Electrophysiological control of ventricular rate during atrial fibrillation.

Thirteen anesthetized canine subjects (17-29 kg) were used to demonstrate that mild cervical left vagal stimulation could control ventricular rate effectively during atrial fibrillation (AF). Two studies are presented. The first study used six subjects to demonstrate the inverse relationship between (manually applied) left vagal stimulation and ventricular excitation (R wave) rate during AF. As left vagal stimulation frequency was increased, ventricular excitation rate decreased. In these studies, a left vagal stimulus frequency of 0-10 per second reduced the ventricular excitation rate from > 200/min to < 50/min. The decreasing ventricular excitation rate with increasing left vagal stimulation frequency was universal, occurring in all 26 trials with the six subjects. This fundamental principle was used to construct an automatic controller for use in the second study, in which seven subjects were used to demonstrate that ventricular rate can be brought to and maintained within a targeted range with the use of an automatic (closed-loop) controller. A 45-minute record of automatic ventricular rate control is presented. Similar records were obtained in all seven subjects.

Treatment of granular cell tumor via complete right lung resection in a horse.

A 7-year-old warmblood mare was referred because of a respiratory tract disorder; pulmonary granular cell tumor was diagnosed. Pulmonary granular cell tumor is a locally invasive but rare type of tumor with low metastatic potential. The entire right lung was resected to ensure removal of all neoplastic tissue. The horse recovered well and has minimal difficulties functioning with one lung. Most of these tumors are diagnosed during postmortem examination. To our knowledge, this is the first report of pulmonary granular cell tumor treated by complete lung resection in a horse.

Hypothermia for cardiac surgery.

If the protocol described here is followed, good results will be obtained in the majority of animal patients. However, as with any procedure involving critically ill animal patients, many factors enter in to determine the results in any given case.

Clinical, clinicopathologic, and pathologic alterations in acute monensin toxicosis in cattle.

Twenty beef calves weighing approximately 180 kg were allotted to 3 groups. In group A, 6 calves were given 25 mg of mycelial monensin/kg of body weight orally and were evaluated at 1, 2, and 4 days for clinical, ECG, clinicopathologic, and pathologic alterations. In group B, 7 calves were given a single dose of monensin (40 mg/kg) and 5 were given a 2nd 40 mg/kg dose on day 7; calves were evaluated at days 1, 2, 4, 7, 8, 9, and 11. In group C, 2 calves served as controls. Monensin-treated calves developed anorexia, diarrhea, and lethargy after day 1. One group B calf died on day 7 with lesions of congestive heart failure. Electrocardiographic abnormalities were not observed in group A calves; in group B, prolongation of Q-T and QRS intervals occurred from days 2 to 11 and first degree heart block was seen from days 7 to 11. Clinicopathologic alterations included: increased serum activities of aspartate aminotransferase and creatine kinase in group B calves after day 2; decreased serum K+, Na+, and Ca2+ concentrations in both groups, and postdosing occurrence of leukocytosis. Calves were euthanatized sequentially and the lesions of monensin toxicosis were present in the heart, skeletal muscles, and rumen in groups A and B. Disseminated pale yellowish-brown areas of necrosis were present in the ventricular myocardium of 6 of 12 group B calves. Gross lesions were not present in the skeletal muscles or rumen. Microscopically, the myocardial and skeletal muscular lesions were characterized by sarcoplasmic vacuolation from mitochondrial swelling and lipid accumulation in calves killed after day 1 in groups A and B, and by myocardial necrosis with contraction bands, but without calcification, in group B calves killed by day 4. Acute rumenitis was present in groups A and B calves. Myotoxic effects of monensin may be related to its action as an ionophore producing altered intracellular ion concentrations and initiating degeneration and necrosis in striated muscle fibers.

Relationship of toxoplasma infections to other diseases in dogs.

Toxoplasma infection as detected by the immunofluorescent antibody (IFA) test was found in 13.2% of 448 dogs examined at the Purdue University Small Animal Clinic. Only titres of 1/64 and above were considered positive, but lesser titers were encountered more frequently. The highest titer observed was 1/1024 in 2 dogs one of which had idiopathic epilepsy and the other had dirofilariasis as well as hip dysplasia. The incidence of positive sera from male and female dogs were 11.7 and 14.5%, respectively. The highest frequency of infection occurred in young dogs up to 4 years of age and the lowest was in older animals. The presence of the high toxoplasmosis IFA titers in the sera of dogs seems to be associated with other disease conditions. Stress such as joint dislocations, fractures, helminth parasitism, and concomitant bacterial and viral infections, etc., was observed in 62.7% of the positive cases. Presence of tumors and renal disease conditions were associated with 28.8 and 5.2%, respectively, of the positive sera.

Pathologic alterations in congestive cardiomyopathy of dogs.

Eleven large-breed dogs with congestive cardiomyopathy were studied at necropsy. Seven of 11 dogs were Great Dane and 9 of 11 were male. The most common clinical signs in affected dogs were dyspnea, abdominal distention by ascites, and weight loss. Three dogs had severe congestive cardiac failure. At necropsy, gross alterations in the hearts were cardiomegaly, dilation of all chambers, opacity of the endocardium, atrial thrombosis, and disseminated foci of myocardial necrosis. Extracardiac changes included hepatic congestion, pulmonary congestion and edema, ascites, and infarction of kidney, liver, lung, and spleen. Microscopically, the affected hearts had disseminated foci of subendocardial myocardial necrosis, scattered areas of myocardial fibrosis, and medial hyperplasia of intramyocardial arteries. Ultrastructurally, degenerated cardiac muscle cells had myocytolysis, proliferated elements of sarcoplasmic reticulum, numerous myelin figures and autophagic vacuoles, large numbers of lipofuscin granules, and mitochondrial alterations. These ultrastructural alterations are similar to those described for cardiomyopathy in persons and cats.

Pathologic alterations in hypertrophic and congestive cardiomyopathy of cats.

Pathologic alterations were studied in 15 cats with cardiomyopathy. Ten of these had hypertrophic cardiomyopathy, characterized by cardiomegaly, diffuse myocardial hypertrophy, small left ventricular cavities, and dilated left atria; the ventricular septum and left ventricular free walls were thick, but asymmetric septal hypertrophy was not present. Aortic thromboembolism, renal infarction, and pulmonary congestion and edema were frequent. Histopathologic and ultrastructural study revealed hypertrophy and disarray of cardiac muscle cells (most severe in left ventricle and ventricular septum), interstitial fibrosis, and fibromuscular hyperplasia of small intramural coronary arteries. The hypertrophied fibers had large nuclei, prominent Golgi complexes, and numerous polysomes; some fibers had crisscrossing myofibrils. Degenerative alterations in hypertrophied myocytes were: perinuclear distension of elements of sarcoplasmic reticulum, focal myofibrillar lysis, numerous thick clumps of Z-band material, and abundant lipofuscin granules. The interstitium showed accumulations of collagen fibrils, increased numbers of fibroblasts, and scattered remnants of external lamina. One cat had dilated chambers, but also had typical histologic and ultrastructural alterations of hypertrophic cardiomyopathy and was considered to have a late stage of this disorder. Four cats had congestive cardiomyopathy, with cardiomegaly and dilatation of all chambers. Hydrothorax and pulmonary congestion and edema were generally present. Cardiac histopathologic and ultrastructural alterations consisted only of mild interstitital edema and fibrosis. Detailed comparisons reveal many similarities in the spectrum of morphologic features of hypertrophic cardiomyopathy in human beings and cats; there are not marked differences in the morphologic features of congestive cardiomyopathy in human beings and cats. Thus, cardiomyopathies in the cat constitute useful models for the study of these diseases in human beings.

Cardiac disease induced by chronic adriamycin administration in dogs and an evaluation of vitamin E and selenium as cardioprotectants.

Chronic adriamycin (ADR) intoxication was produced in three groups of beagle dogs by weekly intravenous injections (1 mg/kg body weight) for 20 weeks (cumulative dose 400 mg/sq m). Group A (6 dogs) received ADR only; Group B (6 dogs) were given ADR and weekly doses of vitamin E (17 mg/kg body weight) as alpha-tocopherol acetate; and Group C (6 dogs) received ADR and weekly doses of vitamin E as did Group B and selenium (0.06 mg/kg body weight as selenite). Each of the 18 dogs developed ADR-induced cardiomyopathy (CMY), and death occurred in 11 dogs during Weeks 17-20. Mortality was lowest in Group B (2 of 6), but no differences between groups were seen either in survival time of the dogs that died or in severity of CMY. Cardiomyopathy was more severe in dogs that died than in survivors. Congestive heart failure with transudation was present in 4 of 11 dogs that died. Cardiac histopathology was characterized by vacuolar degeneration of myocytes. Myocardial damage was most severe in the left ventricle and the ventricular septum, intermediate in the right ventricle and the left atrium, and least in the right atrium. Ultrastructural study showed that an early alteration in damaged myocytes was distention of sarcoplasmic reticulum to form sarcoplasmic vacuoles. Occasional damaged fibers had myofibrillar lysis and focal proliferation of sarcoplasmic reticulum. This study demonstrates that the dog offers a suitable model for studies of chronic ADR cardiotoxicity in man. The lack of cardioprotection from vitamin E and selenium supplementation fails to support the proposed role of lipoperoxidative damage in the development of chronic ADR-induced CMY.

Effects of hypothermia on the visual-evoked brain potential in dogs.

Visual-evoked potentials, as seen on a signal-averaged electroencephalogram, demonstrated clearly recognizable changes in 6 normal dogs undergoing deep hypothermia and rewarming. These changes were more clearly recognizable than changes in the unevoked electroencephalogram with or without signal averaging.