Potassium and lactate uptake by noncontracting tissue during strenuous exercise.

Efflux of potassium (K+) and lactate (lac-) from active skeletal muscle during high intensity exercise leads to increased plasma [K+] and [lac-] in venous and arterial blood. The exercise-induced increases in these ions in human athletes is ameliorated, in part, by uptake by noncontracting tissue, reflected by an increase in the arteriovenous difference across these tissues from rest to exercise. To test the hypothesis that these ions are taken up by noncontracting tissue in strenuously exercising horses, plasma [K+] and [lac-] were measured in blood samples collected simultaneously from the carotid artery (CA), femoral vein (FV), and transverse facial vein (TFV) in 5 unconditioned Standardbred horses performing 4.5 min of strenuous treadmill exercise. Further, the arteriovenous differences ((a-v)diff) in [K+] and [lac-] were calculated across active tissue (CA-FV) and noncontracting tissue (CA-TFV). After 3 min of strenuous exercise, plasma [K+] in FV blood (mean +/- s.e. 7.1 +/- 0.2 mmol/l) was greater (P<0.05) than in CA blood (6.8 +/- 0.2 mmol/l) and both of these concentrations were greater (P<0.05) than a value of 5.7 +/- 0.1 mmol/l in TFV blood. Similarly, plasma [lac-] increased to 20.6 +/- 0.8 and 21.1 +/- 0.8 mmol/l in CA and FV blood, respectively, and these concentrations were greater (P<0.05) than a value of 19.1 +/- 0.8 mmol/l in TFV blood. The magnitude of the (a-v)diff for both [K+] and [lac-] increased (P<0.05) across active and noncontracting tissue during high-speed exercise but the directions were opposite, supporting release by active tissue and uptake by noncontracting tissue. These results confirm that uptake of K+ and lac- by noncontracting tissue contributes to regulation of the plasma concentrations of these ions in strenuously exercising horses.

Retrospective analysis of detomidine infusion for standing chemical restraint in 51 horses.

OBJECTIVE: To assess the effectiveness of a detomidine infusion technique to provide standing chemical restraint in the horse. DESIGN: Retrospective study. ANIMALS: Fifty-one adult horses aged 9.5 ± 6.9 years (range 1-23 years) and weighing 575 ± 290.3 kg. METHODS: Records of horses presented to our clinic over a 3-year period in which a detomidine infusion was used to provide standing chemical restraint were reviewed. Information relating to the types of procedure performed, duration of infusion, drug dosages and adjunct drugs administered was retrieved. RESULTS: Detomidine was administered as an initial bolus loading dose (mean ±â€ŠSD) of 7.5 ± 1.87 µg kg-1. The initial infusion rate was 0.6 µg kg-1 minute-1, and this was halved every 15 minutes. The duration of the infusion ranged from 20 to 135 minutes. Twenty horses received additional detomidine or butorphanol during the procedure. All horses undergoing surgery received local anesthesia or epidural analgesia in addition to the detomidine infusion. A wide variety of procedures were performed in these horses. CONCLUSIONS: Detomidine administered by infusion provides prolonged periods of chemical restraint in standing horses. Supplemental sedatives or analgesics may be needed in horses undergoing surgery. CLINICAL RELEVANCE: An effective method that provides prolonged periods of chemical restraint in standing horses is described. The infusion alone did not provide sufficient analgesia for surgery and a significant proportion of animals required supplemental sedatives and analgesics.