Melbourne Veterinary School - Research Publications
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ItemComplete upper airway collapse and apnoea during tethered swimming in horses.(Wiley, 2020-05)BACKGROUND: There is limited knowledge of the breathing strategy and impact on the patency of the upper respiratory tract (URT) in swimming horses. OBJECTIVES: To describe the respiratory responses and endoscopic appearance of the URT during tethered swimming in horses. STUDY DESIGN: Prospective descriptive study. METHODS: Ten race-fit horses, with no history of URT obstruction, were examined during tethered swimming. Endoscopic examination, heart rate, sound recordings and above and below water video recordings were obtained. Plasma lactate concentration was measured before and 5 min after swimming and tracheal endoscopy was performed 30 min after exercise to assess for presence of blood or mucus. Four horses also underwent endoscopy during exercise on the track. RESULTS: Mean (±s.d.) breathing frequency was 28 ± 5 breaths/min during swimming, with a brief inspiration (mean ± s.d. TI = 0.51 ± 0.08 s), followed by a period of apnoea (1.59 ± 0.53 s) and then a short, forced expiration (TE = 0.42 ± 0.5 s). During apnoea all horses exhibited complete collapse of the URT including closure of the external nares, nasopharynx and rima glottidis (with bilateral adduction of the arytenoid cartilages and vocal folds) and, in two horses, epiglottic retroversion. No horses had URT collapse during overground exercise. Locomotor-respiratory coupling was not observed during swimming. Median (IQR) plasma lactate post swim was 4.71 mmol/L (2.08-8.09 mmol/L) vs 0.68 mmol/L (0.65-0.71 mmol/L) preswim. Post swim endoscopy revealed grade 1 exercise-induced pulmonary haemorrhage (EIPH) in 2 horses. Median mucus grade was 1 (range 0-3). MAIN LIMITATIONS: Overground endoscopy was not performed in all horses. CONCLUSIONS: Horses experienced complete URT collapse associated with post inspiratory apnoea when swimming. The reason for this is unknown but may be to aid buoyancy or associated with the mammalian dive response - a survival reflex to preserve oxygen stores and prevent water entering the lungs.
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ItemThe effect of serial administration of bicarbonate on plasma total CO2 concentrations in horses(John Wiley and Sons, 2021-02)The administration of alkalinising agents including bicarbonate is of concern to racing authorities because resultant alkalosis may enhance performance and interfere with the detection of drugs in post-race urine. A threshold for total carbon dioxide (TCO2) of 36.0 mmol/L in plasma (with action limit of 37.0 mmol/L) has been set. Serial dosing of sodium bicarbonate has gained popularity in human athletes but has not been studied in horses previously. Sodium bicarbonate (200 g per horse) and 60 g of an electrolyte-vitamin complex was administered in 2-L water via nasogastric intubation to five Standardbred horses for three consecutive days (total dose bicarbonate 0.42 ± 0.02 g/kg). Serial blood samples were taken over Days 1–5, with the final day (5) intended to simulate a ‘clear day’, and TCO2 was analysed. Following the first bicarbonate administration, plasma TCO2 peaked at 6 h (34.8 ± 1.3 mmol/L), returning to baseline by 23 h. On Day 2, four out of the five horses showed a peak greater than 36.0 mmol/L (mean 37.0 ± 2.1 mmol/L). With daily repeated dosing, plasma TCO2 peaked progressively earlier, and by Day 3, the peak occurred at 2 h and concentrations declined more rapidly. On Days 4 and 5, TCO2 levels remained low (<32.1 mmol/L on Day 4 and between 27.0–31.2 mmol/L on Day 5). These studies demonstrate that serial dosing of a ‘split dose’ of sodium bicarbonate on three consecutive days does not result in the accumulation or carry-over of plasma TCO2 levels beyond the levels observed following a single dose.
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ItemImmunohistochemical analysis of laryngeal muscle of horses clinically affected with recurrent laryngeal neuropathy(WILEY, 2020-10-27)Background As myosin heavy chain (MyHC) profile of muscle fibres is heavily influenced by neural input, changes in MyHC expression are expected in horses clinically affected with recurrent laryngeal neuropathy (RLN) yet, this has not been thoroughly investigated. Objectives To describe the changes in MyHC and fibre diameter in left cricoarytenoideus dorsalis (L-CAD) muscle of horses with clinical signs of RLN. Study design Observational cohort study. Methods Immunohistochemistry was used to assess the MyHC-based fibre-type proportion, size and grouping in the L-CAD of 10 Thoroughbred horses, five clinically affected with RLN and five unaffected controls based on resting endoscopic examination. The Mann-Whitney U test was used to compare the two groups. Results Compared to controls (of mean age 3.0 ± 1.7 years) which only expressed type I, IIA and IIX MyHC, the L-CAD of affected horses (of mean age 2.8 ± 0.8 years) had obvious fibre-type grouping, and despite apparent compensatory hypertrophy of a small number of fibres, a decrease in overall fibre diameter (median difference −35.2 µm, 95% CI −47.4 to −7.9, P = .02) and diameter of type IIA fibres (median difference −46.8 µm, 95% CI −52.1 to −5.0, P = .03) was observed. Anti-fast MyHC (MY32) cross-immunoreacted with embryonic-MyHC. Whereas MY32-positive fibres were identified as type IIX in controls, in affected horses these fibres were less than 50 µm diameter with internal nuclei and were MYH3-positive for embryonic myosin indicating depletion of type IIX fibres, yet active regeneration and fibre renewal. Main limitations Small sample size that did not include subclinical cases. Fibre size and appearance rather than staining colour were relied upon to differentiate embryonic from type IIX MyHC. Conclusions Horses clinically affected with RLN have overall atrophy of fibres, loss of IIX fibres and expression of embryonic myosin indicating regenerative capacity. Despite hypertrophy of some remaining fibres, the overall decline in the bulk of fibres, including those most fatigue-resistant, may be the critical change that results in failure to maintain arytenoid abduction during exercise although direct comparison to subclinical cases is needed to confirm this.