The effect of two different intra-operative end-tidal carbon dioxide tensions on apnoeic duration in the recovery period in horses.

To compare the effect of two different intraoperative end-tidal carbon dioxide tensions on apnoeic duration in the recovery period in horses.Prospective randomized clinical study.Eighteen healthy client-owned adult horses (ASA I-II) admitted for elective surgery. Horses were of a median body mass of 595 (238-706) kg and a mean age of 9 ± 5 years.A standardized anaesthetic protocol was used. Horses were positioned in dorsal recumbency and randomly allocated to one of two groups. Controlled mechanical ventilation (CMV) was adjusted to maintain the end-tidal carbon dioxide tension (Pe'CO2 ) at 40 ± 5 mmHg (5.3 ± 0.7 kPa) (group 40) or 60 ± 5 mmHg (8.0 ± 0.7 kPa) (group 60). Arterial blood gas analysis was performed at the start of the anaesthetic period (T0), at one point during the anaesthetic (T1), immediately prior to disconnection from the breathing system (T2) and at the first spontaneous breath in the recovery box (T3). The time from disconnection from the breathing system to return to spontaneous ventilation (RSV) was recorded. Data were analysed using a two sample t-test or the Mann-Whitney U-test and significance assigned when p < 0.05.Horses in group 60 resumed spontaneous breathing significantly earlier than those in group 40, [52 (14-151) and 210 (103-542) seconds, respectively] (p < 0.001). Arterial oxygen tension (PaO2 ), pH, base excess (BE) and plasma bicarbonate (HCO3-) were not different between the groups at RSV, however, PaO2 was significantly lower in group 60 during (T1) and at the end of anaesthesia (T2).Aiming to maintain intra-operative Pe'CO2 at 60 ± 5 mmHg (8.0 ± 0.7 kPa) in mechanically ventilated horses resulted in more rapid RSV compared with when Pe'CO2 was maintained at 40 ± 5 mmHg (5.3 ± 0.7 kPa)

Objective methods of nerve localisation to facilitate performing locoregional anaesthetic techniques for horses undergoing surgical procedures

SummaryPerineural anaesthesia is a useful technique in equine surgery, providing pre‐emptive targeted anaesthesia of the surgical site, reducing volatile anaesthetic requirements, improving recovery quality and providing postoperative pain relief. Surgery under standing sedation in horses has increased in popularity, mandating the need for effective locoregional anaesthesia and analgesic techniques. Nerve location techniques offer greater accuracy than blind techniques when placing injectate. These methods can help to avoid structures such as blood vessels and minimise direct nerve damage during needle placement, reducing the risk of procedure‐related complications. This review will discuss the most pertinent research in the veterinary literature where objective methods of nerve location have been used to perform peripheral nerve blocks in horses. The efficacy of using objective methods to perform nerve blocks in equine anaesthesia is discussed by the authors, providing useful information to equine anaesthetists, and potentially improve the quality of anaesthesia and analgesia in horses.</jats:p

Epigenetic mechanisms in tendon ageing

Introduction Tendon is a composite material with a well-ordered hierarchical structure exhibiting viscoelastic properties designed to transfer force. It is recognized that the incidence of tendon injury increases with age, suggesting a deterioration in homeostatic mechanisms or reparative processes. This review summarizes epigenetic mechanisms identified in ageing healthy tendon. Sources of data We searched multiple databases to produce a systematic review on the role of epigenetic mechanisms in tendon ageing. Areas of agreement Epigenetic mechanisms are important in predisposing ageing tendon to injury. Areas of controversy The relative importance of epigenetic mechanisms are unknown in terms of promoting healthy ageing. It is also unknown whether these changes represent protective mechanisms to function or predispose to pathology. Growing point Epigenetic markers in ageing tendon, which are under-researched including genome-wide chromatin accessibility, should be investigated. Areas timely for developing research Metanalysis through integration of multiple datasets and platforms will enable a holistic understanding of the epigenome in ageing and its relevance to disease

miR-24 and its target gene Prdx6 regulate viability and senescence of myogenic progenitors during aging

Satellite cell-dependent skeletal muscle regeneration declines during aging. Disruptions within the satellite cells and their niche, together with alterations in the myofibrillar environment, contribute to age-related dysfunction and defective muscle regeneration. In this study, we demonstrated an age-related decline in satellite cell viability and myogenic potential and an increase in ROS and cellular senescence. We detected a transient upregulation of miR-24 in regenerating muscle from adult mice and downregulation of miR-24 during muscle regeneration in old mice. FACS-sorted satellite cells were characterized by decreased levels of miR-24 and a concomitant increase in expression of its target: Prdx6. Using GFP reporter constructs, we demonstrated that miR-24 directly binds to its predicted site within Prdx6 mRNA. Subtle changes in Prdx6 levels following changes in miR-24 expression indicate miR-24 plays a role in fine-tuning Prdx6 expression. Changes in miR-24 and Prdx6 levels were associated with altered mitochondrial ROS generation, increase in the DNA damage marker: phosphorylated-H2Ax and changes in viability, senescence, and myogenic potential of myogenic progenitors from mice and humans. The effects of miR-24 were more pronounced in myogenic progenitors from old mice, suggesting a context-dependent role of miR-24 in these cells, with miR-24 downregulation likely a part of a compensatory response to declining satellite cell function during aging. We propose that downregulation of miR-24 and subsequent upregulation of Prdx6 in muscle of old mice following injury are an adaptive response to aging, to maintain satellite cell viability and myogenic potential through regulation of mitochondrial ROS and DNA damage pathways