Effect of metoclopramide on gastro-esophageal reflux in anesthetized dogs

Administration of morphine before anesthesia leads to gastro-esophageal reflux (GER) in over 50% of dogs during the subsequent anesthetic. This GER is clinically silent but can lead to aspiration pneumonitis, esophagitis and esophageal stricture. In this prospective clinical study we aimed to determine the effect of metoclopramide on gastro-esophageal reflux (GER) in dogs undergoing elective orthopedic surgery. Dogs were admitted to the study if they were healthy, and had no history of vomiting or dysphagia. Dogs were fasted for an average of 18.2 ± 4.3 (mean ± SD) hours prior to induction of anesthesia. Anesthesia in all dogs included acepromazine, morphine, thiopental and isoflurane in oxygen. By random allocation, half the dogs received metoclopramide (M) as an IV bolus (0.4 mg kg^–1) and then infusion (0.3 mg kg^–1hour^–1), the others received equivalent volumes of saline (S). To measure esophageal pH a sensor-tipped catheter was placed with the tip 5–7 cm cranial to the lower esophageal sphincter, and connected to a computer for continual data collection. The pH of any fluid running from the mouth or nose was measured. Gastro-esophageal reflux was defined as a decrease in esophageal pH below 4 or an increase above 7.5. Fisher's Exact test was used to test significance of differences in incidence between groups. Separate multivariable logistic regression models were created for each outcome to assess the effects of risk factors on outcome. There were seven cases of GER in 16 dogs receiving M and 8/14 in those receiving S. There were no significant differences between M and S treated dogs in age, weight, duration of anesthesia and fasting, thiopental dose or incidence of vomiting. The administration of metoclopramide at this dose did not significantly reduce the incidence of GER in these anesthetized dogs.     

Flunixin meglumine attenuation of endotoxin-induced damage to the cardiopulmonary vascular endothelium of the pony

Endotoxic shock was induced in 5 ponies by intraperitoneal injections of 20, 40, 60, 80, and 80 micrograms of Escherichia coli endotoxin (LPS)/kg of body weight at 0, 6, 12, 18, and 24 hours, respectively. At 24 hours, the ponies also were given 20 micrograms of LPS/kg via catheter in the left ventricle of the heart. A 2nd group of 4 ponies was given 1.1 mg of flunixin meglumine (FM)/kg, IV, at 6, 12, 18, and 24 hours just before the corresponding LPS injection. Two hours after the 24-hour LPS injection, the ponies in both groups were anesthetized, the lungs were perfused with fixative, and portions of the pulmonary arteries and veins and right and left ventricles were prepared for scanning and transmission electron microscopy. In ponies that were given only LPS, some areas of pulmonary vascular endothelium appeared normal when compared with untreated controls, but other areas had disoriented endothelial cells or had varying amounts of sloughing, which ranged from focal areas of a few cells to large areas of denuded endothelium. Ponies treated with FM before LPS had less severe and less extensive endothelial cell damage. In both groups, leukocytes were attached to areas of the vessel wall; endothelial cell damage was greater in these regions. Administration of FM before LPS administration attenuated the LPS-induced endothelial cell damage.     

ENLARGING BILATERAL FEMORAL CONDYLAR BONE CYSTS WITHOUT SCINTIGRAPHIC UPTAKE IN A YEARLING FOAL

Bilateral subchondral bone cysts of the femoral condyles were diagnosed by conventional radiography in a 14 month old Appaloosa colt. Surgical debridement was performed, and over the next 18 months the appearance of the cysts was evaluated with radiography and bone scintigraphy. On the preoperative scintigrams, increased radiopharmaceutical uptake was associated with the cysts. Despite continued radiographic enlargement, the cysts did not demonstrate increased radiopharmaceutical uptake post-operatively.     

Hemodynamics, plasma eicosanoid concentrations, and plasma biochemical changes in calves given multiple injections of Escherichia coli endotoxin

Twelve male neonatal calves (39 to 50 kg) were allotted to 3 groups of 4 calves each. All calves were anesthetized with halothane, and then Escherichia coli endotoxin was given intravenously (3 times) and intraperitoneally (3 times) during a 6-hour period. Group-1 calves were untreated, group-2 calves were pretreated with a low dose of flunixin meglumine (1.1 mg/kg of body weight), and group-3 calves were pretreated with a high dose of flunixin meglumine (4.4 mg/kg). In calves of group 1, the mean systemic arterial blood pressure (MABP) and cardiac output (CO) decreased, but pulmonary arterial pressure increased after the initial intravenous and intraperitoneal injections of endotoxin. In calves of this group, these changes were accompanied by increased plasma thromboxane B2 (TxB2) concentration. During this period, increased plasma TxB2 concentration or hemodynamic changes were not detected in calves of groups 2 and 3. Only calves of group 1 had altered hemodynamics early in the experiment; however, after 6 hours, calves of all 3 groups had similarly decreased CO and MABP. In calves of the untreated group, plasma 6-keto-prostaglandin (PG)F1 alpha concentration increased steadily from the beginning of the experiment until 3 hours later. The CO and MABP were low at the time when serum 6-keto-PGF1 alpha concentration was high; however, these 2 measurements also were low in treated calves who did not have correspondingly high plasma 6-keto-PGF1 alpha concentration. Regional blood flow analysis did not reveal correlations between prostanoid concentrations and altered blood flow to selected tissues.(ABSTRACT TRUNCATED AT 250 WORDS)     

Umbilical cord remnant infections in foals: 16 cases (1975-1985)

Infection of the umbilical cord remnants was diagnosed in 16 foals. The infection was found in the urachus alone in 3 foals, the umbilical arteries in 2 foals, the urachus and umbilical arteries in 3 foals, the urachus and umbilical vein in 2 foals, and the urachus, umbilical vein, and umbilical arteries in 2 foals. The specific location of the infection was not determined in 4 foals. Eleven foals developed an acquired patent urachus between 4 and 16 days of age. Seven foals had one or more joints infected. All foals with umbilical cord remnant infections were treated with orally, intramuscularly, or intravenously administered antibiotics and 9 foals had the umbilical cord remnants excised. Nine foals survived, 6 of which had had excision of the infected remnants. Only 2 foals with joint infections survived.     

Equine endothelial cells in vitro

Certain in vitro culture conditions were determined for equine endothelial cells obtained from the aorta and pulmonary arteries. Cells were enzymatically isolated from the vessel lumen, using clostridial collagenase (2.5 mg/ml of Hanks's balanced salt solution) incubated at 37 C for 30 minutes. Cells were cultured in alpha minimum essential medium supplemented with plasma-derived and nonplasma-derived bovine fetal sera, endothelial cell-growth supplement, heparin, and antibiotics. Smooth muscle cell growth was not inhibited with nonplasma-derived animal sera, plasma-derived equine serum, or heparin. Heparin and a serum replacement were toxic to the cells used in the present study. Statistically significant differences were not found between the various media supplements.     

Retrospective analysis of detomidine infusion for standing chemical restraint in 51 horses

Objective To assess the effectiveness of a detomidine infusion technique to provide standing chemical restraint in the horse. Design Retrospective study. Animals Fifty‐one adult horses aged 9.5 ± 6.9 years (range 1–23 years) and weighing 575 ± 290.3 kg. Methods Records of horses presented to our clinic over a 3‐year period in which a detomidine infusion was used to provide standing chemical restraint were reviewed. Information relating to the types of procedure performed, duration of infusion, drug dosages and adjunct drugs administered was retrieved. Results Detomidine was administered as an initial bolus loading dose (mean ± SD) of 7.5 ± 1.87 µg kg^?1. The initial infusion rate was 0.6 µg kg^?1 minute^?1, and this was halved every 15 minutes. The duration of the infusion ranged from 20 to 135 minutes. Twenty horses received additional detomidine or butorphanol during the procedure. All horses undergoing surgery received local anesthesia or epidural analgesia in addition to the detomidine infusion. A wide variety of procedures were performed in these horses. Conclusions Detomidine administered by infusion provides prolonged periods of chemical restraint in standing horses. Supplemental sedatives or analgesics may be needed in horses undergoing surgery. Clinical relevance An effective method that provides prolonged periods of chemical restraint in standing horses is described. The infusion alone did not provide sufficient analgesia for surgery and a significant proportion of animals required supplemental sedatives and analgesics.