Pharmacokinetics of cefaronide, ceftriaxone and cefoperazone in sheep

The pharmacokinetics of cefaronide (16 gm/kg dose), ceftriaxone and cefoperazone (47 gm/kg dose), after intravenous (i.v.) administration were determined in six Merino ewes. The mean values for terminal half life, steady state volume of distribution Vd(ss), renal clearance (ClR) and total body clearance (ClB) for cefaronide were 1.5 h, 0.39 l/kg, 0.06 l/h/kg and 0.16 l/h/kg, for ceftriaxone; 1.7 h, 0.30 l/kg, 0.08 l/h/kg, and 0.22 l/h/kg, and 0.7 h, 0.16 l/kg, 0.02 l/h/kg and 0.16 l/h/kg for cefoperazone, respectively. After 5.5 h, approximately 42% cefaronide, and after 8 h, approximately 37% ceftriaxone and 13% cefoperazone, was excreted in urine. The non-renal elimination of ceftriaxone and cefoperazone appeared to be more rapid in sheep than is reported in man. Cefaronide was excreted largely unchanged in the urine of sheep. Therefore, the elimination of cefaronide in sheep was similar to that found in man. Cefaronide was well distributed in sheep, whereas ceftriaxone and cefoperazone appeared to be distributed to a lesser degree. These findings underline the different disposition of drugs in different species.     

Preliminary study of ethylene oxide sterilization of full-thickness cortical allografts used in segmental femoral fracture repair

Full-thickness canine cortical allografts were cleanly harvested, sterilized with ethylene oxide, and stored at room temperature. The allografts were incorporated into canine segmental femoral fracture repairs and compared clinically, radiographically, and morphologically with control femoral cortical autografts for function of the limb, graft acceptance, and bone union. Sterility was maintained and the cortical allografts were well accepted by the host animals, resulting in full use of the limb which was subjected to surgical operation. The allografts showed healing patterns similar to those of the autografts, as determined by radiographic, gross, and histologic evaluation of the proximal and distal host-graft interfaces. Evaluations were made monthly. The host-graft interfaces of the allografts and autograft were filled with woven bone with adjacent vascular invasion and remodeling of the graft at the final 4th-month evaluation.     

The acute phase reaction detected in dogs by concanavalin A binding

Using a kinetic turbidimetric assay based on the binding of serum glycoprotein to concanavalin A the acute phase reaction has been detected in dogs. Raised levels of glycoprotein were found in dogs which had undergone surgery, had been treated with bacterial endotoxin and had various inflammatory conditions.     

Plasmapheresis as adjuvant therapy for autoimmune hemolytic anemia in two dogs

Severe, acute, autoimmune hemolytic anemia in 2 dogs was treated, using prednisone, cyclophosphamide, plasmapheresis, and blood transfusion. In 1 case, splenectomy was performed successfully after plasmapheresis and blood transfusion. Antibody removal by means of plasmapheresis effected short-term stabilization to severe hemolysis in both dogs, but was suspected to have contributed to the death of 1 dog.     

Effect of shock strength on survival and acute cardiac damage induced by open-thorax defibrillation of dogs

The safety of open thorax defibrillation with single damped sine-wave shocks and 6-cm-diameter electrodes was evaluated in healthy anesthetized dogs. Twenty-one dogs were allotted to 6 groups: Group A were nonshocked controls and groups B through F were given single shocks of 4-, 7-, 12-, 19-, or 32-fold, respectively, greater than a defibrillation threshold dose (30 mA/g of heart). Immediate postshock death resulted in group F dogs; group A through E dogs survived and were killed after 2 days. The incidence and severity of cardiac morphologic damage increased with shock strength (mild damage occurred in 1 of 3 dogs in group C and in 3 of 4 dogs in group D and severe damage occurred in 2 of 3 dogs in group E). The cardiac lesions were characterized grossly and microscopically. In dogs that died immediately after shocking, damage was apparent as pale circular zones of edema and myofibrillar degeneration in the ventricular free walls beneath the electrode placement sites on the cardiac surface. In the dogs that survived 2 days, the defibrillator-induced areas of myocardial necrosis and calcification were concentrated in arc or ringlike patterns beneath the periphery of the electrode placement sites. All dogs that were studied 2 days after shocking had mild fibrinous pericarditis. Postshock electrocardiographic changes were not good indicators of cardiac damage because the mild epicardial inflammatory reaction associated with the surgical procedure produced large ST and T wave changes which masked any changes associated with myocardial necrosis induced by the electric shocks. It was concluded that a substantial safety margin exists between the required defibrillation threshold shock dose and the large shocks required to produce marked cardiac damage or death in healthy dogs.     

The rôle of non-specific factors in the production of skin disease in the dog

Non-specific factors may affect the vitality or integrity of the skin, increase its intrinsic reactivity, or aggravate, or promote, other skin disease. External factors such as temperature, humidity, irritant agents and external débris, and internal factors such as diet, psychogenic, neurogenic, hormonal and metabolic abnormalities, may have a profound effect on both the abnormal and normal canine integument.
Résumé. Les facteurs non spécifiques peuvent affecter la vitalité et l'intégrité de la peau, augmenter sa réactivité intrinsèque et soit aggraver, soit favoriser d'autres affections cutanées. Les facteurs externes tels que la température, l'humidité, les agents irritants, les débris externes, ainsi que les facteurs internes comme le régime, les anomalies psychogènes, neurogènes, hormonales, métaboliques peuvent exercer un effet profond sur le tégument du chien normal ou pathologique.
Zusammenfassung. Nichtspezifische Faktoren können die Vitalität oder Integrität der Haut beeinflussen, ihre innere Reaktivität erhöhen oder andere Hautkrankheiten verschlimmern oder fördern. Äussere Faktoren wie Temperatur, Feuchtigkeit, Reizstoffe und äussere Fremdkörper und innere Faktoren wie die Ernährung und psychogene, neurogene, hormonale und Stoffwechselanomalien können einen nachhaltigen Einfluss sowohl auf die anomale als auch die normale Haut des Hundes haben.