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- Author or Editor: Jo Ann C. Eurell x
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Abstract
Objective—To document effects of cisplatin on regenerate bone formation during the distraction and consolidation phases of bone transport osteogenesis.
Animals—10 skeletally mature hounds.
Procedure—Bone transport osteogenesis was performed to reconstruct a 3-cm defect in the radius of each dog. Five dogs were randomly selected to receive cisplatin (70 mg/m2, IV, q 21 d for 4 cycles), and 5 were administered saline (0.9% NaCl) solution. Bone mineral density was measured by use of dual-energy x-ray absorptiometry (DEXA) on days 24, 55, and 90 after surgery. Dogs were euthanatized 90 days after surgery. Histomorphometry was performed on nondecalcified sections of regenerate bone. Bone mineral density and histomorphometric indices of newly formed bone were compared between groups.
Results—Densitometric differences in regenerate bone mineral density were not detected between groups at any time period. Cisplatin-treated dogs had decreased mineralized bone volume, decreased percentage of woven bone volume, decreased percentage of osteoblast-covered bone, increased porosity, and increased percentage of osteoblast-covered surfaces, compared with values for control dogs. Lamellar bone volume and osteoid volume did not differ significantly between groups.
Conclusions and Clinical Relevance—Regenerate bone will form and remodel during administration of cisplatin. Results of histomorphometric analysis suggest that bone formation and resorption may be uncoupled in cisplatin-treated regenerate bone as a result of increased osteoclast activity or delayed secondary bone formation during remodeling. These histomorphometric differences were modest in magnitude and did not result in clinically observable complications or decreased bone mineral density as measured by use of DEXA. (Am J Vet Res 2002;63:703–711)
Abstract
Objective—To study the effects of phenylbutazone, indomethacin, prostaglandin E2 (PGE2), glutamine, and butyrate on restitution of oxidant-injured right dorsal colon of horses in vitro.
Sample Population—Right dorsal colon from 9 adult horses euthanatized for reasons other than gastrointestinal tract disease.
Procedure—Mucosal segments from the right dorsal colon were injured via exposure to HOCl and incubated in Ussing chambers in solutions containing phenylbutazone, indomethacin, indomethacin and PGE2, glutamine, and butyrate. Transepithelial resistance and mucosal permeability to mannitol were measured, and all mucosal segments were examined histologically.
Results—The HOCl-injured mucosa had lower resistance and higher permeability to mannitol, compared with control tissue. Histologic changes were also evident. Resistance of HOCl-injured mucosa recovered partially during the incubation period, and glutamine improved recovery. Phenylbutazone and indomethacin increased resistance, but these increases were not significant. Butyrate and PGE2 had no effects, compared with nontreated HOCl-injured tissues. Mucosal permeability to mannitol was lower in glutamine-treated tissue, compared with nontreated tissue. Histologic changes reflected the resistance and permeability changes.
Conclusions and Clinical Relevance—According to our findings, phenylbutazone and indomethacin do not seem to interfere with restitution of oxidant-injured mucosa of equine colon in vitro, and glutamine could facilitate mucosal restitution. (Am J Vet Res 2004;65:1589–1595)
Abstract
Objectives—To evaluate the in vitro protective effects of acetylcysteine and response of resident mucosal eosinophils in oxidant-induced injury to tissues of right dorsal colon of horses.
Animals—9 adult horses.
Procedure—Gastrointestinal mucosa was damaged in vitro with 3mM hypochlorous acid (HOCl), with and without prior exposure to 6mM acetylcysteine. Control tissues were not exposed to HOCl or acetylcysteine. Control and damaged tissues were incubated in Krebs-Ringer-bicarbonate solution and tissue resistance measured during 240 minutes. Tissue permeability to radiolabeled mannitol was also used to assess mucosal barrier integrity. Tissues were examined by light microscopy before and after HOCl exposure and during and after incubation.
Results—Exposure to HOCl caused tissue damage and decreased tissue resistance. Restitution did occur during the incubation period. Eosinophils were located near the muscularis mucosae in freshly harvested tissues and migrated towards the luminal surface in response to HOCl-induced injury. Compared with tissues treated with HOCl without acetylcysteine, pretreatment with acetylcysteine prevented HOCl-induced tissue damage, changes in resistance, and histologically detectable eosinophil migration. The permeability to mannitol increased to the same extent in tissues treated with HOCl alone or with acetylcysteine and HOCl.
Conclusions and Clinical Relevance—Eosinophils migrated toward the mucosal surface in equine colon in response to oxidant-induced damage in vitro. This novel finding could be relevant to inflammation in equine colon and a pathophysiologic feature of many colonic diseases. Acetylcysteine protected the mucosa against oxidant-induced injury and may be useful as a treatment option for various gastrointestinal tract disorders in horses. (Am J Vet Res 2003;64:1205–1212)
Abstract
Objective—To determine effects of sodium hyaluronate (HA) on corticosteroid-induced cartilage matrix catabolism in equine articular cartilage explants.
Sample Population—30 articular cartilage explants from fetlock joints of 5 adult horses without joint disease.
Procedure—Articular cartilage explants were treated with control medium or medium containing methylprednisolone acetate (MPA; 0.05, 0.5, or 5.0 mg/mL), HA (0.1, 1.0, or 1.5 mg/mL), or both. Proteoglycan (PG) synthesis was measured by incorporation of sulfur 35-labeled sodium sulphate into PGs, and PG degradation was measured by release of radiolabeled PGs into the medium. Total glycosaminoglycan (GAG) content in media and explants and total explant DNA were determined.
Results—Methylprednisolone acetate caused a decrease in PG synthesis, whereas HA had no effect. Only the combination of MPA at a concentration of 0.05 mg/mL and HA at a concentration of 1.0 mg/mL increased PG synthesis, compared with control explants. Methylprednisolone acetate increased degradation of newly synthesized PGs into the medium, compared with control explants, and HA alone had no effect. Hyaluronate had no effect on MPAinduced PG degradation and release into media. Neither MPA alone nor HA alone had an effect on total cartilage GAG content. Methylprednisolone acetate caused an increase in release of GAG into the medium at 48 and 72 hours after treatment. In combination, HA had no protective effect on MPA-induced GAG release into the medium. Total cartilage DNA content was not affected by treatments.
Conclusions and Clinical Relevance—Our results indicate that HA addition has little effect on corticosteroid- induced cartilage matrix PG catabolism in articular cartilage explants. (Am J Vet Res 2005;66:48–53)
Abstract
OBJECTIVE To evaluate the eosinophilic response in intestinal mucosa of horses with intestinal ischemia and reperfusion or with strangulation of the jejunum or colon.
SAMPLE Mucosal samples from horses with naturally occurring strangulation (n = 24 horses) or distention (n = 6) of the jejunum or colon (11), with experimentally induced ischemia and reperfusion of the jejunum (6) or colon (15), or that were euthanized for reasons other than gastrointestinal tract disease (13).
PROCEDURES Mucosal samples were collected and grouped by type of intestinal injury. Slides were stained with Luna eosinophil stain and histologically examined to determine eosinophil accumulation and distribution. Number of eosinophils per mm2 of mucosa was calculated as a measure of eosinophil accumulation. Additionally, mucosa was categorized into 5 regions; the percentage of eosinophils in each of the 5 regions, relative to the total eosinophil count in all regions, was determined.
RESULTS Eosinophil migration toward and onto the luminal surface was evident in tissues after ischemia and reperfusion and after naturally occurring strangulating disease of the jejunum and colon, as indicated by a decrease in the number of eosinophils near the muscularis mucosa and an increase in the number of eosinophils on or near the luminal surface. Ischemia alone did not change eosinophil distribution in the jejunum or colon.
CONCLUSIONS AND CLINICAL RELEVANCE Eosinophils responded to mucosal damage evoked by ischemia and reperfusion by migration toward and onto the luminal surface. This migration could represent an important component of the inflammatory response to injury in equine gastrointestinal mucosa.
Abstract
Objectives—To establish reference values for the range of the number of eosinophils found in equine gastrointestinal mucosa and to describe the distribution of this cell within the equine gastrointestinal mucosa.
Sample Population—Gastrointestinal mucosal specimens from 14 adult horses euthanatized for reasons other than gastrointestinal disease.
Procedures—Gastrointestinal mucosal specimens were collected and grouped according to their anatomic regions. For histologic examination slides were stained with Luna's eosinophil stain to determine eosinophil accumulation and distribution. The mucosa was divided into 5 sections for each anatomic location, and the percentage of eosinophils in each of the 5 sections relative to the total eosinophil count in all sections was determined. Additionally, the number of eosinophils per square millimeter of mucosa was calculated as a measure of the degree of eosinophil accumulation.
Results—Lowest numbers of eosinophils were found in the stomach, and numbers increased from there to the cecum, then decreased from the ascending colon (right ventral colon, left ventral colon, pelvic flexure, left dorsal colon, and right dorsal colon) to small colon. In all gastrointestinal sections, most eosinophils were located near the muscularis mucosae and were rarely found near or on the luminal surface of the mucosa.
Conclusions and Clinical Relevance—The distribution of eosinophils in the gastrointestinal tract of horses followed a pattern within the mucosa and between different sections of the gastrointestinal tract. The derived reference values and distribution data could be used to detect changes in eosinophil response in the equine gastrointestinal mucosa caused by diseases states.
Abstract
Objective—To evaluate the effect of an osteoconductive resorbable calcium phosphate cement (CPC) on the holding power of bone screws in canine pelvises and to compare the effect with that for polymethylmethacrylate (PMMA).
Sample Population—35 pelvises obtained from canine cadavers.
Procedure—Each pelvis was sectioned longitudinally. Within each pair of hemipelvises, one 4.0-mm cancellous screw was placed in the sacroiliac (SI) region and another in the iliac body. Similar regions on the contralateral- matched hemipelvis were assigned 1 of 3 augmentation techniques (CPC-augmented 4.0-mm cancellous screws, PMMA-augmented 4.0-mm cancellous screws, and CPC-augmented 3.5-mm cortical screws). Pullout force was compared between matched screws and between treatment groups prior to examination of cross sections for evaluation of cement filling and noncortical bone-to-cortical bone ratio.
Results—CPC and PMMA augmentation significantly increased pullout force of 4.0-mm screws inserted in the SI region by 19.5% and 33.2%, respectively, and CPC augmentation significantly increased pullout force of 4.0-mm cancellous screws inserted in the iliac body by 21.2%. There was no difference in the mean percentage augmentation between treatment groups at either location. Cement filling was superior in noncortical bone, compared with filling for cortical bone. Noncortical bone-to-cortical bone ratio was significantly greater in the sacrum (6.1:1) than the ilium (1.3:1).
Conclusions and Clinical Relevance—CPC and PMMA improve the ex vivo holding strength of 4.0-mm cancellous screws in the SI and iliac body regions and SI region, respectively. Cement augmentation may be more effective in areas with greater noncortical bone-to-cortical bone ratios. (Am J Vet Res 2005;66:1954–1960)
