Blood concentration of bupivacaine and duration of sensory and motor block following ultrasound-guided femoral and sciatic nerve blocks in dogs.

Peripheral nerve blocks are becoming increasingly popular for perioperative use as anesthetics and analgesics in small animals. This prospective study was performed to investigate the duration of motor and sensory blockade following use of bupivacaine for ultrasound-guided femoral and sciatic nerve blocks in dogs and to measure the plasma concentrations of bupivacaine that result from these procedures. Six dogs were anesthetized twice using a randomized cross-over design. At the first anesthetic, dogs were assigned to receive either an ultrasound-guided femoral nerve block or sciatic nerve block with 0.15 mL kg-1 of bupivacaine 0.5%. Two months later, the other nerve block was performed during a second anesthetic. At 5, 10, 15, 20, 30 and 60 minutes after injection, arterial blood samples were collected for laboratory measurement of bupivacaine. After 60 minutes, dogs were recovered from anesthesia. Starting at two hours post-injection, video-recordings of the dogs were made every two hours for 24 hours. The videos were randomized and the degree of motor and sensory blockade was evaluated using a three-point scoring system (0 = no effect, 1 = mild effect, 2 = complete blockade) by two blinded assessors. The median (range) times to full recovery from motor blockade were 11 (6-14) hours (femoral) and 12 (4-18) hours (sciatic), and 15 (10-18) hours (femoral) and 10 (4-12) hours (sciatic) for sensory blockade. There were no differences in the median times to functional recovery for the two techniques. Plasma concentrations of bupivacaine were no different following the blocks and were less than 0.78 µg mL-1 at all times. These results suggest that these ultrasound-guided nerve blocks do not result in potentially toxic systemic levels of local anesthetic and that their duration of action is useful for providing anesthesia and analgesia for pelvic limb procedures.

Workload of horses on a water treadmill: effect of speed and water height on oxygen consumption and cardiorespiratory parameters.

BACKGROUND: Despite the use of water treadmills (WT) in conditioning horses, the intensity of WT exercise has not been well documented. The workload on a WT is a function of water height and treadmill speed. Therefore, the purpose of this study was to determine the effects of these factors on workload during WT exercise. Fifteen client-owned Quarter Horses were used in a randomized, controlled study. Three belt speeds and three water heights (mid cannon, carpus and stifle), along with the control condition (dry treadmill, all three speeds), were tested. Measured outcomes were oxygen consumption (V̇O2), ventilation (respiratory frequency, tidal volume (VT)), heart rate (HR), and blood lactate. An ergospirometry system was used to measure V̇O2 and ventilation. Linear mixed effects models were used to examine the effects of presence or absence of water, water height and speed (as fixed effects) on measured outcomes. RESULTS: Water height and its interaction with speed had a significant effect on V̇O2, VT and HR, all peaking at the highest water level and speed (stifle at 1.39 m/s, median V̇O2 = 16.70 ml/(kg.min), VT = 6 L, HR = 69 bpm). Respiratory frequency peaked with water at the carpus at 1.39 m/s (median 49 breaths/min). For a given water height, the small increments in speed did not affect the measured outcomes. Post-exercise blood lactate concentration did not change. CONCLUSIONS: Varying water height and speed affects the workload associated with WT exercise. The conditions utilized in this study were associated with low intensity exercise. Water height had a greater impact on exercise intensity than speed.

Relationship of oxidative stress in skeletal muscle with obesity and obesity-associated hyperinsulinemia in horses.

In horses, hyperinsulinemia and insulin resistance (insulin dysregulation) are associated with the development of laminitis. Although obesity is associated with insulin dysregulation, the mechanism of obesity-associated insulin dysregulation remains to be established. We hypothesized that oxidative stress in skeletal muscle is associated with obesity-associated hyperinsulinemia in horses. Thirty-five light breed horses with body condition scores (BCS) of 3/9 to 9/9 were studied, including 7 obese, normoinsulinemic (BCS ≥ 7, resting serum insulin < 30 µIU/mL) and 6 obese, hyperinsulinemic (resting serum insulin ≥ 30 µIU/mL) horses. Markers of oxidative stress (oxidative damage, mitochondrial function, and antioxidant capacity) were evaluated in skeletal muscle biopsies. A Spearman's rank correlation coefficient was used to determine relationships between markers of oxidative stress and BCS. Furthermore, to assess the role of oxidative stress in obesity-related hyperinsulinemia, markers of antioxidant capacity and oxidative damage were compared among lean, normoinsulinemic (L-NI); obese, normoinsulinemic (O-NI); and obese, hyperinsulinemic (O-HI) horses. Increasing BCS was associated with an increase in gene expression of a mitochondrial protein responsible for mitochondrial biogenesis (estrogen-related receptor alpha, ERRα) and with increased antioxidant enzyme total superoxide dismutase (TotSOD) activity. When groups (L-NI, O-NI, and O-HI) were compared, TotSOD activity was increased and protein carbonyls, a marker of oxidative damage, decreased in the O-HI compared to the L-NI horses. These findings suggest that a protective antioxidant response occurred in the muscle of obese animals and that obesity-associated oxidative damage in skeletal muscle is not central to the pathogenesis of equine hyperinsulinemia.

Chez les chevaux l'hyperinsulinémie et la résistance à l'insuline (dérèglement de l'insuline) sont associées avec le développement de fourbure. Bien que l'obésité soit associée avec le dérèglement de l'insuline, le mécanisme de l'obésité associée au dérèglement de l'insuline demeure à être établi. Nous émettons l'hypothèse que le stress oxydatif dans les muscles squelettiques est associé avec l'obésité associée à l'hyperinsulinémie chez les chevaux. Trente-cinq chevaux de races légères avec des pointages de conditions corporelles (PCC) de 3/9 à 9/9 ont été étudiés, incluant sept chevaux obèses, normo-insulinémique (PCC ≥ 7, insuline sérique au repos < 30 µIU/mL) et six chevaux obèses, hyperinsulinémique (insuline sérique au repos ≥ 30 µIU/mL). Les marqueurs de stress oxydatif (damage oxydatif, fonction mitochondriale, et capacité antioxydante) furent évalués dans des biopsies de muscles squelettiques. Un coefficient de corrélation de rang de Spearman a été utilisé pour déterminer la relation entre les marqueurs de stress oxydatif et le PCC. De plus, pour évaluer le rôle du stress oxydatif dans l'obésité reliée à l'hyperinsulinémie, les marqueurs de la capacité anti-oxydante et des dommages oxydatifs ont été comparés entre des chevaux minces, normo-insulinémiques (L-NI); des chevaux obèses, normo-insulinémique (O-NI); et des chevaux obèses, hyperinsulinémiques (O-HI). Une augmentation des PCCs était associée avec une augmentation de l'expression des gènes d'une protéine mitochondriale responsable de la biogénèse des mitochondries (récepteur alpha apparenté aux estrogènes, ERRα) et d'une augmentation de l'activité anti-oxydante totale de l'enzyme superoxyde dismutase (TotSOD). Lors de la comparaison des groupes (L-NI, O-NI, et O-HI), l'activité TotSOD était augmentée et les carbonyles protéiques, un marqueur des dommages oxydatifs, avaient diminué chez les chevaux O-HI comparativement aux chevaux L-NI. Ces données suggèrent qu'une réponse anti-oxydante protectrice s'est produite dans le muscle des chevaux obèses et que le dommage oxydatif associés à l'obésité dans les muscles squelettiques n'est pas central à la pathogénèse de l'hyperinsulinémie équine.(Traduit par Docteur Serge Messier).

Comparison of the risks of atherosclerotic events versus death from other causes associated with antiretroviral use.

BACKGROUND: Studies considering the risk of atherosclerotic disease (AtD) associated with the use of HAART have reported inconsistent results. METHODS: Data on antiretroviral therapy (ART) use, risk factors for cardiovascular disease (CVD), AtD and death from other causes in 18 603 HIV-infected patients from two established cohorts were evaluated. The relative hazards of AtD and death from other causes were calculated using a proportional hazards competing risks framework. The impact of protease inhibitor (PI)-containing, non-nucleoside reverse transcriptase inhibitor (NNRTI)-containing or PI + NNRTI-containing regimens on these outcomes were compared to nucleoside reverse transcriptase inhibitor (NRTI)-only regimens or stopping therapy, adjusting for known CVD risk factors. RESULTS: In 77 480 person-years of follow-up (median duration 3.49 years) there were 318 AtD events including 92 myocardial infarctions and 2044 deaths. Older age, hypertension, diabetes mellitus, having smoked and HIV disease stage were significantly associated with increased risk of AtD. PI- and NNRTI-containing regimens significantly reduced the joint risk of either AtD or death from other causes compared to NRTI-only or stopping therapy [hazard ratio (HR) for PI-containing ART, 0.76, 95% confidence interval (CI), 0.73-0.78, P< 0.001; NNRTI-containing ART, 0.69, 95% CI, 0.65-0.74; P< 0.001). PI-containing ART was associated with a borderline significant increased risk of myocardial infarction (cause-specific HR for PI-containing ART 1.19, 95% CI, 1.01-1.40, P = 0.04) but not with increased risk of AtD compared to NRTI-only regimens or stopping therapy (cause-specific HR for PI-containing ART, 1.03, 95% CI, 0.95-1.13, P = 0.44). CONCLUSIONS: Overall benefits of PI- and NNRTI-based ART in reducing mortality significantly outweigh any risks of AtD in the "short-term" follow-up of this study. Traditional cardiac risk factors play an important role in determining AtD risk status.