Objective—To examine the secretory response (in
the presence and absence of prostaglandin inhibition)
in vitro and structural alterations of colonic mucosa in
horses after intragastric administration of black walnut
Animals—14 adult horses.
Procedure—Seven horses were administered
BWE intragastrically and monitored for 11 hours.
Tissue samples were obtained from the right ventral,
left ventral, and right dorsal colons (RVC, LVC,
and RDC, respectively) of the 7 BWE-treated and 7
control horses. Tissue samples were examined via
light microscopy, and the extent of hemorrhage,
edema, and granulocytic cellular infiltration (neutrophils
and eosinophils) was graded. Colonic
mucosal segments were incubated with or without
flunixin meglumine (FLM) for 240 minutes; spontaneous
electrical potential difference and short-circuit
current (Isc) were recorded and used to calculate
Results—Colonic tissues from BWE-treated horses
(with or without FLM exposure) had an overall greater
Isc during the 240-minute incubation period, compared
with tissues from control horses. The resistance
pattern in RVC, LVC, and RDC samples (with or
without FLM exposure) from BWE-treated horses
was decreased overall, compared with control tissues
(with or without FLM exposure). Histologically,
colonic mucosal tissues from BWE-treated horses
had more severe inflammation (involving primarily
eosinophils), edema, and hemorrhage, compared
with tissue from control horses.
Conclusions and Clinical Relevance—In horses,
BWE administration appears to cause an inflammatory
response in colonic mucosal epithelium that results
in mucosal barrier compromise as indicated by
decreased mucosal resistance with presumed concomitant
electrogenic chloride secretory response,
which is not associated with prostaglandin mediation.
(Am J Vet Res 2005;66:443–449)
Objective—To evaluate changes in digital vascular function in horses with carbohydrate overload (CHO)-induced laminitis and determine the effects of an endothelin (ET) receptor antagonist and nitroglycerin on laminitis-associated vascular dysfunction.
Animals—20 adult horses without abnormalities of the digit.
Procedures—Hemodynamic variables were recorded before (baseline) and hourly after all horses were administered a CHO ration via nasogastric tube. In 4 groups of 5 horses each, saline (0.9% NaCl) solution or ET receptor antagonist (10−5M in digital blood) was administered into the digital arterial circulation according to 1 of 2 schedules. During anesthesia, blood flow; arterial, venous, and capillary pressures; and total, precapillary, and postcapillary resistances were measured in an isolated perfused digit of each horse. In all groups, nitroglycerin was infused (10−5M in digital blood), and digital microvascular assessments were repeated.
Results—The CHO caused a significant decrease in right atrial pressure by 14 hours that was not affected by administration of saline solution or ET receptor antagonist. In isolated digits of anesthetized horses, CHO resulted in a significant decrease in digital blood flow associated with a significant increase in total and postcapillary resistances. Treatment with the ET receptor antagonist and nitroglycerin caused a significant decrease in total resistance. Postcapillary resistance was significantly decreased following treatment with the ET receptor antagonist but was not altered by treatment with nitroglycerin.
Conclusions and Clinical Relevance—Treatment with an ET receptor antagonist and nitroglycerin resulted in significant improvement in vascular resistance in isolated perfused digits of anesthetized horses with CHO-induced laminitis.
Objective—To characterize the in vitro effects of
oxytocin, acepromazine, xylazine, butorphanol,
detomidine, dantrolene, isoproterenol, and terbutaline
on skeletal and smooth muscle from the
Animals—14 adult horses without digestive tract disease.
Procedure—Circular and longitudinal strips from
the skeletal and smooth muscle of the esophagus
were suspended in tissue baths, connected to
force-displacement transducers interfaced with a
physiograph, and electrical field stimulation was
applied. Cumulative concentration-response curves
were generated for oxytocin, acepromazine,
xylazine, detomidine, butorphanol, isoproterenol,
terbutaline, and dantrolene. Mean maximum twitch
amplitude for 3 contractions/min was recorded and
compared with predrug-vehicle values for the
skeletal muscle segments, and area under the
curve (AUC) for 3 contractions/min was compared
with predrug-vehicle values for the smooth muscle
Results—No drugs caused a significant change in
skeletal muscle response. In smooth muscle, isoproterenol,
terbutaline, and oxytocin significantly
reduced AUC in a concentration-dependent manner.
Maximum reduction in AUC was 69% at 10–4M for
isoproterenol, 63% at 10–5M for terbutaline, and
64% at 10–4M for oxytocin.
Conclusions and Clinical Relevance—Isoproterenol,
terbutaline, and oxytocin cause relaxation of the
smooth muscle portion of the esophagus. The clinical
relaxant effects on the proximal portion of the esophagus
reported of drugs such as oxytocin, detomidine,
and acepromazine may be the result of centrally mediated
mechanisms. (Am J Vet Res 2002;63:1732–1737)
Objective—To compare effects of oxytocin, acepromazine
maleate, xylazine hydrochloride-butorphanol
tartrate, guaifenesin, and detomidine hydrochloride
on esophageal manometric pressure in horses.
Animals—8 healthy adult horses.
Procedure—A nasogastric tube, modified with 3
polyethylene tubes that exited at the postpharyngeal
area, thoracic inlet, and distal portion of the
esophagus, was fitted for each horse. Amplitude,
duration, and rate of propagation of pressure waveforms
induced by swallows were measured at 5, 10,
20, 30, and 40 minutes after administration of oxytocin,
detomidine, acepromazine, xylazine-butorphanol,
guaifenesin, or saline (0.9% NaCl) solution.
Number of spontaneous swallows, spontaneous
events (contractions that occurred in the absence of
a swallow stimulus), and high-pressure events (sustained
increases in baseline pressure of > 10 mm
Hg) were compared before and after drug administration.
Results—At 5 minutes after administration, detomidine
increased waveform amplitude and decreased
waveform duration at the thoracic inlet. At 10 minutes
after administration, detomidine increased waveform
duration at the thoracic inlet. Acepromazine administration
increased the number of spontaneous events
at the thoracic inlet and distal portion of the esophagus.
Acepromazine and detomidine administration
increased the number of high-pressure events at the
thoracic inlet. Guaifenesin administration increased
the number of spontaneous events at the thoracic
inlet. Xylazine-butorphanol, detomidine, acepromazine,
and guaifenesin administration decreased the
number of spontaneous swallows.
Conclusions and Clinical Relevance—Detomidine,
acepromazine, and a combination of xylazine butorphanol
had the greatest effect on esophageal motility
when evaluated manometrically. Reduction in spontaneous
swallowing and changes in normal, coordinated
peristaltic activity are the most clinically relevant
effects. (Am J Vet Res 2002;63:1738–1744)
Objective—To compare plasma and synovial fluid
endothelin-1 (ET-1) and nitric oxide (NO) concentrations
in clinically normal horses and horses with joint
Animals—36 horses with joint disease, and 15 horses
without joint disease.
Procedure—Horses with joint disease were assigned
to 1 of the 3 groups (ie, synovitis, degenerative joint
disease [DJD], or joint sepsis groups) on the basis of
findings on clinical and radiographic examination and
synovial fluid analysis. Endothelin-1 and NO concentrations
were measured in plasma from blood samples,
collected from the jugular vein and ipsilateral
cephalic or saphenous vein of the limb with an affected
or unaffected joint, as well as in synovial fluid samples
obtained via arthrocentesis from the involved
Results—Plasma ET-1 concentrations between
affected and unaffected groups were not significantly
different. Median concentration and concentration
range of ET-1 in synovial fluid obtained from the joint
sepsis group (35.830 pg/mL, 7.926 to 86.614 pg/mL;
n = 7) were significantly greater than values from the
synovitis (17.531 pg/mL, 0.01 to 46.908 pg/mL; 18),
DJD (22.858 pg/mL, 0.01 to 49.990 pg/mL; 10), and
unaffected (10.547 pg/mL, 0.01 to 35.927 pg/mL; 10)
groups. Plasma and synovial fluid NO concentrations
between affected and unaffected groups were not
Conclusions and Clinical Relevance—Endothelin-1
is locally synthesized in the joints of horses with various
types of joint disease. Synovial fluid concentrations
of ET-1 varied among horses with joint disease,
with concentrations significantly higher in the synovial
fluid of horses with joint sepsis. These results
indicate that ET-1 may play a role in the pathophysiologic
mechanism of joint disease in horses.
(Am J Vet Res 2002;63:1648–1654)