Procainamide in the dog: antiarrhythmic plasma concentrations after intravenous administration

Procainamide hydrochloride was administered to ouabain-intoxicated dogs to determine an antiarrhythmic plasma concentration of procainamide. Ventricular arrhythmias were produced in dogs following intravenous injections of ouabain. After a sustained ventricular tachycardia was achieved, procainamide was administered and plasma samples collected for assay. Plasma procainamide was assayed by fluorescence polarization immunoassay. Procainamide was administered at increasingly higher constant rate infusions in order to achieve intermittent, steady-state plasma concentrations. Infusion rates were calculated on the basis of previous pharmacokinetic information. All six dogs that received procainamide converted to a normal sinus cardiac rhythm after attaining a mean plasma concentration of 33.8 micrograms/ml with a range of 48.5 micrograms/ml-25.0 micrograms/ml. It was observed that the computer-generated prediction of plasma concentrations based upon previous pharmacokinetic data produced an underestimate of the actual plasma concentrations. These data may suggest that plasma concentrations of procainamide for controlling some cardiac arrhythmias in dogs may be higher than plasma concentrations cited for human patients.     

Cellular morphology of Clostridium spiroforme

The helically-coiled bacterium, Clostridium spiroforme, has been shown to consist of an ordered aggregation of numerous individual semi-circular cells joined end to end.     

A COMPARISON OF MANUAL AND AUTOMATIC ULTRASOUND-GUIDED BIOPSY TECHNIQUES

A manual, ultrasound-guided biopsy technique was compared to a new automatic method using a new biopsy device. The liver and the left kidney of 10 dogs were biopsied using the two methods. The specimens from the biopsies were compared for size and quality. Results demonstrate that larger and higher quality samples were obtained with the new automatic method.     

Nitrogenous constituents in plasma of foals weaned at three, four or six months of age

A study was conducted to measure the nitrogenous constituents in the blood of foals weaned at 3, 4 or 6 months of age (four foals per weaning age).Jugular blood was sampled from one week prior to weaning until one month post-weaning, and was analyzed for total protein, albumin, creatinine, urea Nitrogen and free amino acid content. Results indicated that the concentrations of most of the constituents in the blood of foals were not altered by the age of weaning, however, free amino acids decreased as age at weaning increased and creatinine was significantly higher in foals weaned at 6 months of age. Plasma creatinine, lysine and methionine levels generally decreased between pre-weaning and one month post-weaning. These data establish baseline values for blood nitrogenous constituents in foals at weaning.     

Morphologic studies of uveoscleral outflow in normotensive and glaucomatous beagles with fluorescein-labeled dextran

Aqueous humor leaves the anterior chamber through 2 pathways: the trabecular meshwork of the iridocorneal angle and the unconventional uveoscleral route. In the latter route, aqueous humor leaves the anterior chamber, passes caudally through the trabecular meshwork and sclerociliary cleft to enter the supraciliary and suprachoroidal spaces. The fluid is absorbed by the choroidal and scleral circulation. Fluorescein-labeled dextran was slowly infused into the posterior chamber of healthy and glaucomatous Beagles for 30 minutes. The eyes were fixed in a mixture of 70% alcohol and formalin, placed in epoxy resin for histologic evaluation, and examined by fluorescent microscopy. Fluorescence was detected in the healthy dogs throughout the uveoscleral pathway. In the glaucomatous dogs, the uveoscleral outflow was decreased or completely absent.     

Nephrotic syndrome: a platelet hyperaggregability state

Nephrotic syndrome characterized by hypoalbuminemia and hyperlipidemia is associated with an increased incidence of thromboembolism and increased platelet hyperaggregability. Although plasma coagulation proteins are also abnormal, changes are too inconsistent to attribute thromboembolic complications to the coagulation cascade alone. Antithrombin III (ATIII) has been shown to be deficient in nephrotic syndrome. There is, however, an increase in alpha 2 macroglobulin. It is clear that platelet to platelet interactions require exposure of platelet fibrinogen receptors, the binding of fibrinogen to these receptors, platelet crossbridging, and subsequent platelet aggregation. Fibrinogen is consistently elevated in nephrotic syndrome. Hyperlipidemia and hypoalbuminemia in nephrotic syndrome increases the availability of thromboxane A2 (TxA2) by increasing the availability of TxA2 precursors and the removal of TxA2 inhibitors. Thromboxane A2 is a known inducer of platelet aggregation probably through the exposure of platelet fibrinogen receptors. Recently, fibronectins a group of adhesive proteins, were implicated in platelet to platelet interactions. Since thrombin increases the expression of platelet surface fibronectin, fibronectin may be involved in thrombus formation in nephrotic syndrome. Thromboembolic formation in nephrotic syndrome is a composite mechanism involving the coagulation cascade, platelet-platelet interactions, and platelet-surface interactions.