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SUMMARY

In dogs, gastric dilatation-volvulus (gdv) is characterized by cardiogenic shock, with resulting hypoperfusion. Treatment goals include reperfusion of transiently ischemic tissues, which indicates that reperfusion injury may be a factor in the physiopathogenesis of gdv. Recently, we obtained data that indicate that reperfusion injury may be involved in experimentally induced gdv. Using this gdv model, we evaluated mortality in 24 dogs of 4 equal groups, treated with deferoxamine (an iron chelator), dimethylsulfoxide (a free radical scavenger), a combination of the 2 drugs, or isotonic saline solution. All 6 dogs that were given deferoxamine survived; however, 3 dogs of the dimethylsulfoxide-treated group, 2 dogs of the combination-treated group, and 4 dogs of the saline-treated group died. Results of the study indicate that mortality associated with experimentally induced gdv is reduced by appropriate and timely pharmacologic intervention to prevent or attenuate reperfusion injury, and that deferoxamine may be more effective than dimethylsulfoxide.

Free access
in American Journal of Veterinary Research

Summary

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 MlA/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 MlA-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.

Free access
in American Journal of Veterinary Research

SUMMARY

A mucosal lesion was created in the center of each test sinus of 6 mature, healthy, nonlactating Holstein cows by resecting a circumferential band of mucosa. Each lesion was then treated by implantation of strip grafts of autogenous oral mucosa, temporary silastic tube implant, or a combination of strip grafts and temporary silastic tube implant. All teats were evaluated for patency 6 weeks after treatment, and tube implants were removed through a second thelotomy incision. All teats were reevaluated for gross and radiographic patency 12 weeks after treatment, and teats were collected for histologic evaluation of lesions. All 4 teats treated with grafts only were obstructed at 6 and 12 weeks after treatment. Incomplete coverage of the lesion with mucosa was observed in all 4 teats. The major source of obstruction was proliferation of epithelium and keratin into the lumen. All 8 teats treated with temporary silastic tube implants alone were patent at 6 weeks after treatment, but were obstructed at 12 weeks after treatment. Foci of mucosa at the lesion site were detected in only 2 of the 8 teats. Obstruction resulted from proliferation of granulation tissue into the lumen. All 12 teats treated with grafts and a temporary tube implant were patent at 6 weeks after treatment and 11 of 12 were patent at 12 weeks after treatment, although marked luminal narrowing was evident in 9 of 11 teats. Partial to complete coverage of the lesion with mucosa was seen in all teats. Proliferative granulation tissue, epithelium, and keratin contributed to luminal narrowing in 10 of 11 patent teats. Bacteriologic culture of quarters from 6 of the 11 teats patent at the final evaluation yielded pathogens.

Free access
in American Journal of Veterinary Research

Summary

Sixteen horses were allotted at random to 3 groups: vehicle only; low dosage (vehicle and 3 mg of U-74389G/kg of body weight); high dosage (vehicle and 10 mg of U-74389G/kg). These solutions were given prior to reperfusion. The ascending colon was subjected to 2 hours of ischemia followed by 2 hours of reperfusion. Before, during, and after ischemia, full-thickness colonic tissue biopsy specimens were obtained for measurement of malondealdehyde (mda) concentration and myeloperoxidase activity and for morphologic evaluation.

Although increases were not significant, mda concentration and myeloperoxidase activity increased during ischemia and reperfusion. Administration of U-74389G did not have significant effects on mda concentration and myeloperoxidase activity. However, the lower dosage tended (P = 0.08) to reduce myeloperoxidase activity at 30 and 60 minutes of reperfusion.

In horses of the vehicle-only group, ischemia induced a decrease in mucosal surface area that was continued into the reperfusion period (P ≤ 0.05). Administration of U-74389G at both dosages (3 and 10 mg/kg) prevented the reperfusion-induced reduction in mucosal surface area, which was significant at 60 minutes (high dosage; P = 0.05) and 90 minutes (low and high dosages; P = 0.02). After initial reduction in horses of all groups, mucosal volume increased for the initial 60 minutes of reperfusion.

Our results indicate that lipid peroxidation may be partially involved in continued cellular death after ischemia of the ascending colon of horses. The 21-aminosteroid, U-74389G, prevented further loss of mucosa and partially attenuated the induced increase in myeloperoxidase activity during reperfusion of the ascending colon.

Free access
in American Journal of Veterinary Research

Abstract

Objective

To determine the effects of the 21-amino-steroid, U-74389G, on reperfusion of the equine jejunum, using total (TVO) and partial (PVO) vascular occlusion during the ischemic period.

Design

TVO: 16 healthy horses were randomly allotted to 3 groups—4 horses received the vehicle alone, 6 horses received a low dosage (3 mg/kg of body weight), and 6 horses a high dosage (10 mg/kg) of U-74389G. PVO: 10 healthy horses were randomly allotted to 2 groups—5 horses received the vehicle alone, and 5 horses received the low dosage (3 mg/kg) of U-74389G.

Procedure

TVO was induced for 1 hour followed by 2 hours of reperfusion. During PVO, blood flow was reduced to 20% of baseline for 2 hours, followed by 2 hours of reperfusion.

For both models, either the vehicle alone or the drug was given 15 minutes prior to reperfusion. Samples were obtained before, during, and after ischemia for determination of myeloperoxidase (MPO) activity, malondealdehyde (MDA) concentration, concentration of conjugated dienes (PVO experiment only), and morphometric analysis.

Results

TVO: tissue concentration of MDA and MPO activity were not altered in any group by ischemia or reperfusion. During ischemia, mucosal volume and surface area were reduced. After reperfusion, no further reduction occurred. After initial decrease in submucosal volume during ischemia, there was a significant increase after reperfusion in the vehicle-only group (P < 0.05). PVO: there were no alterations in the concentration of either MDA or conjugated dienes. There was a significant increase in the activity of MPO during ischemia and reperfusion (P< 0.05). These effects were similar for the vehicle-only and drug groups. During ischemia, there was a significant decrease in mucosal surface area and volume (P< 0.05), that was continued during reperfusion for the vehicle-only group (P< 0.05). Submucosal volume increased during reperfusion (P< 0.05). Serosal volume was increased during ischemia and reperfusion.

Conclusions and Clinical Relevance

Reduced blood flow during ischemia (PVO group) caused continued loss in mucosal volume and surface area during reperfusion. At the dosage given, the 21-aminosteroid, U-74389G, was not effective in preventing continued reduction in mucosal volume and surface area after restoration of blood supply in the horses subjected to reduced blood flow. (Am J Vet Res 1996; 57:762–770)

Free access
in American Journal of Veterinary Research

reperfusion. 9–14 In horses, neutrophil infiltration develops after ischemia and reperfusion injury in the small intestine 15 and large colon 16 and after distension of the small colon. 17 In another study, 15 neutrophil infiltration of jejunal serosa and

Full access
in American Journal of Veterinary Research

to joint translation. 1,2 Mechanisms of tendinous injury include acute, chronic, or iatrogenic trauma as well as secondary degenerative inflammatory processes. 1–4 Tendon laceration accounts for 0.7% of all appendicular musculoskeletal diagnoses. 5

Full access
in American Journal of Veterinary Research

mural inflammation induced by preoperative distention, hypoperfusion, reperfusion injury, and intestinal manipulation. 2–4 Inflammation induced by intestinal manipulation in laboratory animals can release proinflammatory cytokines and prostaglandins

Full access
in American Journal of Veterinary Research

Thickening of the patellar tendon, termed patellar tendinopathy, patellar tendinosis, or patellar tendinitis, is a common postoperative complication in dogs following TPLO for treatment of cranial cruciate ligament injuries. The condition in dogs

Full access
in American Journal of Veterinary Research

SUMMARY

After a detailed anatomic study to determine puncture sites, 10 cadaver elbows from 5 dogs were examined arthroscopically to study the normal intraarticular anatomy, as viewed from the medial side. Subsequent dissection revealed absence of neurovascular injury and only minor iatrogenic damage to the cartilage. The technique was clinically applied and evaluated in 13 dogs (26 joints). The dogs recovered without complications. The technique proved to be safe and reliable for direct examination of nearly the entire joint. More specifically, it allowed systematic inspection of the medial and lateral humeral condyles, the medial and lateral coronoid processes, the caudal and middle parts of the head of the radius, the olecranon (including the anconeal process), and the medial collateral ligament.

Free access
in American Journal of Veterinary Research