Single doses (2.2 mg/kg of body weight) of phenylbutazone (PBZ) were administered IV to 6 neonatal horses (5 to 17 hours old at time of dosing). Plasma concentrations of PBZ and its metabolite oxyphenbutazone were monitored serially for 120 hours after drug administration. Pharmacokinetic variables were calculated, using 1- and 2-compartment open models. Descriptive equations from the best model for each foal were then used to derive model-independent variables describing PBZ disposition. Median volume of distribution at steady-state was 0.274 L/kg (range, 0.190 to 0.401 L/kg). Median terminal half-life was 7.4 (6.4 to 22.1) hours, and median total plasma clearance of PBZ for foals in this study was 0.018 L/kg/h (range, 0.013 to 0.038 L/kg/h). Volume of distribution was larger, half-life was longer, and total clearance was lower, compared with similar values reported for administration of PBZ to adult horses.

Selective parathyroidectomy (PTX) is preferred to thyroparathyroidectomy (TPTX) when specific effects of parathyroid hormone depletion are being studied. However, because of the anatomic proximity of thyroid and parathyroid glands, TPTX often is performed, leaving animals depleted of thyroxine (T4) and calcitonin as well as parathyroid hormone (PTH). In the present study, six normal dogs had parathyroid tissue and about seven-eighths of thyroid tissue removed. This quantity of thyroid tissue was inadequate to maintain normal serum T4 concentrations, despite allowance of 168 days for thyroid recovery. Five of six dogs with reduced renal mass had successful selective PTX and normal serum T4 concentrations at 28 days, when one-half or more of thyroid tissue was spared. We conclude that with attention to the surgical technique, selective PTX can be achieved in a high percentage of dogs and sufficient thyroid tissue spared to maintain euthyroidism.

Existence of ultradian variation in serum progesterone concentration and the relation between progesterone and luteinizing hormone (LH) secretory patterns were investigated in nonpregnant and pregnant mares. Blood samples were taken every 15 minutes for a 24-hour period on day 8 of the estrous cycle and day 18 of pregnancy, respectively. Progesterone and LH concentrations were determined by radioimmunoassay. Progesterone was secreted in pulsatile manner in nonpregnant and pregnant mares. Luteinizing hormone also was secreted in a pulsatile manner in both groups of mares. There was little temporal relation between LH and progesterone pulses in either pregnant or nonpregnant mares.

To determine blood supply in the area, dye or radioopaque contrast material was injected into the named arteries supplying the terminal colon and rectum in 10 dogs. The cranial rectal artery appeared to supply most of the blood to the terminal colon and rectum. The middle and caudal rectal arteries supplied variable and relatively insignificant amounts. The intrapelvic rectum had a less adequate blood supply than did the terminal colon or proximal rectum. A ventral midline laparotomy and pubic osteotomy were performed in an additional 11 dogs to provide access to the terminal colon and rectum. When the cranial rectal artery was ligated and the colorectal junction was transected and anastomosed, the intrapelvic rectum developed marked congestion, edema, and discoloration. Rectal fluorescence, after IV administration of fluorescein, was either poor or absent. Histologically, partial- to full-thickness mucosal necrosis was evident in most tissue specimens taken from the rectum, and muscle necrosis was evident in some. These findings suggest that, in dogs, the cranial rectal artery should be preserved if at all possible and, if the cranial rectal artery is ligated, most of the intrapelvic rectum should be resected to ensure adequate blood supply to the anastomosis.

A sensitive and specific DNA probe for detection and identification of bovine herpesvirus 4 (BHV-4) was developed. Cloned fragments from a library of HindIII fragments of the BHV-4 (DN-599) genome were labeled with 32P or digoxigenin and were tested for sentitivity and specificity in detecting viral DNA by dot-blot hybridization. Two probes were identified that detected 10 pg of purified viral DNA, and detected viral DNA in 0.001 microgram of total DNA extracted from BHV-4-infected cells. Both probes labeled with 32P and 1 labeled with digoxigenin detected viral DNA in samples prepared from cells infected with 2 prototype strains (DN-599 and Movar 33/63) and 4 field isolates of BHV-4. The DNA probes did not hybridize to total DNA prepared from uninfected bovine cells or from cells infected with BHV-1, BHV-2, alcelaphine herpesvirus 1, pseudorabies virus, or equine herpesvirus 1. One probe, labeled with digoxigenin, was tested further by dot-blot hybridization with infected cell lysates that were simply treated with sodium dodecyl sulfate and proteinase K prior to application to the membrane, avoiding extensive DNA purification procedures. This simplified procedure also resulted in specific detection of field isolates of BHV-4 and prototype strains of BHV-4.

Corynebacterium pseudotuberculosis phospholipase D (PLD) significantly affected viability of ovine neutrophils after 24 hours' exposure, This effect was more marked in cells that ingested PLD emulsified in oil. Treatment of neutrophils with PLD significantly (P < 0.05) reduced the ability of these cells to migrate toward activated sheep serum. The PLD was not chemotactic, but it activated normal sheep serum, producing factors that were chemotactic for neutrophils.

A protocol was developed for preparation of platelet concentrates (PC) to support thrombocytopenic dogs. Four clinically normal dogs with platelet counts that ranged from 200 to 330 X 10(9) platelets/L were used as donors. One unit (450 ml) of blood was collected by venipuncture into a double blood bag. Whole blood (WB) was centrifuged for 4 minutes at 1,000 X g (braking time = 2 minutes, 30 seconds) to prepare platelet-rich plasma (PRP). The PRP was expressed into the satellite bag and was centrifuged for 10 minutes at 2,000 X g (braking time = 2 minutes, 36 seconds). The platelet-poor plasma was expressed, leaving 40 to 70 ml of plasma and the pelleted platelets in the satellite bag. The resulting PC was left undisturbed for 60 minutes to promote disaggregation, and the platelets were then resuspended by gentle manual agitation. Forty-eight PC were prepared. Mean (+/- SD) platelet yield from WB to PRP was 78 +/- 13)% (range, 35 to 97%); yield from PRP to PC was 94 (+/- 6) % (range, 75 to 100%); and overall yield (PC from WB) was 74 (+/- 13) % (range, 36 to 91%). Mean PC platelet count was 8.0 (+/- 3.0) X 10(10) platelets/PC (range, 2.3 to 13.4 X 10(10) platelets/PC). The WBC content was 0.1 to 2.3 X 10(9) platelets/PC, representing 3 to 74% of WBC in the WB. Hematocrit was 0.1 to 26.2%. Results of bacterial and fungal culturing were negative.

Eight dogs were determined to be orthopedically normal on the basis of prelavage physical examination, stifle radiography, synovial fluid analysis, and force plate analysis (peak vertical force normalized for body weight, and time on the force plate). Each dog had 1 stifle randomly assigned to be lavaged with 100 ml of a commercially available 0.05% (w/v) chlorhexidine diacetate solution, and the contralateral stifle was lavaged with lactated Ringer's solution. Difference was not detected between the chlorhexidine diacetate and lactated Ringer's solution-treated joints, with regard to results of synovial fluid analysis and clinical lameness evaluations on days 4 and 8 after lavage. Chlorhexidine diacetate caused a more intense synovitis than did lactated Ringer's solution, as determined by histologic evaluation of synovial membrane specimens after necropsy on day 8; however, a difference in the intensity of toluidine blue staining of articular cartilage was not found between treatments. Chlorhexidine diacetate, as a 0.05% (w/v) solution, cannot be recommended as a joint lavage fluid until the duration of inflammatory changes in the synovial membrane are determined or until the chemical constituents of chlorhexidine diacetate causing the synovitis can be identified and removed.

Twelve healthy dogs were used to determine the cardiorespiratory effects of IV administered ketamine (10 mg/kg of body weight) and midazolam (0.5 mg/ kg). Half the dogs received a ketamine-midazolam combination (K-M) as a bolus over 30 seconds and the other half received the K-M as an infusion over 15 minutes. Induction of anesthesia by use of K-M was good in all dogs. Ketamine-midazolam combination as a bolus or infusion induced minimal cardiorespiratory effects, except for significant (p < 0.05) increases in mean heart rate and rate-pressure product. The increase in heart rate was greater in dogs of the infusion group. Mild and transient respiratory depression was observed in dogs of both groups immediately after administration of K-M, but was greater in dogs of the bolus group than in dogs of the infusion group. Duration of action of K-M for chemical restraint was short. Salivation and defecation were observed in a few dogs. Extreme muscular tone developed in 1 dog after K-M bolus administration.

Cardiopulmonary and behavioral responses to detomidine, a potent alpha 2-adrenergic agonist, were determined at 4 plasma concentrations in standing horses. After instrumentation and baseline measurements in 7 horses (mean +/- SD for age and body weight, 6 +/- 2 years, and 531 +/- 48.5 kg, respectively), detomidine was infused to maintain 4 plasma concentrations: 2.1 +/- 0.5 (infusion 1), 7.2 +/- 3.5 (infusion 2), 19.1 +/- 5.1 (infusion 3), and 42.9 +/- 10 (infusion 4) ng/ml, by use of a computer-controlled infusion system. Detomidine caused concentration-dependent sedation and somnolence. These effects were profound during infusions 3 and 4, in which marked head ptosis developed and all horses leaned heavily on the bars of the restraining stocks. Heart rate and cardiac index decreased from baseline measurements (42 +/- 7 beats/min, 65 +/- 11 ml.kg of body weight-1.min-1) in linear relationship with the logarithm of plasma detomidine concentration (ie, heart rate = -4.7 [log(e) detomidine concentration] + 44.3, P < 0.01; cardiac index = -10.5 [log(e) detomidine concentration] + 73.6, P < 0.01). Second-degree atrioventricular block developed in 5 of 7 horses during infusion 3, and in 6 of 7 horses during infusion 4. Mean arterial blood pressure increased significantly from 118 +/- 11 mm of Hg at baseline to 146 +/- 27 mm of Hg at infusion 4. Similar responses were observed for mean pulmonary artery and right atrial pressures. Systemic vascular resistance (baseline, 182 +/- 28 mm of Hg.ml-1.min-1.kg-1) increased significantly during infusions 3 and 4 (to 294 +/- 79 and 380 +/- 58, respectively). Plasma atrial natriuretic peptide concentration was significantly increased with increasing detomidine concentration (20.4 +/- 3.8 pg/ml at baseline to 33.5 +/- 9.1 at infusion 4). There were few significant changes in respiration rate and arterial blood gas and pH values. We conclude that maintenance of steady-state detomidine plasma concentrations resulted in cardiopulmonary changes that were quantitatively similar to those induced by detomidine bolus administration in horses.