Figure 1.
Figure 1.

American Association of Equine Practitioners (AAEP) lameness scores (0 to 5; least squares means ± SEM) after intra-articular lipopolysaccharide (LPS; derived from Escherichia coli O55:B5) injection at 0 to 24 h postinjection. Treatments were control (lactated Ringer’s solution only; n = 6), 0.25 ng LPS solution (n = 7), and 0.50 ng LPS solution (n = 6). Main effect is time (P ≤ 0.01). a,bDifferent superscripts denote a difference (P ≤ 0.05) among treatments.

 


Figure 2.
Figure 2.

Carpal circumference (cm; least squares means ± SEM) after intra-articular lipopolysaccharide (LPS; derived from Escherichia coli O55:B5) injection at 0 to 24 h postinjection. Treatments were control (lactated Ringer’s solution only; n = 6), 0.25 ng LPS solution (n = 7), and 0.50 ng LPS solution (n = 6). a–dDifferent superscripts denote the main effect of time (P ≤ 0.01).

 


Figure 3.
Figure 3.

Clinical assessment of heart rate (least squares means ± SEM) after intra-articular lipopolysaccharide (LPS; derived from Escherichia coli O55:B5) injection at 0 to 24 h postinduction. Treatments were control (lactated Ringer’s solution only; n = 6), 0.25 ng LPS solution (n = 7), and 0.50 ng LPS solution (n = 6).

 


Figure 4.
Figure 4.

Clinical assessment of respiration rate (least squares means ± SEM) after intra-articular lipopolysaccharide (LPS; derived from Escherichia coli O55:B5) injection at 0 h to 24 h postinduction. Treatments were: control (lactated Ringer’s solution only; n = 6), 0.25 ng LPS solution (n = 7), and 0.50 ng LPS solution (n = 6).

 


Figure 5.
Figure 5.

Clinical assessment of rectal temperatures (least squares means ± SEM) after intra-articular lipopolysaccharide (LPS; derived from Escherichia coli O55:B5) injection at 0 to 24 h postinduction. Treatments were control (lactated Ringer’s solution only; n = 6), 0.25 ng LPS solution (n = 7), and 0.50 ng LPS solution (n = 6). a–dDifferent superscripts denote the main effect of time (P ≤ 0.01).

 


Figure 6.
Figure 6.

Mean synovial fluid concentrations (pg/mL) of PGE2 after intra-articular lipopolysaccharide administration (LPS; derived from Escherichia coli O55:B5). Treatments were control (lactated Ringer’s solution only; n = 6), 0.25 ng LPS solution (n = 7), and 0.50 ng LPS solution (n = 6). a–cDifferent superscripts indicate differences (P ≤ 0.05) in PGE2 concentration among treatments at specific time points after LPS injection.

 


Figure 7.
Figure 7.

Mean synovial fluid concentrations (ng/mL) of catabolic collagenase cleavage neopeptide (C2C) after intra-articular lipopolysaccharide administration (LPS; derived from Escherichia coli O55:B5). Treatments were control (lactated Ringer’s solution only; n = 6), 0.25 ng LPS solution (n = 7), and 0.50 ng LPS solution (n = 6). a–cDifferent superscripts denote the main effect of time (P ≤ 0.01).

 


Figure 8.
Figure 8.

Mean synovial fluid concentrations (ng/mL) of carboxypeptide of type II collagen (CPII) after intra-articular lipopolysaccharide administration (LPS; derived from Escherichia coli O55:B5). Treatments were control (lactated Ringer’s solution only; n = 6), 0.25 ng LPS solution (n = 7), and 0.50 ng LPS solution (n = 6). a,bDifferent superscripts indicate differences (P ≤ 0.05) in CPII concentration among treatments at specific time points after LPS injection.