Objective—To provide a quantitative description of the
architecture of superficial digital flexor (SDF) and deep
digital flexor (DDF) muscles in adult horses to predict
muscle-tendon behavior and estimate muscle forces.
Sample Population—7 forelimb specimens from 7
Procedure—Muscle and tendon lengths and volumes
were measured from 6 fixed forelimbs. After processing,
fiber bundle and sarcomere lengths were
measured. Optimal fascicle lengths and muscle
length-to-fascicle length, muscle length-to-free tendon
length, and fascicle length-to-tendon length ratios
were calculated, as were tendon and muscle physiologic
cross-sectional areas (PCSAs). Pennation angles
were measured in 1 embalmed specimen.
Results—The SDF optimal fascicle lengths were uniformly
short (mean ± SD, 0.8 ± 0.1 cm), whereas DDF
lengths ranged from 0.9 ± 0.2 cm to 10.8 ± 1.6 cm.
The DDF humeral head had 3 architectural subunits,
each receiving a separate median nerve branch, suggestive
of neuromuscular compartmentalization.
Pennation angles were small (10o to 25o). The PCSAs
of the SDF and DDF muscle were 234 ± 51 cm2 and
259 ± 30 cm2, with estimated forces of 4,982 ± 1148
N and 5,520 ± 544 N, respectively.
Conclusions and Clinical Relevance—The SDF
muscle appears to provide strong tendinous support
with little muscle fascicular shortening and fatigueresistance
properties. The DDF muscle combines
passive and dynamic functions with larger tension
development and higher shortening velocities during
digital motion. Architectural parameters are useful for
estimation of forces and have implications for analysis
of muscle-tendon function, surgical procedures
involving muscle-tendon lengthening, and biomechanical
modeling. (Am J Vet Res 2004;65:819–828)
To evaluate effects of poly(ADP-ribose) polymerase-1 (PARP1) inhibitors on the production of tumor necrosis factor-α (TNF-α) by interferon-γ (IFN-γ)– and lipopolysaccharide (LPS)-stimulated peripheral blood mononuclear cells (PBMCs) of horses as an in vitro model of inflammation in horses.
1,440 samples of PBMCs from 6 healthy research horses.
From heparinized whole blood samples, PBMC cultures were obtained. An initial dose-response trial on 48 PBMC samples from 2 horses (24 samples each) was used to determine concentrations of IFN-γ and LPS for use as low- and high-level stimulation concentrations. Seventy-two PBMC samples from 6 horses were assigned equally to 1 of 4 PARP1 inhibition categories: no PARP1 inhibitor (PARP1 inhibition control); 2-((R)-2-methylpyrrolidin-2-yl)-1H-benzimidazole-4-carbozamide dihydrochloride (ABT888);4-(3-(1-(cyclopropanecarbonyl)piperazine-4-carbonyl)-4-fluorobenzyl)phthalazin-1(2H)-one (AZD2281); or N-(6-oxo-5,6-dihydrophenanthridin-2-yl) -N,N-dimethylacetamide hydrochloride (PJ34). Samples of PBMCs from each horse and each PARP1 inhibition category were then assigned to 1 of 3 levels of IFN-γ and LPS stimulation: none (control), low stimulation, or high stimulation. After a 24-hour incubation period, a TNF-α ELISA was used to measure TNF-α concentration in the supernatant. Results were compared across treatments and for each horse. Data were analyzed with repeated-measures ANOVA.
Median TNF-α concentration was significantly lower for PJ34-treated, high-level stimulated PBMCs than for PARP1 inhibition control, high-level stimulated PBMCs; however, no other meaningful differences in TNF-α concentration were detected among the inhibition and stimulation combinations.
CONCLUSIONS AND CLINICAL RELEVANCE
Findings suggested that PJ34 PARP1 inhibition may reduce TNF-α production in horses, a potential benefit in reducing inflammation and endotoxin-induced damage in horses.