Hypoglycin A (HGA) in seeds of Acer spp. is suspected to cause seasonal pasture myopathy in North America and equine atypical myopathy (AM) in Europe, fatal diseases in horses on pasture. In previous studies, this suspicion was substantiated by the correlation of seed HGA content with the concentrations of toxic metabolites in urine and serum (MCPA-conjugates) of affected horses. However, seed sampling was conducted after rather than during an outbreak of the disease. The aim of this study was to further confirm the causality between HGA occurrence and disease outbreak by seed sampling during an outbreak and the determination of i) HGA in seeds and of ii) HGA and MCPA-conjugates in urine and serum of diseased horses. Furthermore, cograzing healthy horses, which were present on AM affected pastures, were also investigated. AM-pastures in Germany were visited to identify seeds of Acer pseudoplatanus and serum (n = 8) as well as urine (n = 6) from a total of 16 diseased horses were analyzed for amino acid composition by LC-ESI-MS/MS, with a special focus on the content of HGA. Additionally, the content of its toxic metabolite was measured in its conjugated form in body fluids (UPLC-MS/MS). The seeds contained 1.7–319.8 μg HGA/g seed. The content of HGA in serum of affected horses ranged from 387.8–8493.8 μg/L (controls < 10 μg/L), and in urine from 143.8–926.4 μg/L (controls < 10 μg/L), respectively. Healthy cograzing horses on AM-pastures showed higher serum (108.8 ± 83.76 μg/L) and urine concentrations (26.9 ± 7.39 μg/L) compared to control horses, but lower concentrations compared to diseased horses. The range of MCPA-carnitine and creatinine concentrations found in diseased horses in serum and urine were 0.17–0.65 mmol/L (controls < 0.01), and 0.34–2.05 μmol/mmoL (controls < 0.001), respectively. MCPA-glycine levels in urine of cograzing horses were higher compared to controls. Thus, the causal link between HGA intoxication and disease outbreak could be further substantiated, and the early detection of HGA in cograzing horses, which are clinically normal, might be a promising step in prophylaxis.

Summary A glass combined pH‐reference electrode was placed in the stomachs of 5 adult horses and pH was recorded every 6 mins for 24 h while (1) feed and all bedding materials were withheld for 24 h (unfed), (2) horses had free access to Timothy grass hay for 24 h (fed), and (3) horses had free access to Timothy grass hay and were treated with ranitidine, 6.6 mg/kg body weight, orally, every 8 h for 48 h (fed + ranitidine). There was a significant (P= 0.007) difference in median 24‐h gastric pH amongst the 3 protocols, the value being 3.1 in fed horses and 1.55 in unfed horses (P= 0.05) and 4.6 in fed + ranitidine horses (P= 0.05 compared with fed horses). The percentage of pH readings <2.0 was significantly greater (P= 0.05) in unfed (76%) than in fed (30%) horses, and in fed horses than in fed + ranitidine (9%) horses. The percentage of readings >2.0, 3.0, 4.0, 5.0 and 6.0 were each significantly (P= 0.05) greater in fed + ranitidine horses than in fed horses, and in fed than in unfed horses. There was no difference (P= 0.13) between median gastric pH values from different times of day in unfed horses (00:00 to 06:00 h, 1.5; 06:00 to 12:00 h, 1.6; 12:00 to 18:00 h, 1.7; and 18:00 to 24:00 h, 1.5). We conclude that gastric acidity is greatest when horses do not have access to feed material and that ranitidine effectively suppresses gastric acidity in horses under conditions of free access to hay.

SummaryHydroxyethyl starch (HES) solution is an effective colloidal infusion solution in humans for treatment of hypovolaemic shock, but it has not been compared with fluids currently available for use in horses. On the basis of plasma-expanding effect of HES in normal horses, a 10% medium-molecular 200/ 0.5 solution of HES was subsequently tested in hypovolaemic horses. Six normal horses were given five protocols of a single infusion of HES at varying dosage rates (5, 10, 15 ml HES/kg), as well as isotonic saline (15 ml/kg) and hypertonic saline (4 ml/kg b.w.). Dehydrated horses suffering from acute colitis or those which had been treated surgically for ileus of the small or large intestine were given an i.v. infusion of 10 ml HES/kg in combination with 10 ml saline/kg. Clinical data and blood samples for testing were taken before the infusion, and then 10 min, 1 h, 2, 4, 6, 8, 10, 12 and 24 h after infusion (a.i.). A significant decrease in haematocrit was observed in protocol 1-5 for a period of up to 4, 4, 10 h, 10 min and up to 10 min; in group of colitis, during the entire 24-h testing period, and in groups of ileus of small intestine and of large intestine, up to 4 and 10 h a.i. HES decreases better and longer-lasting haematocrit and total protein than either isotonic or hypertonic saline. Half-life of HES increases due to higher dosage (5.83, 7.63 and 11.48 h) and distribution is exclusively intravascular. In normal horses of protocol 1-3 using HES aPTT, sodium and potassium were within the physiological range. Serum amylase activity is increased in horses using HES. On the basis of this clinical study, the decreasing effect of urea and creatinine in colic patients after surgery and fewer instances of postoperative ileus a dosage of 10 ml HES/kg could be recommended.