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
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
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.
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.
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
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
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)
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
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
Sample Population—35 pelvises obtained from
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
Objective—To determine effects of sodium
hyaluronate (HA) on corticosteroid-induced cartilage
matrix catabolism in equine articular cartilage
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
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)