Middle carpal cartilage explants from 4 horses with mild osteoarthritis involving that joint were maintained in tissue culture to test the effects of a polysulfated glycosaminoglycan (PSGAG) on proteoglycan synthesis and degradation. Cultures were exposed to 0.025 or 25 mg of PSGAG/ml for 48 hours, after which the medium was replaced with medium containing similar doses of PSGAG and 35S. Subsequently, the sulfated proteoglycan content of the medium and extracts of the explants was measured. Gel filtration chromatography was used to estimate the size and to purify the principal, large proteoglycan monomer, which was further characterized by digestion, using glycosidic enzymes. In a second experiment, explants were incubated with 35S for 48 hours, and were subsequently exposed to the same concentrations of the PSGAG for an additional 48 hours. The amount of remaining labeled proteoglycan was determined for culture medium and cartilage extracts. Gel filtration chromatography was used to assess the hydrodynamic size of the large proteoglycan monomer. Aliquots of proteoglycans from the second experiment were incubated in high-molecular weight hyaluronate and chromatographed to assess reaggregation. Polysulfated glycosaminoglycan caused a significant (P < 0.04) decrease in sulfated proteoglycan synthesis by cartilage explants. Radioactive proteoglycan content in explants labeled prior to exposure to PSGAG were similar. Large proteoglycan monomer size was similar in both experiments (median partition coefficient [K(AV)] = 0.40), and was not influenced by PSGAG treatment. Prelabeled explants exposed to hyaluronate and chromatographed under associative conditions had similar proportions of the radiolabel eluting as proteoglycan aggregate. Enzymatic digestion of newly synthesized large monomer revealed a mild dose-dependent increase in the proportion of keratan sulfate substitution on core protein. It was concluded that PSGAG in vitro, at the dosages evaluated, caused a decre.

The effect of urine pH on plasma disposition of ampicillin sodium was evaluated. A single dose of 10 mg/kg of body weight was administered IV to Thoroughbreds with alkaline (pH > 8.0) or acidic (pH < 4.5) urine. Urine alkalinity was achieved and maintained by oral administration of up to 400 mg of sodium bicarbonate/kg/d, and acidity was achieved and maintained by oral administration of up to 400 mg of ammonium chloride/kg/d. Ampicillin sodium was measured in the plasma of horses by use of an agar diffusion microbiological assay with Bacillus subtilis as the test organism. The plasma disposition kinetics of ampicillin sodium best fitted a 2-exponential decay pattern, and statistically significant differences were not evident in elimination half-life, area under the plasma concentration time curve, volume of distribution, or body clearance rate between horses with alkaline or acidic urine. Results indicate that changes in urine pH over a range encountered in clinically normal horses are unlikely to affect plasma pharmacokinetic variables of ampicillin sodium after IV administration of the drug.

Viscosity of synovial fluid (SF) from 29 clinically normal horses was determined by use of a rotational cone and plate microviscosimeter. Total protein concentration in the SF of the 29 horses, as measured with a refractometer, was < 2.5 g/dl. When the Coomassie brilliant blue test was used to determine total protein concentration in SF for 15 horses, the mean value was 1,088 mg/dl. Viscosity values at 60, 30, 12, 6, 3, and 1.5 revolutions/min (rpm) spindle speed were 4.41 +/- 1.54 centipoise (cp), 5.29 +/- 1.94 cp, 6.76 +/- 2.76 cp, 8.52 +/- 4.27 cp, 10.41 +/- 6.30 cp, and 13.07 +/- 9.05 cp, respectively. Synovial fluid viscosity increased with decreasing rpm and shear rate, but the shape of the curve for each horse fitted the asymptotic curve. The rotational cone and plate microviscosimeter was an accurate instrument in measuring SF viscosity at multiple rpm or shear rates in horses. The values obtained on clinically normal horses in this study will serve as a baseline for comparison in the evaluation of horses with joint disease.

Four hours prior to exercise on a high-speed treadmill, 4 dosages of furosemide (0.25, 0.50, 1.0, and 2.0 mg/kg of body weight) and a control treatment (10 ml of 0.9% NaCl) were administered IV to 6 horses. Carotid arterial pressure (CAP), pulmonary arterial pressure (PAP), and heart rate were not different in resting horses before and 4 hours after furosemide administration. Furosemide at dosage of 2 mg/kg reduced resting right atrial pressure (RAP) 4 hours after furosemide injection. During exercise, increases in treadmill speed were associated with increases in RAP, CAP, PAP, and heart rate. Furosemide (0.25 to 2 mg/kg), administered 4 hours before exercise, reduced RAP and PAP during exercise in dose-dependent manner, but did not influence heart rate. Mean CAP was reduced by the 2-mg/kg furosemide dosage during exercise at 9 and 11 m/s, but not at 13 m/s. During recovery, only PAP was decreased by furosemide administration. Plasma lactate concentration was not significantly influenced by furosemide administration. Furosemide did not influence PCV or hemoglobin concentration at rest prior to exercise, but did increase both variables in dose-dependent manner during exercise and recovery. However, the magnitude of the changes in PCV and hemoglobin concentration were small in comparison with changes in RAP and PAP, and indicate that furosemide has other properties in addition to its diuretic activities. Furosemide may mediate some of its cardiopulmonary effects by vasodilatory activities that directly lower pulmonary arterial pressure, but also increase venous capacitance, thereby reducing venous return to the atria and cardiac filling.

Six nontrained mares were subjected to steady-state, submaximal treadmill exercise to examine the effect of exercise on the plasma concentration of atrial natriuretic peptide (ANP) in arterial, compared with mixed venous, blood. Horses ran on a treadmill up a 6 degree grade for 20 minutes at a speed calculated to require a power equivalent to 80% of maximal oxygen uptake. Arterial and mixed venous blood samples were collected simultaneously from the carotid and pulmonary arteries of horses at rest and at 10 and 20 minutes of exercise. Plasma was stored at -80 degrees C and was later thawed; ANP was extracted, and its concentration was determined by radioimmunoassay. Exercise caused significant (P < 0.05) increases in arterial and venous plasma ANP concentrations. Mean +/- SEM arterial ANP concentration increased from 25.2 +/- 4.4 pg/ml at rest to 52.7 +/- 5.2 pg/ml at 10 minutes of exercise and 62.5 +/- 5.2 pg/ml at 20 minutes of exercise. Mean venous ANP concentration increased from 24.8 +/- 4.3 pg/ml at rest to 67.2 +/- 14.5 pg/ml at 10 minutes of exercise and 65.3 +/- 13.5 pg/ml at 20 minutes of exercise. Significant differences were not evident between arterial or mixed venous ANP concentration at rest or during exercise, indicating that ANP either is not metabolized in the lungs or is released from the left atrium at a rate matching that of pulmonary metabolism.

Sixteen healthy ponies were inoculated IV with Ehrlichia risticii-infected P388D1 mouse monocytes. Of the 16 ponies, 15 developed clinical signs of equine ehrlichial colitis. Twenty-four hours after onset of fever (rectal temperature > 38.8 degrees C), 7 ponies were treated with 25 mg of erythromycin stearate/kg of body weight and 10 mg of rifampin/kg, given orally every 12 hours for 5 days. The remaining 8 ill ponies served as nontreated controls. All ponies were observed for progression of clinical signs typical of equine ehrlichial colitis. Within 12 hours of initiation of treatment, 4 of the 7 treated ponies had rectal temperature < 38.4 C and, within 24 hours, 6 of the 7 ponies had rectal temperature < 38.3C. In contrast, all control ponies had rectal temperature > 39.2 C at 24 hours (P < 0.05). Of the 7 treated ponies, 4 no longer had signs of mental depression after the second day of treatment, and only 1 of the 7 ponies had mild signs of depression after the third day of treatment. In contrast, control ponies had high mental depression score during the observation period (P < 0.05). Feed intake improved in ponies of the treatment group, with feed intake of 4 of the 7 ponies returning to normal; the other 3 ponies were only mildly anorectic by the second day of treatment. Control ponies progressively decreased their feed intake during the observation period (P < 0.05). One control pony and 2 treated ponies developed diarrhea before the treatment/observation period began. Only 1 treated pony developed diarrhea after treatment began. Of the 8 control ponies, 7 developed diarrhea. Profound decrease in borborygmal sounds with silent periods lasting longer than 3 minutes was observed in 7 of the 8 control ponies. Only 1 of the 7 treated ponies had such profound decrease in borborygmi (P < 0.05). The decrease in borborygmal sounds progressed in the control ponies during the observation period. None of the treated ponies continued to have decreased borborygmi after treatment day 2 (P < 0.05). Of the 8 control ponies, 2 were euthanatized; all treated ponies survived. In survivors, signs lasted 8 to 17 (mean, 10) days in control ponies but only 1 to 5 (mean, 2.9) days in treated ponies.

We compared the frequency and severity of osteochondrosis lesions in young Thoroughbred horses with cervical stenotic myelopathy (CSM) vs that in clinically normal Thoroughbreds of the same age. All lesions of the cervical vertebrae and appendicular skeleton were classified histologically as osteochondrosis or nonosteochondrosis and were measured for severity. Minimal sagittal diameter was significantly smaller in horses with CSM from C2 through C6; no difference was detected at C7. Severity of cervical vertebral osteochondrosis was greater in the horses with CSM, however frequency was not different. Frequency and severity of nonosteochondrosis lesions were not different in cervical vertebrae or appendicular skeleton. Frequency and severity of appendicular skeleton osteochondrosis lesions were both greater in horses with CSM. Osteochondrosis and nonosteochondrosis lesions were more severe on facets at sites of compression than on facets at noncompressed sites in horses with CSM. However, compression was also observed at sites with no articular facet lesions. The association of widespread osteochondrosis and spinal canal narrowing with CSM suggests CSM may represent a systemic failure in the development or maturation of cartilage and bone.

Microvascular circulation of the ascending colon in healthy horses was studied using microangiography, light microscopy, and scanning electron microscopy. The pelvic flexure with 30 cm of ventral and dorsal colon attached was removed from 14 adult horses immediately after horses were euthanatized. The lumen was flushed with warm water, and this section of the ascending colon was placed in a 37-C bath of isotonic NaCl. In sections from 8 horses, colic vessels were perfused with a radio-opaque medium for microangiography. After angiographic evaluation, tissue sections were prepared for light microscopic observation, using standard histologic methods. In sections from 6 horses, injection replicas were made by perfusing the vessels with 2 types of plastics. The results of microangiography, light microscopy, and scanning electron microscopy of vascular replicas were correlated, providing acomprehensive documentation of the microvasculature of the ascending colon at the pelvic flexure. Arteries branched from mesenteric colic vessels approximately every 2 cm toward the colonic tissue. Immediately after branching, arterial vessels formed an anastomotic plexus, the colonic rete. However, each branch from the colic vessel eventually continued into the colonic tissue. A second set of vessels originated from the colonic rete and supplied the mesenteric lymph nodes. Arterial vessels penetrated the tunica muscularis into the sub-mucosa 3 to 4 cm toward the antimesenteric border forming a submucosal vascular network. From the submucosal arterioles, branching took place at right angles to supply the mucosal capillaries. Capillaries surrounded the colonic glands and anastomosed at the luminal surface, forming a superficial luminal honeycomb-appearing vascular plexus. Venules, sparsely distributed, drained the superficial plexus. Arterial venous anastomoses were not observed within the mucosa.