To differentiate the origin of high total lactate dehydrogenase (LD) activity in canine sera, a spectrophotometric method based on the preferential inhibition of cardiac LD isoenzymes by pyruvate was performed. Comparison with the electrophoretic separation of LD isoenzyme activities and determination of the hydroxybutyrate dehydrogenase-to-LD ratio indicated that the method proposed gave a better discrimination between cardiac and hepatic LD activities than did the other tests.

Protein kinase (PK) C activity in the liver of cattle with fatty liver syndrome was evaluated and compared with that in liver of healthy cattle. The PKC activities in cytosolic and particulate fractions were reduced in fatty livers, compared with those in livers from healthy cattle. The decrease of PKC activity was more distinct in cytosolic (P = 0.0016) than particulate (P = 0.069) fractions. Protein kinase activities other than PKC were not substantially changed. Seemingly, PKC was involved in the pathogenesis of fatty liver syndrome in cattle.

The Langendorff isolated heart preparation was adapted to determine the effect of furazolidone (0.5 and 2 migrogram/ml of perfusate) on hearts of 3-week-old broiler chickens. Following 115 minutes of perfusion, both concentrations of furazolidone caused approximately a two-fold increase in myocardial vascular resistance and a six-fold increase in myocardial vascular resistance and a six-fold increase in lactate dehydrogenase release into the effluent fluid, compared with a control perfused group of isolated hearts (P less than 0.01). Ultrastructural alteration differences were not found between the drug-treated and control groups. It was concluded that: (i) furazolidone, at concentrations only moderately above therapeutic plasma concentrations, caused detrimental changes in myocardial vascular resistance and lactate dehydrogenase release and (ii) the isolated chicken heart preparation is an example of a cost-effective, reliable laboratory tool for screening potential cardiotoxins.

Serum vitamin E and blood glutathione peroxidase values were determined in 40 horses with a histologically confirmed diagnosis of degenerative myeloencephalopathy and in 49 age-matched control horses with normal neurologic function. Significant differences were not detected in serum vitamin E or blood glutathione peroxidase values between horses affected with degenerative myeloencephalopathy and control horses. These findings fail to support a reported role of vitamin E deficiency as a cause of equine degenerative myeloencephalopathy.