Serial blood samples were collected and plasma concentrations of florfenicol (FLO) were measured following the administration of an intravenous bolus of 50 mg/kg FLO to five healthy non-lactating dairy cows. A triexponential equation provided the best fit of the data for four of the five cows. The mean value for beta corresponded to a half-life of 3.2 h. The mean apparent volume of distribution was 0.67 l/kg, and the mean body clearance was 0.15 l/kg/h. The extent of binding of FLO to bovine plasma proteins was determined in vitro at concentrations of 5 micrograms/ml and 50 micrograms/ml by equilibrium dialysis and ultrafiltration. The drug was 18% and 19% bound by equilibrium dialysis, and 23% and 19% bound by ultrafiltration, at 5 micrograms/ml and 50 micrograms/ml, respectively. Phagocytosis of 32phosphorus-labelled Staphylococcus aureus by bovine blood neutrophils was compared in vitro between neutrophils incubated in phosphate-buffered saline alone or in combination with 5, 125, or 1000 micrograms/ml chloramphenicol or FLO. There was no significant effect of chloramphenicol at any concentration. Florfenicol significantly inhibited phagocytosis at all concentrations, but the percentage inhibition was small. The clinical significance, if any, of this effect of FLO remains to be demonstrated.

The effects of intravenous xylazine (1.1 mg/kg) were studied in six thoroughbred horses (five mares and a stallion). Plasma glucose concentration increased to 168% of control at 45 min and decreased to 112% of control at 180 min. Insulin had decreased to 31% of control at 15 min. Thereafter, insulin concentration increased, reaching its highest concentration at 150 min. The mechanism for these changes is not fully understood and further investigation is indicated.

Calcium gluconate was administered to conscious horses at 3 different rates (0.1.0.2, and 0.4 mg/kg/min for 15 minutes each). Serum calcium concentrations and parameters of cardiovascular function were evaluated. All 3 calcium administration rates caused marked increases in both ionized and total calcium concentrations, cardiac index, stroke index, and cardiac contractility (dP/dt,,,).Mean arterial pressure and right atrial pressure were unchanged; heart rate deypocalcemia may occur in horses with acute renal dis-H ease, gastrointestinal disease (colic), exertional rhabdomyolysis, transport tetany, lactation tetany, and idiopathic hypocalcemia syndrome.'.' Endot~xemia,~.' sepsis,'-* cantharidin toxicity,' and pancreatitis' can also result in low serum calcium concentrations. Sequelae of hypocalcemia include muscle weakness and fasciculations, tetany, cardiac arrhythmias, synchronous diaphragmatic flutter, ileus, convulsions, and death.' Calcium plays a crucial role in a variety of physiological processes, including muscle contractility (cardiac, skeletal, and smooth muscle), cardiac automaticity and rhythmicity, neuromuscular excitation, enzyme function, coagulation, secretion of certain hormones, bone formation, and milk production.'.' Calcium is most commonly provided to the body through dietary intake and is maintained at appropriate physiological concentrations by interactions of parathyroid hormone, calcitonin, and vitamin D.',' However, in severe acute hypocalcemia or in hypocalcemia due to anorexia, IV calcium supplementation may be necessary. Because calcium can have marked effects on the cardiovascular system,' an understanding of the effects of calcium administered IV is essential.The primary goal of this study was to determine the cardiovascular effects of calcium gluconate administered to normal conscious horses. A second goal was to document and compare the ionized and total serum calcium concentrations during IV calcium administration. Materials and MethodsSix thoroughbred horses (3 fillies, 3 geldings) aged 2 to 4 years and weighing from 440 to 500 kg were used in this study. Horses were cared for according to the guidelines of the University of Illinois Lab Animal Care Committee. InstrumentationAll horses were catheterized while standing quietly in the stocks. An area over each jugular furrow was clipped and surgically scrubbed for aseptic placement of intravascular and intracardiac catheters. Each catheter site was infused with 1 mL of 2% lidocaine hydrochloride. Two 8F catheter introducers (Desilet Hoffman Introducers; Cook Medical, Bloomington, IN) were placed approximately 20 cm apart in the right jugular vein, and one 8F catheter introducer was placed in the left jugular vein. A 150-cm 7F thermodilution catheter ( 150-cm Swan-Ganz catheter; Columbus Instruments, Columbus, OH) was advanced through the right caudal catheter introducer until the distal port of the catheter was positioned in the pulmonary artery. Polyethylene tubing was inserted through the cranial right catheter introducer int...

The pharmacokinetics of lidocaine in dogs were investigated following the intravenous and intramuscular administration of single doses of lidocaine hydrochloride. The mean elimination rate constant and the mean specific clearance determined for the intravenous portion of the study were 0.786 h-1 and 2.40 1/kg/h, respectively. Following intramuscular administration the mean absorption rate constant was 7.74 h-1. Absorption was nearly complete as the percentage of an intramuscular dose absorbed averaged 91.9%. Concentrations of two N-deethylated metabolites, determined following the administration of lidocaine suggest that monoethylglycinexylidide is eliminated rapidly while glycinexylidide is more slowly eliminated. The relative contribution of these metabolites to the therapeutic and toxic effects of lidocaine and the potential for glycinexylidide accumulation during lidocaine administration remain to be investigated.

Lidocaine was infused at a fixed zero-order rate to eight healthy mongrel dogs until tonic extension (n = 5) and cortical seizures (n = 7) were produced. Lidocaine concentrations determined at 5-min intervals were used to calculate concentrations at which these effects occurred. The tonic extension phase occurred at a mean lidocaine concentration of 8.21 +/- 1.69 micrograms/ml. After a 1-month rest period, the same dogs were anaesthetized and ventricular tachycardia was produced by administering ouabain. Lidocaine was again infused at a fixed zero-order rate until all beats of ventricular origin were abolished. This occurred at a mean lidocaine concentration of 6.25 +/- 1.49 micrograms/ml.