Equine veterinary journal. Supplement最新文献

The plasma proteins are a significant contributor to the total weak acid concentration as a net anionic charge. Due to potential species difference, species-specific values must be confirmed for the weak acid anionic concentrations of proteins (Atot) and the effective dissociation constant for plasma weak acids (Ka). We studied the net anion load Atot of equine plasma protein in 10 clinically healthy mature Standardbred horses. A multi-step titration procedure, using a tonometer covering a titration range of PCO2 from 25 to 145 mmHg at 37 degrees C, was applied on the plasma of these 10 horses. Blood gases (pH, PCO2) and electrolytes required to calculate the strong ion difference ([SID] = [(Na(+) + K(+) + Ca(2+) + Mg(2+))-(Cl(-) + Lac(-) + PO4(2-))]) were simultaneously measured over a physiological pH range from 6.90-7.55. A nonlinear regression iteration to determine Atot and Ka was performed using polygonal regression curve fitting applied to the electrical neutrality equation of the physico-chemical system. The average anion-load Atot for plasma protein of 10 Standardbred horses was 14.89 +/- 0.8 mEq/l plasma and Ka was 2.11 +/- 0.50 x 10(-7) Eq/l (pKa = 6.67). The derived conversion factor (iterated Atot concentration/average plasma protein concentration) for calculation of Atot in plasma is 0.21 mEq/g protein (protein-unit: g/l). This value compares closely with the 0.24 mEq/g protein determined by titration of Van Slyke et al. (1928) and 0.22 mEq/g protein recently published by Constable (1997) for horse plasma. The Ka value compares closely with the value experimentally determined by Constable in 1997 (2.22 x 10(7) Eq/l). Linear regression of a set of experimental data from 5 Thoroughbred horses on a treadmill exercise test, showed excellent correlation with the regression lines not different from identity for the calculated and measured variables pH, HCO3 and SID. Knowledge of Atot and Ka for the horse is useful especially in exercise studies and in clinical conditions to quantify the mechanisms of the acid-base disturbances occurring.

This study compared the study of a pectin-lecithin complex (Pronutrin) on gastric ulcer healing during an 11 day period in 2 groups of 12 horses each. Twenty-four horses suffering from gastric lesions of differing severity were selected from a larger group of clinical cases on the basis of gastroscopic examination. Both gastric mucosal erosions as well as gastric ulcers were found in the 2 mucosal regions (pars nonglandularis and pars glandularis). The gastric mucosal lesions occurred predominantly in the pars nonglandularis in the vicinity of the margo plicatus. The 24 horses were divided equally into a treated group (Group A) and a control group (Group B). Twelve horses in Group A received Pronutrin, in a dose of 300 g/horse/day over a period of 10 days, whereas horses in Group B received no active substance. Gastroscopic examination was performed on Days 0 and 11. The degree of severity of the gastric erosions or gastric ulcers was evaluated independently in the 2 mucosal regions with the aid of a scoring system. Group A horses showed good acceptance of the product and no side effects were recorded. After the 10 day treatment phase, Group A showed a marked reduction in gastric mucosal lesions or disappearance of lesions, while untreated horses showed no change or, even, a deterioration on Day 11. Statistical calculation of efficacy revealed a highly significant reduction in gastric mucosal lesions in the pars nonglandularis and a significant reduction in gastric mucosal lesions in the pars glandularis in the treated horses. It would appear, however, that the treatment period of 10 days was too short, since the gastric mucosal lesions had often not completely healed in all horses. The results of this study in 24 horses with gastric lesions suggest that a pectin-lecithin complex can have a beneficial effect on the healing of gastric ulcers.

Gastric ulceration has been found to occur in 80-90% of Thoroughbreds in active race training. Previously, variable success has been reported using mucosal surface protectants and H2 receptor antagonist. Omeprazole, a substituted benzimidazole, has been shown to inhibit gastric acid secretion in both man and animals. Fourteen horses, in active race training and with endoscopic evidence of moderated to severe gastric ulceration were divided into 2 groups: Group 1 (7 horses) were given placebo paste orally once daily for 28 days; Group 2 (7 horses) received 1.54 g active omeprazole in the placebo once daily for 28 days. Logs detailing administration and acceptability of the paste, and the horse's feeding and training regime were maintained by the trainer of each horse. Endoscopic examination of the stomach occurred at the beginning of the trial, and at 13-17 days and 27-31 days following commencement of the trial. Those horses that were free of ulceration on Days 27-31 were reexamined on Days 35-49. Acceptability of the paste, whether with or without active omeprazole, was deemed excellent in all horses except on one occasion, when one horse swallowed the paste following initial mild reluctance. Of the horses given the placebo (Group 1), 3 were withdrawn after the 13-17 day endoscopic examination: 1 horse to be given a H2 receptor antagonist, 1 horse was removed from training due to aryepiglottic entrapment and 1 horse had a greater than 10% fall in bodyweight from the start of the trial. Of the horses given active omeprazole (Group 2), one horses was relocated to another race track following the 13-17 day endoscopic examination. For the horses given placebo (Group 1), there was no change in the severity of ulceration. In contrast, the severity of ulceration in the horses given active omeprazole was significantly reduced at 13-17 days and 27-31 days. In 2 Group 2 horses, ulcers that had been completely eliminated subsequently returned when reexamined at 35-49 days. The results of this study suggest that omeprazole, employing a once daily dosing schedule, is effective at reducing the severity or eliminating gastric ulcers in Thoroughbreds in active race training.

Ulceration of the nonglandular, stratified squamous mucosa of the equine and porcine stomach is a common event in both species, although in pigs the fatality rate is significant and it is an economically important disease. Because the barrier function of this mucosa in horses and pigs appears similar, it is probable that similar pathophysiological mechanisms may be responsible for the initiating lesions and reparative events. Recent studies of ulcer pathogenesis in the pig have shown that feed preparation or prolonged fasting can result in disruption of the normal stratification of gastric contents, thereby allowing high concentrations of HCl, pepsin and refluxed bile to mix in the proximal stomach. Conditions simulating those found in vivo have been shown to damage this mucosa in vitro and indicate that luminal products, such as short chain fatty acids and bile salts, which act in synergy with HCl, probably are necessary to induce significant damage to this mucosa. Studies of the equine stomach have shown a similar proximal to distal pH gradient in the fed stomach, a significant duodenal-gastric reflux, and induction of squamous ulcers with fasting, thereby illustrating that similar conditions may be responsible for damage to the equine nonglandular mucosa.

Equine gastric ulcer syndrome (EGUS) is very common among performance horses, with a reported prevalence of approximately 90% in racehorses, and also > 50% in foals. Omeprazole, an acid pump inhibitor 5 times more potent than ranitidine, has been used with great success to treat EGUS. This multicentre study of Thoroughbred racehorses with endoscopically verified gastric ulcers was designed to demonstrate the efficacy of an equine oral paste formulation of omeprazole in the treatment and prevention of recurrence of EGUS. Of the 100 horses entered into the study, 25 were sham-dosed for the full 58 days of the study. The remaining 75 horses all received omeprazole paste, 4 mg/kg bwt/day once daily for 28 days. At Day 28, 25 of treated horses continued on this dosing regimen while 25 received a half dose (2 mg/kg bwt once daily) and 25 horses were sham-dosed. By Day 28, gastric ulcers were completely healed in 77% of omeprazole-treated horses, while 92% were significantly (P < 0.01) improved. In contrast, 96% of the sham-dosed horses still had gastric ulcers at Day 28. The improvement was maintained in horses that continued on either a full dose or half dose of omeprazole paste until Day 58. However, in those horses that were removed from omeprazole treatment at Day 28, the incidence and severity of the gastric ulcers at the end of the study were similar to those horses that did not receive the omeprazole paste. This study demonstrates that omeprazole paste, 4 mg/kg bwt per os, once daily, is highly effective in healing gastric ulcers in Thoroughbred racehorses and that either a full dose or half dose of omeprazole paste effectively prevents the recurrence of EGUS. The study also indicates that gastric ulcers in untreated horses did not demonstrate a significant rate of spontaneous healing.

A paste formulation of the H+,K(+)-ATPase inhibitor omeprazole was evaluated in Thoroughbred foals and yearlings for its safety and acceptability. Twenty foals age 11-16 weeks and 20 yearling horses age 15-17 months were included and gastroscopic examinations performed 1-3 days before and at the end of each trial. Lesions were scored on a scale of 0 to 3 and animals allocated based on endoscopic lesion score and sex, with 4 animals in each of 5 replicates. Dosages of 4 mg omeprazole/kg bwt or sham treatment were administered once daily for 28 days, from a syringe graduated in 50 lb (22.68 kg) increments, the amount of paste administered being rounded up to the nearest corresponding weight in pounds. Acceptability of the paste or sham treatment was assessed and recorded by the individual administering the treatment on the basis of the tolerance or resistance to insertion of the syringe into the mouth, administration of the paste and if the paste was swallowed or actively expelled by the animal. Safety was determined on the basis of daily observation recordings and physical examination findings during and at the conclusion of the trial. Treatment was judged to have been accepted for all 420 doses of omeprazole paste and all 140 sham doses given to foals during the trial and for 418/420 doses of paste and all 140 sham doses given to yearlings. Two doses of paste were entirely rejected by yearlings. On the initial endoscopic examination, lesions were observed in the gastric squamous epithelial mucosa in 4 foals and 3 yearlings, and single small, superficial erosions were seen in the gastric glandular mucosa of 2 foals. On the second examination there were small, superficial erosions in the squamous mucosa in 3 foals and 2 yearlings, multi-focal superficial erosions in 1 foal and 1 yearling, and 1 foal had large areas of erosion extending from the margo plicatus toward the dorsal fundus. No lesions in the glandular mucosa were seen in foals or yearlings. There were no significant differences (P < 0.05) in lesion scores between the beginning and the end of the trials in the omeprazole-treated or sham-treated groups of foals or yearlings. A paste formulation of omeprazole, administered at a dose of 4 mg/kg bwt once daily for 28 days, was determined to be highly acceptable to the foals and yearlings we studied, and no adverse effects attributable to the medication were noted.