Objective—To determine whether intestinal ischemia
would alter activity of the jejunum in vitro or alter
staining characteristics for certain types of enteric
Sample Population—Jejunal samples obtained from
Procedure—Jejunal samples were obtained from
locations proximal and distal to an area of small intestine
made ischemic for 60 minutes. A portion of each
sample was stained to detect substance P-like
immunoreactivity, cholinergic and adrenergic neurons,
and nitric oxide synthase. Portions of the
remaining samples were suspended in muscle baths.
General activity patterns (frequency and amplitude of
contraction), responses to neuronal depolarization
induced by electrical field stimulation (EFS), and
responses to 1 µM norepinephrine (NE) were compared
with responses of a normal section of small
intestine obtained prior to ischemic insult.
Results—Staining patterns were not altered.
Proximal and distal sections had evidence of
decreased contractility, compared with the normal
section. Contraction frequency also was decreased,
and distal sections had lower contraction frequency
than proximal sections. Relaxation responses were
decreased in distal sections. Responses to NE differed
significantly for distal and proximal sections,
compared with normal sections.
Conclusions and Clinical Relevance—Short-term
ischemia can significantly affect adjacent bowel.
Contractile and relaxation responses are impaired.
Discrepancies in intestinal motility patterns and alterations
in response to NE for sections proximal and
distal to ischemic intestine could lead to clinical ileus
or slowed transit of ingesta. (Am J Vet Res 2001;
Objective—To determine whether substance P (SP)
functions as a neurotransmitter in equine jejunum.
Sample Population—Samples of jejunum obtained
from horses that did not have lesions in the gastrointestinal
Procedure—Jejunal smooth muscle strips, oriented
in the plane of the circular or longitudinal muscle,
were suspended isometrically in muscle baths.
Neurotransmitter release was induced by electrical
field stimulation (EFS) delivered at 2 intensities (30
and 70 V) and various frequencies on muscle strips
that were maintained at low tension or were under
contraction. A neurokinin-1 receptor blocker (CP-
96,345) was added to baths prior to EFS to interrupt
SP neurotransmission. Additionally, direct effects of
SP on muscle strips were evaluated, and SP-like
immunoreactivity was localized in intestinal tissues,
using indirect immunofluorescence testing.
Results—Substance P contracted circularly and longitudinally
oriented muscle strips. Prior treatment with
CP-96,345 altered muscle responses to SP and EFS,
suggesting that SP was released from depolarized
myenteric neurons. Depending on orientation of muscle
strips and stimulation variables used, CP-96,345
increased or decreased the contractile response to
EFS. Substance P-like immunoreactivity was detected
in the myenteric plexus and circular muscle layers.
Conclusions and Clinical Relevance—Substance P
appears to function as a neurotransmitter in equine
jejunum. It apparently modulates smooth muscle contractility,
depending on preexisting conditions. Effects
of SP may be altered in some forms of intestinal dysfunction.
Altering SP neurotransmission in the
jejunum may provide a therapeutic option for motility
disorders of horses that are unresponsive to adrenergic
and cholinergic drugs. (Am J Vet Res 2000;61:
Objective—To determine whether triamcinolone acetonide diffuses from the distal interphalangeal joint (DIPJ) to the navicular bursa, diffusion is direct or systemic, and addition of sodium hyaluronan has an effect on diffusion in horses.
Animals—11 adult horses without forelimb lameness.
Procedures—1 randomly chosen forelimb DIPJ of each horse received an injection of 10 mg of triamcinolone acetonide plus 20 mg of sodium hyaluronan (group 1), and the contralateral forelimb DIPJ received an injection of 10 mg of triamcinolone acetonide plus 2 mL of lactated Ringer's solution (group 2). Synovial fluid samples were taken from both forelimb navicular bursae and 1 hind limb navicular bursa (systemic control group) at 6 hours. Triamcinolone acetonide concentrations in synovial fluid were quantified by use of high-performance liquid chromatography plus tandem mass spectrometry. Data were logarithmically transformed, and contrast analysis was performed on the 3 groups.
Results—Triamcinolone acetonide was detected in navicular bursal samples in all groups. Groups 1 and 2 had significantly greater concentrations of triamcinolone acetonide than the systemic control group. There was no significant difference between groups 1 and 2.
Conclusions and Clinical Relevance—Triamcinolone acetonide diffused directly from the DIPJ into the navicular bursa in clinically normal horses, and diffusion was not affected by addition of hyaluronan. Injection into the DIPJ with triamcinolone acetonide or a triamcinolone acetonide–hyaluronan combination can potentially be used for treatment of navicular syndrome, but further studies are needed to determine whether triamcinolone acetonide diffuses similarly in horses with navicular syndrome.