Using an applanation tonometer, 5 replicate intraocular pressure (IOP) measurements were obtained from each eye of 12 young, clinically normal, American alligators. Alligator length ranged from 46 to 117 cm, measured from snout to tail tip. All IOP were recorded by a single observer at an ambient temperature of approximately 25 C, and ranged from 5 to 35 mm of Hg. Observer reliability was excellent (intraclass r = 0.93), and IOP did not change over the ordered sequence of 5 replicate measurements/eye. Replicate IOP measurements were, therefore, averaged in each eve for comparison between eyes of the same alligator. Left and right eye IOP were highly correlated within individual alligators (r = 0.92), whereas the mean within-animal difference between left and right eye IOP was not statistically significant (95% confidence interval [CI] for the left eye-right eye mean difference, -1.9 to 1.5 mm of Hg). Mean IOP determined for 5 confirmed females and 3 confirmed males did not differ significantly between the sexes (95% CI for the male-female difference in means, -2.1 to 3.7 mm of Hg). Mean +/- SEM IOP of 23.7 + 2.1 mm of Hg determined for 4 alligators < 50 cm long was significantly (P = 0.009) greater than mean IOP of 11.6 + 0.5 mm of Hg determined for 8 alligators > 50 cm long (95% CI for the difference in means, 8.5 to 15.7 mm of Hg). In young alligators, the relation between body length and IOP appears to be nonlinear, possibly with a negative exponent.

The vasculature of the jejunum was studied in 6 llamas and 1 alpaca, using a combination of microangiography, standard light microscopy, and vascular cast imaging. The casts were examined by use of scanning electron microscopy and low-power dissecting microscopy. After administration of 40,000 IU of heparin, all animals were euthanatized by administration of an overdose of sodium pentobarbital. Three sections of jejunum and their respective arcuate vessels were isolated from each animal. One section was immediately placed in formalin for later H&E staining. The second and third sections were placed in warm saline solution, and the vasculature was flushed free of all blood by repeated infusions of the solution. Once flushed of all blood, one section was infused with a radio-opaque medium and subsequently evaluated by microangiography, and the remaining section was perfused with a methylmethacrylate polymer for creation of vascular casts. The arcuate vessels branched into extensive primary and secondary arcades prior to giving rise to the marginal rete. Muscular arteries and small veins left the marginal rete and penetrated the tunica serosa and tunica muscularis to provide nutrients or drain the mesenteric angle, respectively, or entered into the circumferential submucosal network. The primary penetrating vessels in the submucosa formed an extensive submucosal plexus that supplied the tunica serosa, tunica muscularis, and tunica mucosa. The primary penetrating vessels anastomosed with vessels from oral and aboral sections and with their counterparts from the opposite side at the antimesenteric border. Vessels supplied the tunica serosa and tunia muscularis by branching centrifugally from the submucosal plexus supplying the inner circular and outer longitudinal muscle layers parallel to their respective muscle layers. The arterioles supplying the tunica mucosa branched at right angles, penetrated the muscularis mucosa, and gave rise to clusters of arterioles supplying either the villi or the intervening crypts; anastomosis occurred between these 2 systems toward the base of the villus. The arterioles gradually developed a discontinuous smooth muscle layer as they approached the base of the villus. Each villus was supplied by a single centrally placed metarteriole that spiraled to the tip of the villus, divided, and descended in a fountaining capillary network. The individual capillaries in the cascade coalesced to drain via 2 to 4 venules at the base of the villus. Branches from the venules entered into an anastomosing network in the lamina propria to drain the crypts. Venules drained in the submucosal plexus and continued paralleling the arterial supply toward the mesenteric border and the arcuate veins. The jejunal vasculature of South American camelids contains an extensive set of anastomotic connections at all levels after formation of the arcuate vessels. Within the scope of this examination into the microvasculature of llamas and alpacas, differences were not detected between the individual species.

Pharmacokinetic variables of bupivacaine (BPV) were determined after IV and epidural administrations in the same 6 dogs. Plasma BPV concentration curves after IV administration were adjusted to biexponential kinetics: a rapid distribution phase was followed by a slower elimination phase, with half-life of 34.5 +/- 7.8 minutes. Mean plasma clearance was 20.2 +/- 7.4 ml/min/kg of body weight, and mean volume of distribution at steady state was 0.7 +/- 0.2 L/kg. After epidural administration, absorption was rapid. Peak plasma concentration, 1.4 +/- 0.4 microgram/ml, was detected approximately 5 minutes after BPV administration. The half-life corresponding to epidural administration (179 +/- 33.6 minutes) was 5 to 6 times longer than that observed after IV administration, possibly because of the slow release of BPV from the epidural space. Induction times were short (2.3 +/- 2.2 minutes); anesthesia quickly began and lasted for more than 2 hours (158 +/- 48.8 minutes). During that period, BPV plasma concentration ranged between 1.4 and 0.2 microgram/ml. Changes in systolic blood pressure and heart rate were correlated to high plasma concentration of BPV. These modifications were observed for the first 30 minutes, reaching baseline values after 60 minutes.

Eight Holstein cows, 4 inoculated intracisternally in 1 quarter of the mammary gland with Escherichia coli and 4 noninfected controls, were administered ceftiofur sodium (3 mg/kg of body weight, IV, q 12 hours) for 24 hours, beginning at 14 hours after inoculation of infected cows. All challenge-exposed cows became infected, with mean +/- SEM peak log10 bacterial concentration in milk of 5.03 +/- 0.69 colony-forming units/ml. The infection resulted in systemic signs (mean peak rectal temperature, 41.5 +/- 0.3 C; anorexia; signs of depression) and local inflammation (mean peak albumin concentration in milk, 7.89 +/- 1.71 mg/ml). Ceftiofur was detectable in milk from all challenge-exposed cows, compared with only 1 of 4 noninfected cows, and the mean period after inoculation that ceftiofur was detectable in milk was longer (P < 0.05) in infected (147.7 +/- 27.5 hours) than noninfected cows (1.3 +/- 1.3 hours). However, maximal ceftiofur concentration attained in milk for all cows was 0.28 micrograms/ml, and was 0.20 micrograms/ml or less for all but 2 milk samples collected for 10 days after challenge exposure. Mean serum concentration of ceftiofur peaked at 1.0 +/- 0.3 micrograms/ml and 0.7 +/- 0.1 micrograms/ml for infected and noninfected COWS, respectively. After each ceftiofur dose, mean peak and trough concentrations of ceftiofur in serum did not differ between groups; however, concentration of ceftiofur in serum was higher at 7 hours after each dose in noninfected cows, suggesting more rapid clearance of the drug in infected cows. Ceftiofur was not detected in serum (< 0.05 micrograms/ml) of any cow at or after 120 hours following inoculation of infected cows. Storage of serum samples at -20 C for 3 weeks resulted in a 98.8% decrease in ceftiofur activity, compared with that in fresh serum samples. Eighty-seven percent of this loss occurred 30 minutes after mixing serum and ceftiofur; thus, about 13% of the original activity was lost in storage. Storage of milk samples under similar conditions did not result in loss of ceftiofur activity. Despite acute inflammation, the dosage of ceftiofur used in this trial would not result in drug concentrations in milk above FDA safe concentrations, or above the reported minimum inhibitory concentration for coliform bacteria.

We examined the electromyographic activity of the costal portion of the diaphragm and the transverse abdominal and external oblique muscles in 6 chronically instrumented awake adult horses during eupneic breathing during 2 levels of hypercapnia (fractional concentration of inspired CO2; FICO2 = 0.4 and 0.6), and during 2 levels of hypocapnic hypoxia (FIO2 = 0.15 and 0.12). Using the inert gas technique, we also measured the end-expiratory lung volumes of the 6 horses during eupnea, 6% CO2 challenge, and 12% O2 breathing. During eupneic breathing, phasic electrical activity of these 3 muscles was always present and was preceded by the onset of mechanical flow. At progressive levels of hypercapnia, the magnitude of inspiratory and expiratory electrical activity increased, and for the expiratory muscles, this recruitment coincided with significant (P < 0.05) increases in peak expiratory gastric pressure. However, during hypocapnic hypoxia, differential recruitment patterns of the respiratory muscles were found. The electrical activity of the diaphragm increased in magnitude and occurred sooner relative to the onset of mechanical flow. The magnitude and onset of abdominal expiratory activity failed to increase significantly during these episodes of hyperpnea and this pattern of activity coincided with decrements in peak expiratory gastric pressure. Despite alterations in muscle recruitment patterns during these hyperpneic episodes, end-expiratory lung volume remained unchanged. Thus, we conclude that adult horses respond similarly to awake dogs during peripheral and central chemoreceptor stimulation.

Sixteen German Shepherd Dogs from 4 litters were IgA-deficient on the basis of at least 1 of 2 serum IgA determinations, and all had small intestinal bacterial overgrowth, as documented by quantitated small intestinal bacterial culture in another study. These dogs were fed 2 diets that differed principally in their protein source (chicken vs beef, milk, and wheat). All dogs were fed each diet for 2 weeks before the study began. Next, all dogs were fed the chicken-based diet for 2 months. Then, half the dogs (group 1) were randomly assigned to continue eating the chicken-based diet, while the other half (group 2) ate a diet containing beef, milk, and wheat proteins. The small intestine was biopsied at the beginning of the study and after dogs had eaten the assigned diet for 2 and 4 months. At 2 months, group-2 dogs had more colonic mucosal mast cells, but this difference did not persist at 4 months. At the end of the study (ie, 4 months), although all dogs were clinically normal, group-2 dogs had significantly (P = 0.010) decreased numbers of jejunal villus plasma cells. However, these histologic changes were not considered clinically important. There were no significant differences in blood eosinophil counts, serum trypsin-like immunoreactivity, or cobalamin, folate, or IgA concentration. Clinical differences were not detected between the 2 groups, before or after the study. Changes were seen in serum IgM and IgG concentrations. Although results of this study suggest that dietary protein may influence intestinal mucosal cell populations, there was no evidence that the protein sources in these 2 diets caused intestinal disease in these dogs under the conditions of this study.

To determine whether abnormal airway pressures have a role in development of dorsal displacement of the soft palate (DDSP), measurements of tracheal and pharyngeal pressures were correlated with nasopharyngeal morphology in exercising horses. Exercising videoendoscopy and measurement of tracheal and pharyngeal pressures were used in 14 clinically normal horses and 19 horses with intermittent DDSP. The pressure signals were superimposed on the videoendoscope image, and both images were saved simultaneously on a videocassette for slow motion analysis to determine the instant displacement occurred in the respiratory cycle. Horses were submitted to an escalating 8-minute high-speed test with a maximal speed of 14 m/s. Compared with clinically normal horses, horses with intermittent DDSP did not have excessively negative inspiratory pressures during exercise. Eight horses displaced the soft palate during inspiration, 4 horses displaced it during expiration, and 7 displaced it by swallowing. Some horses displaced the soft palate at the beginning of the exercise trial, before reaching maximal speed, some horses displaced it at the peak speed, and some horses displaced it when slowing down. Epiglottic size in horses with DDSP was within normal limits, ruling out epiglottic hypoplasia as a cause of DDSP during exercise. Airway pressures were significantly (P < 0.002) altered after DDSP. Pharyngeal and tracheal inspiratory pressures were less negative, whereas pharyngeal expiratory pressure became less positive and tracheal expiratory pressure became more positive after displacement, suggesting a decrease in airflow and an increase in expiratory resistance in the upper airway.

Thirty healthy male horses were allotted to 3 groups and treated blindly during 4 days. Group-1 horses received unfractioned calcium heparin (100 IU/kg of body weight, SC, q 12 h). Group-2 horses received a single dose of a low-molecular-weight heparin (50 anti-Xa IU/kg, SC) every morning, and a similar volume of saline solution every evening. Group-3 horses received the vehicle (saline solution), SC, every 12 hours. Citrated and EDTA-anticoagulated blood samples were collected before starting the medication (T-0) and once daily 3 hours after each morning injection (T-3, T-27, T-51, and T-75). The PCV, hemoglobin concentration, RBC and platelet counts, and clotting times (activated partial thromboplastin time and thrombin time) were determined, and a microscopic examination to detect hemagglutination was performed. Plasma concentration of heparin was measured by use of the antifactor Xa activity assay. Bleeding time was determined on the first and fourth days, using a double-template method. The horses given unfractioned heparin had marked agglutination of erythrocytes after the first injection that became more pronounced as treatment progressed. Also, significant decrease in PCV, hemoglobin concentration, and RBC count was observed during treatment. Platelet count was significantly decreased after the first day, and clotting times were significantly prolonged. In contrast to the horses given unfractioned heparin, those given low-molecular-weight heparin did not have any agglutination of erythrocytes during the 4 days of treatment, and there were no significant changes in PCV, hemoglobin concentration, or RBC and platelet counts. Activated partial thromboplastin time increased slightly in the horses given low-molecular-weight heparin, although the values remained within reference range. Both groups of horses achieved adequate concentrations of heparin in plasma for prophylactic purposes, but those given low-molecular-weight heparin achieved those values after the first injection. Bleeding times were not significantly different between heparin-treated horses and horses given saline solution during treatment. We conclude that low-molecular-weight heparin may be used more safely and conveniently in horses, because it does not affect equine erythrocytes, platelets, or clotting and bleeding times.

Systemic administration of dexamethasone led to a significant reduction in the size of the tuberculin reaction in response to intradermal injection of bovine purified protein derivative in 18 cattle experimentally sensitized to Mycobacterium bovis (P < 0.01) and 8 cattle naturally infected with M bovis (P < 0.001). The reaction in 6 of the 7 M bovis-infected cattle that received dexamethasone was classified as negative for the standard interpretation of the single intradermal comparative tuberculin test. Significantly fewer BoCD2+ (P < 0.05) and BoCD4+ T cells (P < 0.001) were present at the reaction site and in blood of dexamethasone-treated cattle, compared with untreated control cattle. Significantly fewer cells expressing the interleukin-2 receptor and WC1+ gamma delta T cells (P < 0.001), and a significantly greater number of cells expressing the ACT2 antigen (P < 0.05) were found at the reaction site in dexamethasone-treated cattle than in controls. The number of BoCD8+ T cells at the reaction site and in blood was not significantly affected by administration of dexamethasone. In vitro production of interferon-gamma by lymphocytes incubated with bovine purified protein derivative also was significantly lower (P < 0.01) in the dexamethasone-treated cattle.

Objective-To develop a flow cytometric assay for detection of platelet-bound IgG in dogs. Sample Population-Negative-control platelets were obtained from 5 clinically normal Greyhounds. Positive-control platelets were platelets from 1 clinically normal dog, sensitized with dog anti-canine platelet alloantibodies. Procedure-Washed platelets were incubated with mouse anti-canine IgG conjugated to fluorescein isothiocyanate and analyzed by flow cytometry. Optimal dilution of antibody reagent and dose-response were determined, as were effects on platelet-bound IgG detection of storage time and temperature of K3EDTA-anticoagulated blood samples, variable platelet numbers, and variable filling of K3EDTA evacuated tubes. Results-A 1:128 dilution of antibody reagent was optimal. There was a linear increase in platelet-bound IgG when normal canine platelets were incubated with increasing concentrations of positive-control serum. Variable numbers of positive-control platelets tested and variable filling of K3EDTA evacuated tubes had no significant effect on platelet-bound IgG concentration. Platelet-bound IgG concentration increased with storage time at room temperature (P = 0.0003), but not when blood was kept cool. Sufficient platelets for assay were able to be isolated from 3 ml of blood from 5 dogs with < 10,000 platelets/microliter. Conclusion-This assay for platelet-bound IgG in dogs is simple, repeatable, and practical. The assay is not affected by platelet count or variable filling of evacuated tubes, and requires only 3 ml of K3EDTA-anticoagulated blood. Blood samples for testing require packaging on ice and overnight delivery but, after arrival at the laboratory, can be refrigerated and analyzed within 72 hours of collection. Clinical Relevance-Assays for platelet-bound IgG may help in assessing causes and treatment of thrombocytopenia.