The role of platelet-activating factor in mediating the cardiovascular and peripheral cellular responses to large-colon ischemia and reperfusion, was explored in anesthetized ponies. A specific platelet. activating factor (PAF) antagonist (WEB 2086) was administered to a group of 6 ponies, and another 6 ponies (controls) were given an equivalent volume of saline solution, prior to 1 hour of large-colon torsion. After correction of the torsion, ponies were monitored during the reperfusion period. Significant (P < 0.05) hypotension and metabolic acidosis developed in afl ponies after correction of colonic torsion, cardiac index increased initially, but then decreased significantly (P < 0.05) over the study period. Mean times between correction of torsion and onset of cardiac failure and death were not different between groups. Significant (P < 0.05) thrombocytopenia developed during the reperfusion period in control ponies, but not in WEB-treated ponies. Blood leukocyte concentration in control ponies was more variable and significantly (P < 0.05) decreased immediately upon reperfusion, compared with that in WEB-treated ponies. We conclude that although the cardiovascular responses to colonic ischemia and reperfusion are not prevented by use of a specific PAF-antagonist, specific peripheral cellular responses are mediated by PAF.

Transcutaneous oxygen (PO2.TC) monitoring is commonly used in human medicine for evaluating skin viability. The application of transcutaneous monitoring for evaluating skin viability in dogs was investigated. The changes in PO2-TC values were measured from 16 avascular skin flaps created along the lateral hemithoraces of 4 dogs. Transcutaneous oxygen values were serially recorded from the vascular base and avascular apex of each flap for 12 hours after surgery. A single transcutaneous measurement was obtained from each flap base and apex 24 hours after surgery. Serial arterial blood gas analyses were obtained to compare central oxygen values with PO2-TC values. Full-thickness skin biopsy specimens were harvested from the base and apex of each flap 24 hours after surgery. The flaps were observed for 4 days and then excised for histologic examination. A subjective grading scale was used to assess histologic changes. Throughout the 12-hour period and at 24 hours, a statistically significant difference was found between the PO2-TC values for apices and bases of the flaps. The mean PO2-TC for all bases was 90.9 mm of Hg +/- 3.3 SEM, and the mean PO2-TC for all apices was 21.2 mm of Hg +/- 1.8 SEM. The mean regional perfusion index (apex PO2.TC/base PO2-TC) was 0.23 +/- 0.02. The subjective numbers assigned to the biopsy specimens were statistically evaluated by using a paired Student's t test and a Wilcoxon signed-rank test. A significant difference was found between the numbers for the collective bases and apices with both tests. A statistically significant difference was found between the numbers for the apex biopsy specimens taken 24 hours after creation of the skin flap and those taken when the flap was excised, whereas no difference was found between the numbers for the base biopsy specimens. On the basis of our findings, PO2-TC monitoring is a useful technique for assessing skin viability in dogs.

In horses with noninduced, reversible airway obstruction (heaves), pulmonary function is improved after sedation with the alpha-adrenergic agonist xylazine. The mechanism of this effect is undetermined. Because the predominant excitatory innervation of equine airways is cholinergic, the influence of alpha 2-adrenergic receptor stimulation on the response of isolated distal airways to cholinergic stimulation was determined. Distal bronchial segments from 22 healthy horses were suspended in isolated organ baths where their mechanical responses to various stimuli could be studied. Each tissue was incubated with one of several concentrations of clonidine, clonidine vehicle, or clonidine plus tolazoline. Then, the contractile response of the tissues to either cumulative acetylcholine (ACh) addition or cumulative electrical field stimulation (EFS) was recorded. All contractile responses evoked by EFS were mediated through stimulation of cholinergic airway nerves. Clonidine had no effect on the contractile response of distal airway segments to exogenous ACh. However, clonidine (at concentrations > 10(-5) M) significantly (P < 0.05) diminished the contractile response of the distal airway segments to EFS. This inhibitory effect of clonidine was not observed in the presence of tolazoline. Similar results were observed when the less-selective alpha 2-adrenergic agonist xylazine was exposed to the isolated segments instead of clonidine. Because EFS-but not exogenous ACh-induced contractions were inhibited, alpha 2-adrenergic receptor stimulation apparently causes presynaptic inhibition of the cholinergic nerves innervating distal portions of the bronchi of horses.

The purpose of this study was to investigate the mechanism by which 5-hydroxytryptamine (5-HT) modifies respiratory function, specifically, hyperventilation, diffuse bronchoconstriction, and pulmonary arterial hypertension in cattle. We determined whether the IV response to 5-HT in calves was attributable to stimulation of 5-HT2 receptors. Six healthy unsedated young bull calves of the Friesian (n = 4) and of the Belgian White and Blue (n = 2) breeds were used. A specific 5-HT2 antagonist (metrenperone, 0.05 mg/kg of body weight) was administered IM 30 minutes before the cattle were given a 5-minute IV 5-HT infusion. Pulmonary function values were registered before, during, and after the 5-HT challenge infusion. Minute volume increased significantly, because of an increase in respiratory rate. Conversely, lung dynamic compliance, total pulmonary resistance, and pulmonary arterial pressure were not changed. We concluded that in cattle, 5-HT-induced ventilatory response is not mediated through activation of 5-HT2 receptors. However, the 5-HT2 receptors are involved in 5-HT-induced broncho- and pulmonary vasoconstriction.

Prednisone was administered orally for 4 weeks at a dosage of 1.1 mg/kg of body weight/d, in divided dose every 12 hours, to a group of healthy adult dogs (n = 12). Intravenous glucose tolerance testing was performed before and after the 28-day regimen in each dog, as well as in dogs of a control group (n = 6). Glucose metabolism was evaluated by measurement of preprandial plasma insulin and glucose concentrations, total insulin secretion, and fractional clearance of glucose. Mean preprandial plasma insulin and glucose concentrations were not increased after the 4-week regimen of prednisone. Total insulin secretion in response to an IV administered glucose load was not increased in treated dogs, compared with pretreatment values or with values for control dogs. The fractional clearance of glucose was also not altered in dogs given prednisone. Results indicate that anti-inflammatory doses of prednisone, given orally for 4 weeks, probably do not alter insulin sensitivity or glucose tolerance in clinically normal dogs.

The sodium-dependent transporter system responsible for L-glutamine uptake by brush border membrane vesicles prepared from equine jejunum was characterized. Vesicle purity was ascertained by a 14- to 17-fold increase in activity of the brush border enzyme markers. Glutamine uptake was found to occur into an osmotically active space with negligible membrane binding. The sodium-dependent velocity represented approximately 80% of total uptake and demonstrated overshoots. Kinetic studies of sodium-dependent glutamine transport at concentrations between 5 micromolar and 5 mM revealed a single saturable high-affinity carrier with a Michaelis constant of 519 +/- 90 micromolar and a maximal transport velocity of 3.08 +/- 0.97 nmol/mg of protein/10 s. Glutamine uptake was not affected by changes in environmental pH. Lithium could not substitute for sodium as a contransporter ion. 2-Methylaminoisobutyric acid inhibited the sodium-dependent carrier only minimally, but marked inhibition (> 90%) was observed in the presence of histidine, alanine, cysteine, and nonradioactive glutamine. Kinetic analysis of the sodium-independent transporter revealed it to have a Michaelis constant = 260 +/- 47 micromolar and a maximal transport velocity of 0.32 t 0.06 nmol/mg of protein/10 s. We conclude that glutamine transport in equine jejunal brush border membrane vesicles occurs primarily via the system B transporter and, to a lesser extent, by a sodium-independent carrier.

Complete atrioventricular block was induced in 26 pentobarbital-anesthetized dogs to determine the effects of the alpha 2-adrenergic receptor agonists, xylazine and medetomidine, on supraventricular and ventricular automaticity. Prazosin and atipamezole, alpha-adrenoceptor antagonists, were administered to isolate alpha 1- or alpha 2-adrenoceptor effects. Six dogs served as controls and were given glycopyrrolate (0.1 mg/kg of body weight, IV) and esmolol (50 to 75 microgram/kg/min, IV) to induce parasympathetic and beta 1-adrenergic blockade, respectively. Eight dogs were given sequentially increasing doses of xylazine (n = 5), 0.000257 mg (10(-9)M) to 25.7 mg (10(-4)M) and medetomidine (n = 3), 0.000237 mg (10(-9)M) to 2.37 mg (10(-5) < M) after parasympathetic and beta 1-adrenergic blockade. Twelve dogs were given xylazine (n = 6, 1.1 mg/kg, IV) or medetomidine (n = 6, 0.05 mg/kg, IV) after parasympathetic and beta 1-adrenergic blockade. Three dogs given xylazine and 3 dogs given medetomidine were administered prazosin (0.1 mg/kg, IV) followed by atipamezole (0.3 mg/kg, IV). The order of prazosin and atipamezole was reversed in the remaining 3 dogs given either xylazine or medetomidine. Complete atrioventricular block and administration of glycopyrrolate and esmolol resulted in stable supraventricular and ventricular rates over a 4-hour period. Increasing concentration of xylazine or medetomidine did not cause significant changes in supraventricular or ventricular rate. Xylazine and medetomidine, in the presence of the alpha-adrenoceptor antagonists, prazosin (alpha(1)) and atipamezole (alpha(2)), did not cause significant changes in supraventricular or ventricular rate. alpha 2-Adrenoceptor agonists do not induce direct alpha 1- or alpha 2-adrenoceptor-mediated depression of supraventricular or ventricular rate in dogs with complete atrioventricular block.

Power spectral analysis and digital filtering of brain stem auditory evoked potentials (BAEP) were performed in dogs. The BAEP were recorded in 7 dogs, using alternating clicks at frequency of 20 Hz. The clicks were delivered monaurally at intensity of 90-dB normal hearing level. Power spectral analysis indicated that the frequency compositions of the averaged responses were divisible into 4 frequency bands: A (30 to 390 Hz), B (390 to 680 Hz), C (680 to 910 Hz) and D (910 to 1960 Hz). The frequency limits of digital high-pass (HP) and low-pass (LP) filters, at which neither peak-to-peak nor absolute amplitudes were reduced, were 1,170 and 1,270 Hz for P1, 290 and 1,170 Hz for P2, 290 and 980 Hz for P3, 290 and 980 Hz for P4, and 200 and 880 Hz for P5, respectively. The dual structure of BAEP was confirmed in dogs. Below 200 Hz for the HP filter, peak-to-peak and absolute amplitudes of afl waves were not significantly reduced. Therefore, this frequency may be a boundary frequency between low- and high-frequency components of BAEP in dogs. The main source for the high- frequency components that constituted each positive peak and the following trough was derived from frequency bands C and D. The frequency limits of 200 Hz for a digital HP filter and of 1,270 Hz for a digital Lp filter, at which amplitudes of aU waves were not reduced, support the analog filter settings recommended for dogs (ie, less than and qual to 53 and 3,000 Hz for analog HP and LP filters, respectively).

Plasma concentrations of hypoxanthine, uric acid, and allantoin, which are breakdown products of adenine nucleotides, were measured in Standardbred and Finnhorse trotters during and after an exercise test on a high-speed treadmill, after an incremental exercise test performed on a racetrack, and after a racing competition. Fiber-type composition of the middle gluteal muscle and the muscle concentrations of adenine nucleotides and inosine monophosphate were measured after the racetrack test. Changes in the concentration of hypoxanthine were not observed in any of the tests. Peak concentration of uric acid was measured between 5 and 30 minutes after exercise, and it was three- to tenfold higher than the value at rest. The variability can be explained by intensity of the exercise test and variation among horses. The concentration of allantoin after exercise was 2 to 3 times as high as that at rest, depending on the intensity of the exercise, although the absolute increase was about 10 times as high as the increase in the concentration of uric acid. Peak values of allantoin for the treadmill and the racetrack tests were obtained 4 to 6 minutes after exercise and < 30 minutes after the races. Peak concentration of allantoin correlated positively with the percentage of type-II (IIA + IIB) fibers in the middle gluteal muscle. Significant correlations were not observed between plasma concentration of uric acid or allantoin and muscle concentrations of adenosine triphosphate (ATP) or inosine monophosphate. It can be concluded that in horses, breakdown of ATP during and after exercise continues until allantoin is produced. The peak concentration of allantoin increases with the intensity of exercise, is reached rapidly after exercise, and the variation in the time to the peak value is small among horses. It is suggested that the main source of allantoin is the fast-twitch, type-II fibers and that the mixed muscle concentrations of adenine nucleotides are of limited value when estimating the effects of exercise on ATP content of the muscle tissue.

Random fragments of DNA were obtained from a cosmid library of Salmonella agona genomic DNA. from this library, 2 fragments were chosen and pooled to probe isolates of S typhimurium obtained during an episode of salmonellosis in a veterinary medical teaching hospital. Chromosomal DNA from the Salmonella isolates was digested with restriction endonucleases, and was probed with the random fragments of chromosomal DNA. This procedure resulted in a fingerprint pattern for each isolate. We found that the method permitted discrimination between isolates involved in the disease episode and S typhimurium obtained prior to the episode. We conclude that random fragments of chromosomal DNA are useful for fingerprinting isolates of S typhimurium. Analysis of plasmid DNA obtained from the isolates was not as useful. Some isolates found to be identical by restriction site analysis, had plasmids of different molecular weight. These results indicate that plasmid analysis may not be as useful a fingerprinting tool as previously reported.