of cell number/volume distribution observed between the 2 cell populations when all ducks were studied. Females had a greater change than did males when population density and volume percentage comparisons were made on erythrocyte compartments.

We studied the antibody responses to transmissible gastroenteritis (TGE) in serum, colostrum, and milk from sows vaccinated with 2 attenuated (1 IM and 1 oral-IM) and 1 nonattenuated live vaccines and the relationship of these responses with the survivability of the sow's suckling pigs after challenge exposure with virulent TGE virus. Contrary to previous studies, the anti-TGE virus-neutralizing geometric mean titers (GMT) in the milk of sows vaccinated with attenuated vaccines at 3 and 5 days of lactation were similar to that found in the colostrum. Colostral and serum antibody titers were highest in sows given 2 injections of the IM attenuated vaccine. Half of the sows given the oral-IM attenuated vaccine did not seroconvert after 2 oral doses. Only sows vaccinated with the nonattenuated live vaccine had milk GMT that remained high for 21 days after farrowing. The linear relationship between colostral GMT and percentage of survivability of suckling pigs challenge exposed at 3 days of age was significant (P less than 0.05), although the relationship between serum GMT and percentage of survivability and the relationship between milk GMT and percentage of survivability were not significant (P greater than 0.10). The linear relationship between colostral (P less than 0.10) or pre-challenge exposure milk (P less than 0.05) GMT and percentage of survivability of suckling pigs challenge exposed at 5 days of age was significant. We have no adequate explanation for the relatively low colostral GMT, the relatively high milk GMT at 3 and 5 days of lactation in vaccinated sows, or the lack of significant linear relationship between milk GMT and survivability of pigs challenge exposed at 3 days of age.

Serum concentrations of relaxin and progesterone were measured by specific radioimmunoassays in pregnant, pseudopregnant, or ovariectomized (between gestation weeks 4 and 5) pregnant Labrador Retriever bitches. Daily administration of 17 alpha-ethyl-19-nortestosterone was performed to maintain gestation in the ovariectomized pregnant bitches. This synthetic gestagen was selected because it did not interfere with the assay for endogenously secreted progesterone concentration in serum. Serum progesterone concentration was high in ovarian-intact pregnant or pseudopregnant bitches, but the mean progesterone concentration in pseudopregnant bitches (evaluated at 4 weeks after mating) was only 56% of the concentration in pregnant bitches. After ovariectomy, serum progesterone concentration decreased to undetectable values. Unlike progesterone, serum relaxin concentration increased during the latter half of pregnancy in the ovarian-intact and in the ovariectomized pregnant bitches, but relaxin was not detectable at any time in the pseudopregnant bitches. The amount of relaxin measured in the ovariectomized pregnant bitches was less (P less than 0.05) than that in ovarian-intact bitches, suggesting that the ovaries may have contributed to the total circulating relaxin concentration in the latter. Placental production of relaxin might have accounted for the serum relaxin concentration after ovariectomy; thus, the ovary and placenta each may secrete relaxin during gestation in bitches. Regardless of its source, measurement of serum relaxin concentration may offer a useful way of distinction between pregnancy and pseudopregnancy in dogs.

Uveitis was induced in dogs by intracameral injection of canine lens protein. The lipoxygenase inhibitors phenidone and norhydroguaiaretic acid, and dimethyl sulfoxide decreased fibrin production at 0.5 and 1 hour after induction uveitis. Phenidone and norhydroguaiaretic acid also inhibited the initial increase intraocular pressure early in the course of inflammation. Leukotriene B4 in the aqueous was measured by use of radioimmunoassay at 1 hour after inflammation. In control dogs, 230 to 1,700 pg of leukotriene B4/ml was measured; in dogs treated with phenidone, leukotriene, B4 was not measured.

Oxytetracycline (OTC) pharmacokinetic values in plasma and bile were ascertained after IV administration of the drug. At 6 hours after administration of 1 mg of OTC/kg of body weight, 2.15% of the dose was found in the bile and 37.6% was found in the urine. At 2 hours after administration, the peak bile-to-plasma OTC concentration ratio was 60:1. Bioavailability of OTC was 47.6% when it was administered orally to fasted turkeys and was 9.4% when administered to fed turkeys.

The disposition of theophylline in healthy ruminating calves was best described by a first-order 2-compartment open pharamacokinetic model. The drug had a mean elimination half-life of 6.4 hours and a mean distribution half-life of 22 minutes. Total body clearance averaged 91 ml/kg/h. The mean values for the pharmacokinetic volume of the central compartment, pharmacokinetic volume of distribution during the terminal phase, and volume of distribution at steady state were 0.502, 0.870, and 0.815 L/kg, respectively. Theophylline was readily absorbed after oral administration to the ruminating calf, with a mean fraction of 0.93 absorbed. The plasma concentrations after oral dosing peaked in approximately 5 to 6 hours, with a mean absorption half-life of 3.7 hours. A flip-flop model (rate constant of input is much smaller than the rate constant of output) of drug absorption was not found because the elimination process roughly paralleled that of the study concerning IV administration. In a multiple-dose trial that used a dosage regimen based on single-dose pharmacokinetic values, clinically normal calves responded as predicted. However, diseased calves had higher than expected plasma concentrations after being given multiple oral doses of theophylline at 28 mg/kg once daily. Overt signs of toxicosis were not seen, but this aspect of the drug was not formally investigated. Theophylline can be used as an ancillary therapeutic agent to treat bovine respiratory disease, but not without risk. The suggested oral dose of theophylline at 28 mg/kg of body weight once daily should be tailored to each case. Twice daily oral dosing at 20 mg/kg should reduce the plasma peak:trough ratio and provide plasma concentrations more cnsistently within the human therapeutic range of 10 to 20 micrograms/ml. Even then, therapeutic drug monitoring should be done.

The in vitro reactivity of vasoconstrictive mediators that are implicated in acute laminitis was determined in palmar and plantar digital arteries and veins obtained from healthy horses and in palmar digital vessels of horses with early laminitis (Obel grade I). To obtain baseline reactivity data, 3 experiments were conducted, using healthy horses: (1) the reactivity of palmar and plantar digital arteries and veins to angiotensin II, norephinephrine, and 5-hydroxytryptamine (serotonin) were compared; (2) the direct effects of bacterial endotoxin on vascular reactivity were assessed; and (3) the reactivity of palmar digital arteries and veins to angiotensin II, norepinephrine, prostaglandin F2 alpha (PGF2 alpha), sertonin, and a thromboxane-endoperoxide analog (U46619) were determined. The vascular reactivity of these same 5 vasoconstrictors then was determined in horses with early laminitis and was compared with data from healthy (control) horses. Obel grade-I laminitis was experimentally induced in horses using carbohydrate overload. Dose responses were conducted for each agent at concentrations between 10(-8)M and 10(-4)M. The potency of a drug was defined as the mean effective concentration necessary to induce 50% of maximal contraction (EC50). There were no differences in EC50 concentrations and in maximal contractions between forelimb and hind limb arteries and veins for angiotensin II, norepinephrine, and serotonin. Incubation with endotoxin had no effect on the reactivity of arteries and veins to angiotension II, norepinephrine, and serotonin. In healthy horses, serotonin and U46619 were more potent arterial constrictors than were norepinephrine PGF2 alpha, and angiotensin II. In veins, serotonin, U46619, and angiotension II were similar in potency, and all were significantly (P less than 0.05) more potent than were norepinephrine and PGF2 alpha. Serotonin induced greater arterial constriction than did all other agents tested. There were no differences in the maximal venoconstriction induced by norepinephrine, PGF2 alpha, serotonin, and U46619. Angiotensin II induced the least amount of arterial and venous constriction. Maximal contractions were significantly (P less than 0.05) greater for veins than for arteries for all agents evaluated, except for angiotensin II. In horses with early laminitis, angiotensin II and serotonin were the most potent (smallest EC50 values) constricting agents for the arterial and venous segments and norepinephrine and PGF2 alpha were the least potent. Serotonin and norepinephrine induced significantly (P less than 0.05) greater venoconstriction than did the other agents. Angiotensin II induced the least arterial and venous contraction. For all agonists except angiotensin II, the mean EC50 values for vessels from horses with early laminitis were either similar or greater than those for vessels from control horses. The EC50 values for norepinephrine and the thromboxane analog were significantly (P less than 0.05) greater for vessels from horses with early laminitis, compared with those from control horses. The mean maximal contractions for all vasoconstrictors, except angiotensin II, were significantly (P less than 0.05) less for vessels from horses with early laminitis. Significantly greater venous-to-arterial maximal contraction ratios were found for norepinephrine and serotonin in horses with laminitis, compared with those ratios in control horses. These data suggested that the digital vasculature of horses with early laminitis was not more sensitive to the vasoconstrictor substances tested and that the vessels were significantly less repsonsive than was vasculature from the control horses. However, the venous-to-arterial contraction ratios were either the same or significantly (P less than 0.05) greater in horses with laminitis.

Transrectal ultrasonography was performed on the cranial mesenteric artery and its major branches in 23 conscious adult horses. Ultrasonographically, 25 arterial segments were classified as either normal or abnormal. These ultrasonographic classifications were later compared with the gross and histologic evaluations of each artery following necropsy of each horse. In this study, transrectal ultrasonography as a diagnostic test for verminous arteritis had a 90% sensitivity for detecting normal arteries and an 86% specificity for detecting abnormal arteries, suggesting that ultrasonography may be useful in the antemortem diagnosis of verminous arteritis.