Atracurium besylate, a nondepolarizing neuromuscular blocking agent, was administered as an infusion to 8 anesthetized cats in which neuromuscular blockade was assessed, using the train-of-four response. Once 50% depression of the first-twitch (T1) response was achieved, the infusion was held constant for 60 minutes before being discontinued and the recovery time was determined. The time for recovery was recorded as the time for the train-of-four ratio (T4 ratio) to increase from 50% to 75%. After recovery, atracurium infusion was reinstituted and the cats were again maintained for 60 minutes at 50% depression. A single bolus of gentamicin sulfate (2.0 mg/kg of body weight) was administered IV, and the infusion was continued for another 60 minutes before it was discontinued and the time for recovery was recorded. Within 1 minute of gentamicin administration, the mean +/= SD T1 response decreased from 49 +/- 5% to 33 +/- 8% of baseline and the T4 ratio decreased from 28 +/- 19% to 14 +/- 11%. Peak effect occurred at 5 minutes, with a T1 response of 29 +/- 6% of baseline and a T4 ratio of 13 +/- 12%. By 60 minutes after gentamicin administration, the T1 response had increased to 38 +/- 7% of baseline and the T4 ratio had increased to 21 +/- 13%. The time for recovery significantly (P less than 0.03) increased from 9.9 +/- 3.4 minutes during the control study to 18.1 +/- 10.7 minutes during the gentamicin study. In this study, gentamicin potentiated the neuromuscular blockade induced by atracurium and increased the recovery time. Residual blockade, observed after gentamicin administration was reversed with edrophonium.

Autologous tissue transmission of spontaneously developing feline eosinophilic plaques was attempted in 5 cats. Macerated tissue from the plaque was vigorously rubbed onto 2 scarified skin sites in each cat. The inoculated areas were observed daily for 30 days. During that time, no clinical or histologic evidence of transmission was found.

A study was designed to determine whether phenytoin (PHE) prevents the myocardial necrosis and subsequent fibrosis produced by isoproterenol (ISO). Seven groups of female rats of the Wistar strain were used. Rats in groups 1 and 5 served as controls. Rats in group 3 were injected SC with 85 mg of ISO/kg of body weight for 2 consecutive days. Rats in groups 2 and 6 received 100 mg of PHE/kg orally. Rats in groups 4 and 7 received both PHE and ISO. There were 6 to 9 rats/group. Effects of ISO and PHE were evaluated gravimetrically, histologically, and electrocardiographically. Heart weight/body weight ratios for each group receiving ISO, with or without PHE, were greater than for groups not receiving ISO (P < 0.05). Light microscopic examination of heart sections of rats given ISO alone or ISO + PHE revealed multiple and diffuse areas of fibrosis. Fibrosis in hearts from rats receiving PHE + ISO was less severe than that in hearts from rats receiving ISO alone, but the difference was not statistically significant. Electrocardiographic changes of statistical significance were not observed in rats receiving any compound (alone or in combination), when compared with the control groups of equal age.

The growth hormone (GH) secretagogue activity of variable dosages of clonidine (16.5, 50, 150, and 450 microgram/kg of body weight), given orally mixed with the daily food ration, was evaluated in young and old dogs. Significant (P < 0.05) increase in plasma GH concentration was detected at all dosages tested in young dogs and in response to all but the lowest dose tested in the old dogs fed the clonidine-containing diet. Old dogs had plasma GH concentration that exceeded that of young dogs when higher doses of clonidine were used. A clonidine (100 microgram/kg)-supplemented diet was fed to middle-aged dogs twice daily for 30 days. Significant (P < 0.01) increase of plasma GH concentration was observed on the first day of the feeding trial, but was undetectable by day 30. After feeding the clonidine-enhanced diet for 30 days, the effects on thymic morphology were variable, and there was no effect on plasma thymulin titer. Clonidine-fed dogs had significantly increased lymphocyte blastogenic responsiveness to mitogens, compared with that of control dogs, when evaluated as stimulation index.

A radiopaque marker was injected, using needles of various lengths, into the cervical musculature, the lumbar epaxial musculature, and the cranial and caudal muscular masses of the thighs of anesthetized dogs. After this procedure, the dogs were euthanatized and deep-frozen. The bodies were then sectioned, and the slices were radiographed to determine the fate of the injected material. Material that was injected into the neck or caudal region of the thigh was determined to be located in the muscle bellies or dispensed throughout the intermuscular fascial sheaths. In contrast, material injected into the lumbar area and cranial region of the thigh was located entirely in the muscle bellies. It was concluded that the best sites for injection in dogs are the lumbar epaxial musculature or the quadriceps femoris muscle when IM administration is imperative.

Samples of pleural fluid from 20 horses with effusive pleural diseases of various causes were evaluated; samples from 19 horses were used for the study. There were differences for pH (P = 0.001) and partial pressure of oxygen (P(O2)) between arterial blood and nonseptic pleural fluid (P = 0.0491), but there were no differences for pH, P(O2), partial pressure of carbon dioxide (P(CO2)) and concentrations of bicarbonate (HCO3-), lactate, and glucose between venous blood and nonseptic pleural fluid. Paired comparisons of venous blood and nonseptic pleural fluid from the same horse indicated no differences. There were differences (P = 0.0001, each) for pH, P(O2), P(CO2), and concentrations of HCO3- between arterial blood and septic pleural fluid. Differences also existed for pH (P = 0.0001), P(CO2) (P = 0.0003), and concentrations of HCO3- (P = 0.0001), lactate (P = 0.0051), and glucose (P = 0.0001) between venous blood and septic pleural fluid. Difference was not found for values of P(O2) between venous blood and septic pleural fluid, although 4 samples of septic pleural fluid contained virtually no oxygen. Paired comparisons of venous blood and septic pleural fluid from the same horse revealed differences (P < 0.05) for all values, except those for P(O2). These alterations suggested functional and physical compartmentalization that separated septic and healthy tissue. Compartmentalization and microenvironmental factors at the site of infection should be considered when developing therapeutic strategies for horses with septic pleural disease.

Areas of skin vascularized by large axial vessels potentially suitable for microvascular anastomosis were investigated in 10 horse cadavers. Eleven such areas were dissected, and the skin over the flank region vascularized by the deep circumflex iliac artery was most suitable. The anatomy of this area was further defined, using angiography and latex injection studies on 10 cadavers.

During the first part of a study, cats were inoculated with Cryptococcus neoformans via the following routes: intradermal, intranasal, IV, and intracisternal. Only use of the IV route of inoculation consistently induced disseminated cryptococcosis. In the second part of the study, disseminated cryptococcosis was experimentally induced in cats via IV inoculation of C neoformans. One month after inoculation, 3 cats were treated with ketoconazole (10 mg/kg of body weight/d) and 3 cats were treated with itraconazole (10 mg/kg/d) for 3 months. One of the ketoconzole-treated and 2 of the itraconazole-treated cats also had cryptococcosis of the CNS when treatment was begun. During treatment, serum cryptococcal antigen titer progressively decreased in all cats. Abnormalities in CBC values or the serum biochemical profile were not found in any cat during treatment. However, all ketoconazole-treated cats became anorectic and lost weight. Side effects were not seen in itraconazole-treated cats. During the 3-month posttreatment observation period, all cats remained healthy. At necropsy, histologic evidence of cryptococcosis was not found in the 3 ketoconazole-treated cats or in 2 of the itraconazole-treated cats. In the third itraconazole-treated cat, cryptococcal organisms were found in the kidneys.

A study was conducted to determine whether subcomponent proteins (previously identified as BCSP20, BCSP3l, and BCSP45, and the corresponding recombinant proteins rBCSP20, rBCSP31, and rBCSP45) that were recovered from the cell surface of Brucella abortus strain 19 were immunogenic and protective for mice when compared with Brucella cell surface protein (BCSP) and with a proteinase K-treated lipopolysaccharide (PKLPS) extracted from B abortus strain 2308. Protection was evaluated after challenge exposure with a virulent culture of B abortus strain 2308, using CD-1 or BALB/c mice or both inoculated with vaccines of various combinations and concentrations, with and without PKLPS or BCSP. Protection was assessed by enumeration of splenic colony-forming units, reduced mean splenic weight relative to controls, and the relative serologic responses (immune response) in an ELISA. The general results indicate that BCSP, PKLPS, BCSP20, and BCSP31 are immunogenic or protective or both. Protectiveness was not observed for each of the recombinant proteins; however, results from the combined recombinant protein vaccine study suggest the immunogenicity of the recombinant proteins. The apparent immune-inducing properties of BCSP20 and BCSP3l are thought to be attributable to the presence of an immunogenic and protective BCSP fraction (possibly lipopolysaccharide) still associated. Serologic results support our conclusion that each of the recombinant protein vaccines did not induce a protective response comparable to that of BCSP or PKLPS, even when the subcomponents were combined. Although the results suggest that the subcomponents of BCSP apparently induced partial protection, they are thought to be only a part of the antigens contained in BCSP that influence the serologic response. Our findings may serve as an experimental model to determine the mechanisms involved in the protective responses induced by Brucella antigens.

Evoked potentials were induced by transcranial stimulation and recovered from the spinal cord, and the radial and sciatic nerves in six dogs. Stimulation was accomplished with an anode placed on the skin over the area of the motor cortex. Evoked potentials were recovered from the thoracic and lumbar spinal cord by electrodes placed transcutaneously in the ligamentum flavum. Evoked potentials were recovered from the radial and sciatic nerves by surgical exposure and electrodes placed in the perineurium. Signals from 100 repetitive stimuli were averaged and analyzed. Waveforms were analyzed for amplitude and latency. Conduction velocities were estimated from wave latencies and distance traveled. The technique allowed recovery of evoked potentials that had similar characteristics among all dogs. Conduction velocities of potentials recovered from the radial and sciatic nerves suggested stimulation of motor pathways; however, the exact origin and pathway of these waves is unknown.