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SUMMARY

Thirty horses were randomly assigned to 1 of 5 groups. All horses were anesthetized and subjected to ventral midline celiotomy, then the large colon was exteriorized and instrumented. Colonic arterial blood flow was reduced to 20% of baseline (bl) and was maintained for 3 hours. Colonic blood flow was then restored, and the colon was reperfused for an additional 3 hours. One of 5 drug solutions was administered via the jugular vein 30 minutes prior to colonic reperfusion: group 1, 0.9% NaCl; group 2, dimethyl sulfoxide: 1 g/kg of body weight; group 3, allopurinol: 25 mg/kg; group 4, 21-aminosteroid U-74389G: 10 mg/kg; and group 5, manganese chloride (MnCl2): 10 mg/kg. Hemodynamic variables were monitored and recorded at 30-minutes intervals. Systemic arterial, systemic venous (sv), and colonic venous (cv) blood samples were collected for measurement of blood gas tensions, oximetry, lactate concentration, Pcv, and plasma total protein concentration. The eicosanoids, 6-keto prostaglandin F, prostaglandin E2 and thromboxane B2, were measured in cv blood, and endotoxin was measured in cv and sv blood. Full-thickness biopsy specimens were harvested from the left ventral colon for histologic evaluation and determination of wet weight-to-dry weight ratios (WW:DW). Data were analyzed, using two-way ANOVA for repeated measures, and statistical significance was set at P < 0.05. Heart rate, mean arterial pressure, and cardiac output increased with MnCl2 infusion; heart rate and cardiac output remained increased throughout the study, but mean arterial pressure returned to bl values within 30 minutes after completion of MnCI2 infusion. Other drug-induced changes were not significant. There were significant increases in mean pulmonary artery and mean right atrial pressures at 2 and 2.5 hours in horses of all groups, but other changes across time or differences among groups were not observed. Mean pulmonary artery pressure remained increased through 6 hours in all groups, but mean right atrial pressure had returned to bl values at 3 hours. Mean colonic arterial pressure was significantly decreased at 30 minutes of ischemia and remained decreased through 6 hours; however, by 3.25 hours it was significantly higher than the value at 3 hours of ischemia. Colonic arterial resistance decreased during ischemia and remained decreased throughout reperfusion in all groups; there were no differences among groups for colonic arterial resistance. Colonic venous Po2, oxygen content, and pH decreased, and Pco2 and lactate concentration increased during ischemia but returned to bl values during reperfusion. Compared with bl values, colonic oxygen extraction ratio was increased from 0.5 to 3 hours. By 15 minutes of reperfusion, colonic oxygen extraction ratio had decreased from the bl value in all groups and either remained decreased or returned to values not different from bl through 6 hours. Colonic venous 6-keto prostaglandin F and prostaglandin E2 concentrations increased during ischemia, but returned to bl on reperfusion; there were no changes in thrombox- ane2 concentration among or within groups. Endotoxin was not detected in cv or sv blood after ischemia or reperfusion. There were no differences among or within groups for these variables. Low-flow ischemia and reperfusion (i-r) of the large colon caused mucosal injury, as evidenced by increases in percentage of surface mucosal disruption, percentage depth of mucosal loss, mucosal hemorrhage, mucosal edema, mucosal interstitial-to-crypt ratio, mucosal neutrophil index, submucosal venular neutrophil numbers, and mucosal cellular debris index. There was a trend (P = 0.06) toward greater percentage depth of mucosal loss at 6 hours in horses treated with dimethyl sulfoxide, compared with the vehicle control solution. There were no differences in the remainder of the histologic variables among groups. Full-thickness and mucosal WW:DW increased with colonic I-R, but there were no differences among groups. There was a trend (P = 0.09) toward neutrophil accumulation, as measured by myeloperoxidase activity, in the lungs after colonic I-R, but there were no differences among groups. There was no change in lung WW:DW after colonic I-R. There were no beneficial effects of drugs directed against oxygen-derived free radical-mediated damage on colonic mucosal injury associated with low-flow I-R. Deleterious drug-induced hemodynamic effects were not observed in this study.

Free access
in American Journal of Veterinary Research

Summary

Histomorphologic/morphometric evaluation, leukocyte scintigraphy, and myeloperoxidase activity were used to determine whether neutrophils accumulate in the large colon of horses during low-flow ischemia and reperfusion. Twenty-four adult horses were assigned to 1 of 3 groups: group 1, sham-operated (n = 6); group 2, 6 hours of ischemia (n = 9); and group 3, 3 hours of ischemia and 3 hours of reperfusion (n = 9). Low-flow ischemia of the large colon was induced in horses of groups 2 and 3 by reducing colonic arterial blood flow to 20% of baseline. Radiolabeled (99mTc) autogenous neutrophils were injected at 175 minutes, which corresponded to 5 minutes prior to reperfusion in group-3 horses. Full-thickness biopsy specimens of the left ventral colon were collected at baseline and at 30-minute intervals for 6 hours; a portion of the biopsy specimen was placed in formalin for histologic examination, and the remainder was used to measure mucosal radioactivity and myeloperoxidase activity. There were no differences in baseline mucosal neutrophil index, mucosal neutrophil numbers, submucosal venular neutrophil numbers, mucosal radioactivity, or mucosal myeloperoxidase activity among groups, or over time in group-1 horses. Neutrophils accumulated in the colonic mucosa during ischemia and further increased at reperfusion, as indicated by neutrophil index (morphology) and mucosal neutrophil numbers (morphometry); mucosal neutrophil index was significantly (P < 0.05) greater in group-3 horses during reperfusion than at the corresponding periods of ischemia in group-2 horses. Neutrophil numbers were significantly (P < 0.05) increased in submucosal venules at 10 minutes of reperfusion in group-3 horses and were significantly (P < 0.05) greater in group-3 than in group-2 horses during the interval from 3 to 6 hours. Mucosal radioactivity significantly (P < 0.05) increased at reperfusion in group-3 horses; there was a trend (P = 0.076) toward greater mucosal radioactivity in group-3, compared with group-2 horses, throughout the 3- to 6-hour interval. There were no differences in mucosal myeloperoxidase activity among or within any of the 3 groups over time.

Neutrophils accumulated in the large colon of horses during low-flow ischemia and reperfusion. Neutrophil infiltration was detected by histologic examination and leukocyte scintigraphy, but not by measurement of myeloperoxidase activity. The accumulation of neutrophils during ischemia and the further neutrophil infiltration during reperfusion indicate that neutrophils may contribute to reperfusion injury of the large colon.

Free access
in American Journal of Veterinary Research

Summary

Medical records of 59 racehorses with noncomminuted midsagittal proximal phalanx fractures repaired by means of lag screw fixation between 1973 and 1991 were reviewed. Fractures were classified as short incomplete fractures (7), long incomplete fractures (32), complete fractures extending into the proximal interphalangeal joint (13), and complete fractures extending through the lateral cortex of the proximal phalanx (7). Time from fracture repair to first race following fracture repair, number of racing starts, and fastest race times before and after surgery were obtained from race records and compared among horses grouped by fracture type and between horses that returned to racing and those that did not race. Five horses with short incomplete fractures, 21 horses with long incomplete fractures, 6 horses with complete fractures extending into the proximal interphalangeal joint, and 5 horses with complete fractures extending to the lateral cortex returned to racing. A significantly lower percentage of horses returned to racing following repair of complete fractures extending into the proximal interphalangeal joint (46%), than following repair of short incomplete fractures (71%), long incomplete fractures (66%), or complete fractures extending to the lateral cortex (71%). Time from fracture to repair for horses that returned to racing (mean, 14.7 days; range, 1 to 60 days) was not significantly different from that for horses that did not race (mean, 5.8 days; range, 1 to 21 days). For all fracture groups, median number of races before injury was not significantly different from median number of races after repair, and median fastest race time before fracture was not significantly different from median fastest race time after fracture repair.

Free access
in Journal of the American Veterinary Medical Association

SUMMARY

Twenty-four horses were randomly allocated to 3 groups. Horses were anesthetized, subjected to a ventral midline celiotomy, and the large colon was exteriorized and instrumented. Group-1 horses served as sham-operated controls. Group-2 horses were subjected to 6 hours of low-flow colonic arterial ischemia, and group-3 horses were subjected to 3 hours of ischemia and 3 hours of reperfusion. Baseline (bl) samples were collected, then low-flow ischemia was induced by reducing ventral colonic arterial blood flow to 20% of bl. All horses were monitored for 6 hours after bl data were collected. blood samples were collected from the colonic vein and main pulmonary artery (systemic venous [sv]) for measurement of plasma endotoxin, 6-keto prostaglandin F (6-kPG), thromboxane B2 (txb 2), and prostaglandin E2 (pge 2) concentrations. Tumor necrosis factor and interleukin-6 activities were measured in colonic venous (cv) serum samples. Data were analyzed, using two-way anova, and post-hoc comparisons were made, using Dunnett's and Tu- key's tests. Statistical significance was set at P < 0.05. Endotoxin was not detected in CV or sv plasma at any time. There was no detectable tumor necrosis factor or interleukin-6 activity in CV samples at any time. There were no differences at bl among groups for CV or sv 6-kPG, pge 2, or txb 2 concentrations, nor were there any changes across time in group-1 horses. Colonic venous 6-kPG concentration increased during ischemia in horses of groups 2 and 3; CV 6-kPG concentration peaked at 3 hours in group-3 horses, then decreased during reperfusion, but remained increased through 6 hours in group-2 horses. Systemic venous 6-kPG concentration increased during reperfusion in group-3 horses, but there were no changes in group- 2 horses. Colonic venous pge 2 concentration increased during ischemia in horses of groups 2 and 3, and remained increased for the first hour of reperfusion in group-3 horses and for the 6-hour duration of ischemia in group-2 horses. There were no temporal alterations in sv pge 2 concentration. There was no difference in CV or sv ixb2 concentration among or within groups across time; however, there was a trend (P = 0.075) toward greater CV txb 2 concentration at 3.25 hours, compared with bl, in group-3 horses. Eicosanoid concentrations were significantly lower in sv, compared with CV plasma. Prostaglandin E2 and 6-kPG concentrations were approximately 3 to 8 and 5 to 10 times greater, respectively, in CV than in sv plasma. The increased concentrations of 6-kPG and pge 2 in CV plasma were likely attributable to their accumulation secondary to colonic ischemia. The increased values of these vasodilator eicosanoids may have a role in the reactive hyperemia observed during reperfusion. The increased 6-kPG concentration in sv plasma may represent spillover from the colonic vasculature, but more likely reflects systemic production.

Free access
in American Journal of Veterinary Research

Summary

Effects of low-flow ischemia and reperfusion of the large colon on mucosal architecture were determined in horses. Twenty-four adult horses were randomly allocated to 3 groups: sham-operated (n = 6), 6 hours of ischemia (n = 9), and 3 hours of ischemia and 3 hours of reperfusion (n = 9). Low-flow ischemia was induced in horses of groups 2 and 3 by reducing colonic arterial blood flow to 20% of baseline values. Systemic hemodynamic and metabolic variables were maintained constant and in a normal physiologic range. Full-thickness biopsy specimens were obtained from the left ventral colon for histomorphologic and morphometric examination at baseline and at 30-minute intervals for 6 hours; additional biopsy specimens were collected at 185, 190, and 195 minutes (corresponding to 5-, 10-, and 15-minute periods of reperfusion in group-3 horses). There were no differences among groups at baseline or across time in group-1 horses for any of the histopathologic variables. There were significant (P < 0.05) increases in percentage of surface mucosal disruption, estimated and measured percentage depth of mucosal loss, mucosal hemorrhage, mucosal edema, and cellular debris index during 0 hour to 3 hours, compared with baseline, and from 3 hours to 6 hours, compared with 3 hours in horses of groups 2 and 3. Estimated percentage depth of mucosal loss and cellular debris index were significantly (P < 0.05) greater in group-3 horses, compared with group-2 horses during the interval from 3 to 6 hours. There were trends toward greater percentage of surface mucosal disruption and mucosal edema during the early phase of reperfusion (3 to 4 hours) and greater mucosal hemorrhage, measured percentage depth of mucosal loss, and mucosal interstitial-to-crypt ratio during the late phase (4 to 6 hours) of reperfusion in group-3 horses vs group-2 horses. Reestablishment of colonic arterial blood flow after low-flow ischemia caused greater mucosal injury than did a comparable period of continued ischemia. Thus, reperfusion injury was detected in the large colon of horses after low-flow arterial ischemia. The serial mucosal alterations that developed in the colon were comparable in horses of groups 2 and 3; however, reperfusion exacerbated colonic mucosal injury.

Free access
in American Journal of Veterinary Research

Abstract

Objective—To compare biodegradable magnesium phosphate cement (Mg-cement), calcium phosphate cement (Ca-cement), and no cement on bone repair, biocompatibility, and bone adhesive characteristics in vivo in horses.

Animals—8 clinically normal adulthorses.

Procedures—Triangular fragments (1-cm-long arms) were created by Y-shaped osteotomy of the second and fourth metatarsal bones (MTII and MTIV, respectively). Fragments were replaced in pairs to compare Mg-cement (MTII, n = 8; MTIV, 8) with Ca-cement (MTIV, 8) or with no cement (MTII, 8). Clinical and radiographic evaluations were performed for 7 weeks, at which time osteotomy sites were harvested for computed tomographic measurement of bone density and callus amount, 3-point mechanical testing, and histologic evaluation of healing pattern and biodegradation.

Results—All horses tolerated the procedure without clinical problems. Radiographically, Mg-cement secured fragments significantly closer to parent bone, compared with Ca-cement or no treatment. Callus amount and bone remodeling and healing were significantly greater with Mg-cement, compared with Ca-cement or no cement. Biomechanical testing results and callus density among treatments were not significantly different. Significantly greater woven bone was observed adjacent to the Mg-cement without foreign body reac-tion, compared with Ca-cement or no cement. The Mg-cement was not fully degraded and was still adhered to the fragment.

Conclusions and Clinical Relevance—Both bone cements were biocompatible in horses, and Mg-cementmay assistfracture repair by osteogenesis and fragmentstabilization. Fur ther studies are warranted on other applications and to define degradation characteristics.

Full access
in American Journal of Veterinary Research

Abstract

Objective—To evaluate and correlate patterns of subchondral bone density and articular cartilage degeneration (derived by use of gross, histologic, and computed tomographic [CT] examinations) in equine third metacarpal condyles with and without osteoarthritis.

Sample Population—8 metacarpophalangeal (MCP) joints (n = 4 horses) without osteoarthritis and 6 osteoarthritis-affected MCP joints (4).

Procedures—Horses were euthanized. The third metacarpal condyles of the joints were examined grossly and via CT (3 slice images/condyle). For 6 condylar zones, mean bone density and pattern of density distribution were determined. Data for osteoarthritis-affected and control joints were compared. Histomorphometric point count analyses identified areas of bone density for comparison with CT density measurements.

Results—Osteoarthritis-affected condyles had heterogeneous subchondral bone with focal resorptive lesions and patterned sclerosis, whereas control condyles had symmetric bone density distribution. In osteoarthritis-affected condyles, bone density determined via gray scale image density analysis was greater (dorsal and medial pattern), compared with control condyles, and differed among zones because of resorption and sclerosis. With regard to bone density in osteoarthritis-affected condyles, histologic findings correlated with CT images, and bone lesions were significantly correlated with cartilage lesions.

Conclusions and Clinical Relevance—In horses, heterogeneous distribution and greater subchondral bone density were characteristic of osteoarthritis-affected condyles, compared with control condyles. Subchondral bone lesions correlated with overlying cartilage lesions in osteoarthritis-affected MCP joints. Identification of CT image characteristics appears to predict the presence of a cartilage lesion in MCP joints of horses with osteoarthritis.

Full access
in American Journal of Veterinary Research

Abstract

Objective—To assess analgesia, inflammation, potency, and duration of action associated with intra-articular injection of triamcinolone acetonide (TA), mepivacaine hydrochloride, or both in metacarpophalangeal (MCP) joints of horses with experimentally induced acute synovitis.

Animals—18 horses.

Procedures—Both forelimbs of each horse were injected with lipopolysaccharide (LPS) 3 times. After the first LPS injection, 1 forelimb of each horse was treated with intra-articular injection of mepivacaine (80 mg; n = 6), TA (9 mg; 6), or mepivacaine with TA (same doses of each; 6) 12 hours after the initial LPS injection. Contralateral limbs served as control limbs. Joint pain was assessed via lameness score and measurements of vertical force peak and pain-free range of motion of the MCP joint. Periarticular edema was evaluated. Degree of synovial inflammation was determined via synovial fluid analysis for WBC count and total protein concentration. Samples of plasma and synovial fluid were analyzed for TA and mepivacaine concentrations.

Results—Each injection of LPS induced lameness and joint inflammation. Mepivacaine effectively eliminated lameness within 45 minutes after injection, regardless of whether TA was also administered, whereas TA reduced lameness, edema, and concentration of synovial fluid protein after the second LPS injection, regardless of whether mepivacaine was also injected. Treatment with TA also induced higher WBC counts and mepivacaine concentrations in synovial fluid, compared with results for mepivacaine alone.

Conclusions and Clinical Relevance—Results suggested TA is a potent analgesic and anti-inflammatory medication for acute synovitis in horses and that simultaneous administration of mepivacaine does not alter the potency or duration of action of TA.

Full access
in American Journal of Veterinary Research

Abstract

Objective—To investigate the effect of laser shock peening on the fatigue life and surface characteristics of 3.5-mm-diameter cortical bone screws.

Sample Population—32 stainless steel, 3.5-mm-diameter cortical bone screws.

Procedure—Screws were randomly assigned to an untreated control group or 2 power-density treatment groups, 6 gigawatts (GW)/cm2 and 8.5 GW/cm2, for laser shock peening. Number of cycles to failure and findings on scanning electron microscopy-assisted morphometric evaluation, including the mode of failure, surface debris, surface damage, and thread deformation, were compared between control and treated screws.

Results—The 6 GW/cm2 treated screws had a significant (11%) improvement in fatigue life, compared with untreated control screws. The 8.5 GW/cm2 treated screws had a significant (20%) decrease in fatigue life, compared with control screws. A mild but significant increase in thread deformation was evident in all treated screws, compared with control screws. The 8.5 GW/cm2 treated screws had significantly more surface irregularities (elevations and pits), compared with control or 6 GW/cm2 treated screws.

Conclusions and Clinical Relevance—A modest positive increase in fatigue strength was produced by this design of laser shock peening on the midshaft of cortical bone screws. High laser shock peening power densities were detrimental, decreasing screw fatigue strength probably resulting from structural damage. Greater fatigue life of cortical bone screws can be generated with laser shock peening and could reduce screw breakage as a cause of implant failure; however, future studies will be necessary to address biocompatibility, alternative cleaning techniques, alterations in screw strength and pullout characteristics, and effects on susceptibility to corrosion. ( Am J Vet Res 2004;65:972–976)

Full access
in American Journal of Veterinary Research

Abstract

Objective—To compare biomechanical strength, interface quality, and effects of bone healing in bone-implant interfaces that were untreated or treated with calcium phosphate cement (Ca-cement), magnesium phosphate cement (Mg-cement), or polymethylmethacrylate (PMMA) in horses.

Animals—6 adult horses.

Procedures—4 screw holes were created (day 0) in each third metacarpal and third metatarsal bone of 6 horses. In each bone, a unicortical screw was placed in each hole following application of Ca-cement, Mg-cement, PMMA, or no treatment (24 screw holes/treatment). Screws were inserted to 2.82 N m torque. Horses were euthanized and bones were harvested at day 5 (16 screw holes/treatment) or day 182 (8 screw holes/treatment). Radiography, biomechanical testing, histomorphometry, and micro–computed tomography were performed to characterize the bone-implant interfaces.

Results—Use of Mg-cement increased the peak torque to failure at bone-implant interfaces, compared with the effects of no treatment and Ca-cement, and increased interface toughness, compared with the effects of no treatment, Ca-cement, and PMMA. Histologically, there was 44% less Ca-cement and 69% less Mg-cement at the interfaces at day 182, compared with amounts present at day 5. Within screw threads, Ca-cement increased mineral density, compared with PMMA or no treatment. In the bone adjacent to the screw, Mg-cement increased mineral density, compared with PMMA or no treatment. One untreated and 1 Ca-cement–treated screw backed out after day 5.

Conclusions and Clinical Relevance—In horses, Mg-cement promoted bone-implant bonding and adjacent bone osteogenesis, which may reduce the risk of screw loosening.

Full access
in American Journal of Veterinary Research