Castration is among the most common surgical procedures performed in the horse (Equus Caballus) and a variety of post-operative complications can occur. This study aims to determine if a single dose of long-acting ceftiofur crystalline free acid (CCFA) used as a preoperative antimicrobial in equine field castrations offers any reduction in post-operative inflammatory markers when compared to procaine penicillin G (PPG). Sixty-five horses aged 8 months to 2 years were randomly assigned to the CCFA (n = 33) or PPG (n = 32) treatment groups. Horses were castrated under general anaesthesia using a closed castration technique with removal of the median raphe. Quantitative and qualitative inflammatory markers were measured and short-term complications were recorded post-operatively on Days 3, 8 and 14. No clinically significant difference in any postoperative inflammatory markers between the CCFA and PPG group was detected. In the CCFA group, 48% of horses experienced short-term post-operative complications compared to 31% in the PPG group. Regardless of the preoperative treatment, castration induced significant elevation in serum amyloid A (P<0.0001), preputial oedema (P<0.0001) and scrotal oedema (P<0.0001) at Day 3. These values returned to baseline levels by Day 8. Horses with grade 3 or above preputial oedema had elevated serum amyloid A values (P<0.001). The data from this study indicate CCFA used as a preoperative antibiotic for routine castration offers no advantages over PPG. The difference in complication rate between groups is likely of minimal clinical importance, as all complications were mild and self-limiting.

Arterial walls are largely composed of smooth muscle cells. By contracting or relaxing, these cells regulate arterial diameter, thus influencing blood flow and blood pressure. The concentration of calcium in arterial smooth muscle largely determines the degree of arterial contraction. The main source of calcium entry into these cells is through voltage‐gated L‐type calcium channels. We recently reported that local NADPH oxidase‐mediated stimulation of PKC alpha‐dependent L‐type calcium channel activity (“calcium sparklets”) results in increased calcium influx and arterial contraction. However, details regarding the molecular mechanisms underlying redox‐dependent regulation of L‐type calcium channels are poorly understood. Using a combination of TIRF microscopy and patch clamp electrophysiology, here we investigate detailed aspects of redox‐dependent regulation of arterial L‐type calcium channels including experiments examining the molecular composition of the NADPH oxidase complex involved as well as determining the identity of the participating reactive oxygen species. Preliminary data suggest that Rac1‐dependent NADPH oxidase activity results in the generation of hydrogen peroxide that in turn stimulates PKC alpha‐dependent L‐type calcium channel function. This work was supported by the Pew Scholars Program (GCA).