Effects of IV and aerosol administration of 5-hydroxytryptamine (5-HT) on ventilation, pulmonary mechanics values, pulmonary arterial pressure, and heart rate were investigated in healthy unsedated Friesian calves. Minute volume increased significantly, mainly because of an increase in respiratory rate. Except for total pulmonary resistance after bolus injection, continuous administration of 5-HT given by either route caused significant alterations of lung dynamic compliance and total pulmonary resistance, the former decreasing to one-fifth of its baseline value and the latter increasing twofold. Pulmonary arterial pressure increased significantly, whatever the speed or route of administration. Administration of a bolus did not affect heart rate, whereas continuous iv administration of 5-HT as well by perfusion or by aerosol resulted in sustained tachycardia. It was concluded that 5-HT induces reversible bronchoconstriction and pulmonary vasoconstriction in healthy unsedated calves, 5-HT-induced functional alterations depend on the speed of administration, and excess of 5-HT production or depression in uptake by the lungs during bovine respiratory tract diseases could contribute to pulmonary dysfunction.

Newborn pups from 4 large litters were allotted to 6 groups to determine effect of time and route of administration on absorption of an alternate source of immunoglobulin. Selective absorption of specific classes of immunoglobulins was also investigated. The alternate source of immunoglobulin consisted of pooled serum that was administered either PO or SC. Control groups were either left with the dam (group C1) or fed milk replacer (group C2). Blood samples were collected from pups at birth and 24 hours. Immunoglobulin (IgA, IgG, IgM) concentrations were determined by use of radial immunodiffusion on samples of pooled serum, colostrum, and pups' serum (birth and 24 hours). Serum IgA concentration was less than the sensitivity of the procedure and was not included in the statistical analysis. Pups fed 8 ml of pooled serum at birth and 12 hours later (group T1) absorbed more (P < 0.05) IgG and IgM than did group-C2 pups, but less (P < 0.05) than did group-C1 pups. Pups fed 8 ml of pooled serum at 12 hours only had significant (P < 0.05) increase of IgG concentration, but no absorption of IgM (P > 0.05) at 24 hours, compared with control pups (group C2). Pups administered 8 ml of pooled serum SC at birth (group SC1) had similar (P > 0.05) absorption of IgG and higher (P < 0.05) absorption of IgM than did pups of group T1. Pups administered 16 ml of pooled serum SC at birth had the highest increase of IgG and IgM concentrations of all treatment groups, but immunoglobulin concentrations were lower (P < 0.05) than those for group-C1 pups. Absorption of IgG was favored, compared with IgM, when pooled serum was fed. Results indicate clearly that intestinal absorption of immunoglobulins is minimal after 12 hours and thus, another route of administration should be used. Pups in groups SC1 and T1 had similar absorption of IgG, despite lower IgM absorption in pups of group T1. This lower IgM concentration in group-T1 pups may have been the result of selective intestinal absorption or the consequence of low number of pups per group. Subcutaneous administration of 16 ml of pooled serum was the most successful alternative to colostrum, with minimal pain to pups if serum was administered slowly. Serum IgG concentration in C1 pups was higher than expected and probably was attributable to the amount of colostrum available to the pups.

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.

Contact wide-field specular microscopy was performed on eyes of 16 healthy dogs after tissue plasminogen activator at a concentration of 25 microgram/100 (group 1, n = 8) or 50 microgram/100 microliter (group 2, n = 8) was injected into 1 anterior chamber of each dog. The contralateral eye served as a nontreated control. Applanation tonometry was used to measure intraocular pressure in both eyes for up to 168 hours. By use of computerized morphometric analysis and pachymetry, changes from baseline values in endothelial cell density, cell morphologic features, and corneal thickness were evaluated at postinjection, hours 24, 48, and 168. Significant mean differences in intraocular pressure were not detected between treated eyes of group-1 dogs and those in group 2 at designated times, or between treated and nontreated eyes of dogs in either group. Mean corneal thickness of treated and nontreated eyes was similar in both groups through postinjection hour 168. Changes in mean percentage of endothelial cell sides were observed only in treated eyes of group-2 dogs, with the mean percentage of hexagons at postinjection hour 168 decreasing by 18%, a decrease that was significantly (P < 0.05) greater than the decrease in nontreated eyes. The mean percentage of 6-sided cells in treated eyes of group-2 dogs was significantly (P < 0.05) less than that in treated eyes of group-1 dogs at postinjection hour 168.

Communications between the femoropatellar, medial femorotibial, and lateral femorotibial joints were studied, using fresh equine cadaver specimens. A total of 90 specimens from 45 horses were used. Horses were randomly assigned to 3 groups with 15 horses/group. Each group was assigned an injection site (femoropatellar joint, medial femorotibial joint, or lateral femorotibial joint), and red latex was injected into the respective location of each joint in each group. Immediately after injection, the joints were flexed and extended 100 times. The stifles were frozen in slight flexion, then cut into 1-cm sagittal sections. The communications between the femoropatellar and medial and lateral femorotibial joints were determined. None of the specimens in this study had communication between afl 3 joint compartments. When the femoropatellar joint was injected, 18 of 30 joints (60%) communicated with the medial femorotibial joint, and 1 of 30 (3%) communicated with the lateral femorotibial joint. Injection of the medial femorotibial joint revealed 24 of 30 (80%) joints that communicated with the femoropatellar joint, and 1 of 30 (3%) that communicated with the lateral femorotibial joint. Injection of the lateral femorotibial joint resulted in communication with the femoropatellar joint in 1 of 30 (3%) joints. Communication did not exist between the medial and lateral femorotibial joints.

Three doses of sodium monoiodoacetate (MIA) were used to induce degenerative changes in articular cartilage in middle carpal joints of horses. Twelve young (2- to 5-year-old) horses, free of lameness, were randomly allotted to 3 groups. One middle carpal joint of each horse was injected with 0.9% NaCl solution (control joint). The contralateral middle carpal joint was injected with 0.09 mg of MIA/kg of body weight (group 1); 0.12 mg(kg (group 2); or 0.16 mg(kg (group 3). After MIA administration, horses were allowed ad libitum exercise in a 2-acre paddock for 12 weeks. At the end of the study, gross and microscopic tissue changes were evaluated and biochemical analyses of articular cartilage were done. Grossly, diffuse partial-thickness articular cartilage lesions were observed in group-2 (n = 2) and group-3 (n = 4) horses, but not in group-1 horses. Articular cartilage uronic acid content was significantly (P < 0.03) decreased in all MIA-injected joints, compared with controls. Articular cartilage matrix staining with safranin-O was decreased in 3 of 4 MIA-injected joints of group-1 horses and in all MIA-injected joints of group-2 and group-3 horses, compared with controls (P < 0.06). Microscopic degenerative changes in articular cartilage were not significantly different between MIA-injected and control joints in group-1 horses, but were increased (P < 0.06) in all MIA-injected joints of group-2 and group-3 horses, compared with controls. Qualitatively, decreased matrix staining and degenerative changes were more severe in group-3 horses. On the basis of articular cartilage gross and microscopic changes, as well as biochemical changes, 0.12 mg of MIA/kg injected intra-articularly was determined to induce moderate degrees of articular cartilage degeneration. This model of chemically induced articular cartilage injury could be useful for evaluating treatment effects of anti-arthritic drugs in horses.