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Biomedical subjects

S K Liu

Publications and source records attributed to S K Liu.

At least 73 records · Page 4Linked to original sources

Cardiomyopathy and vitamin E deficiency in zoo animals and birds.

Cardiomyopathy associated with vitamin E deficiency was diagnosed in more than 100 ruminants and primates and in 106 embryos and newly hatched chicks and ducklings. Affected bird embryos failed to pip the eggshell and died inside. Newly hatched chicks and ducklings and neonatal ruminants were weak, had difficulty standing or rising, and died within a few days. Death usually occurred without premonitory signs of disease in juvenile and adult animals. On gross examination, the hearts of the neonatal ruminants had areas of mottled, pinkish-tan myocardium. The hearts of the embryos and newly hatched birds were edematous, pinkish, and pale. In the juvenile ruminants, irregular, whitish patches or pale areas were seen in the myocardium. Histologically, there was multifocal myocytolysis in the myocardium of the neonatal and juvenile ruminants and embryos and newly hatched birds. Focal disseminated or diffuse myocardial fibrosis and myocytolysis were observed in the hearts of the adult animals. Plasma alpha tocopherol values were low enough in all species to be considered deficient. These values increased significantly after the addition of alpha tocopherol and/or vitamin E to the diets of the animals. Cardiomyopathy has not been diagnosed in any of the same groups of animals since supplementation was initiated.

Animals↗

Cardiomyopathy associated with vitamin E deficiency in seven gelada baboons.

Between November 1979 and July 1982, 7 captive gelada baboons (Theropithecus gelada) died; 5 of them died unexpectedly, 1 died after a 4-month history of heart failure, and 1 was anemic and dyspneic for 2 days before death. Of those that died unexpectedly, 1 was anemic and 4 were clinically normal. At necropsy, all baboons had white or pale patches of myocardium. Histologically, fibrosis and acute myocytolysis were observed in the myocardium. Three affected baboons were tested for plasma alpha-tocopherol content and were found deficient. Four unaffected baboons were given vitamin E for 24 months, and plasma alpha-tocopherol content returned to normal. Blood selenium content was determined in 1 affected baboon and was normal.

Anemia↗

Listeriosis in seven bushy-tailed jirds.

Listeriosis was diagnosed in 7 bushy-tailed jirds (Sekeetamys calurus). Death in all cases was acute, and there were no clinical signs. Necropsy revealed necrotizing lesions in the liver, intestines, spleen, and hepatic and mesenteric lymph nodes. On histologic examination large numbers of gram-positive coccobacilli were seen in the lesions. Pneumonitis was seen in 6 jirds, and small numbers of bacteria were seen in the lungs in all cases except one. Diagnosis was based on bacterial culture of the liver in 2 jirds and on immunofluorescence of bacteria when tissue specimens from 2 other jirds were stained with fluorescein-labelled antiglobulins specific for Listeria monocytogenes.

Animals↗

Hypertropic cardiomyopathy and hyperthyroidism in the cat.

In a 21/2-year period, hypertrophic cardiomyopathy was found at necropsy of 23 cats that died (13 cats) or were euthanatized (10) because of problems associated with hyperthyroidism. Of these, 4 (17%) also had evidence of cardiac failure (pulmonary edema or pleural effusion). The mean body weight of the cats with hyperthyroidism and hypertrophic cardiomyopathy was significantly less (P less than 0.001) than that of clinically normal cats and cats with primary cardiomyopathy (congestive or restrictive) or excessive moderator band cardiomyopathy. In addition, the ratio of heart weight to body weight was significantly greater (P less than 0.001) in the 23 hyperthyroid cats than in the normal cats and cats with primary cardiomyopathy. Twenty (87%) of the cats had symmetric hypertrophy of the ventricular septum and left ventricular free wall, whereas the remaining 3 cats had disproportionate thickening of the ventricular septum, compared with the free wall, similar to what is found in cats with asymmetric hypertrophic cardiomyopathy. Histologic cardiac abnormalities included large, hyperchromatic nuclei, interstitial fibrosis, endocardial fibroplasia, fibrosis of the atrioventricular node, and marked disorganization of cardiac muscle cells. The study showed that hypertrophic cardiomyopathy develops in most hyperthyroid cats, some of which also develop congestive heart failure. Although the signs of heart disease in primary myocardial disease and thyrotoxic disease are similar, the characteristic signalment and clinical signs of hyperthyroidism should lead one to suspect the association of hypertrophic cardiomyopathy with the hyperthyroidism.

Animals↗

Mechanisms for atrial arrhythmias associated with cardiomyopathy: a study of feline hearts with primary myocardial disease.

The cellular electrophysiologic and structural characteristics of arrhythmic and non-arrhythmic atria isolated from feline hearts with spontaneously occurring cardiomyopathy were studied. The animals were divided into three groups according to the degree of left atrial enlargement: mild (group I), moderate (group II), and severe (group III). The right atria were of relatively normal size. Microelectrode recordings showed that inexcitable cells were present in both left and right atria of all groups but were most numerous in the left atria of group III animals. Most inexcitable cells had low resting membrane potentials. There was also a significant reduction in resting membrane potentials, maximum rate of phase 0 depolarization, and action potential amplitude of excitable cells in left atria of animals in groups II and III, whereas action potentials of excitable cells in the right atria were normal. Acetylcholine or norepinephrine often restored excitability to cells that originally did not generate action potentials. Norepinephrine also caused slow-response action potentials as well as abnormal automaticity and triggered activity due to delayed afterpotentials. The diseased atria showed marked structural abnormalities, which were most pronounced in group III cats, including large amounts of interstitial fibrosis, cellular hypertrophy and degeneration, and thickened basement membranes. Therefore electrophysiologic abnormalities and concurrent changes in cell structure may be involved in the genesis of atrial tachyarrhythmias caused by cardiomyopathy.

Acetylcholine↗

Canine sinonasal skeletal neoplasms: chondrosarcomas and osteosarcomas.

We studied 34 chondrosarcomas and 17 osteosarcomas among 285 sinonasal neoplasms in the dog. Mesenchymal chondrosarcomas (24) were more common than ordinary chondrosarcomas. Ultrastructural studies done in one case confirmed mesenchymal chondrosarcoma. Of the osteosarcomas, fibroblastic osteosarcoma (7) was the most common. In contrast to non-sinonasal skeletal neoplasms which are composed mostly (80%) of osteosarcomas, chondrosarcomas (66%) and mesenchymal chondrosarcomas (47%) were predominant among the sinonasal skeletal neoplasms of this study. The average age (ten years) of the dogs with sinonasal osteosarcoma was higher than that of dogs with non-sinonasal skeletal osteosarcoma, and there was a distinct male predominance in the dogs with osteosarcoma and chondrosarcoma. Large breed dogs and boxers, frequently affected with skeletal neoplasms, were not affected commonly with sinonasal osteosarcoma. The frequency of metastasis in the dogs with chondrosarcoma and osteosarcoma was much lower than that seen in dogs with nonsinonasal skeletal neoplasms.

Age Factors↗

Myelopathy and vitamin E deficiency in six Mongolian wild horses.

Degenerative myelopathy was diagnosed in six Mongolian wild horses. Three of the horses had a history of ataxia dating from birth to 3 months of age. The clinical signs were uncoordinated movement of the hindlimbs and an abnormally wide-based gait and stance. The other 3 horses had mild ataxia. There were no gross lesions in the brain, vertebrae, or spinal cord. Histologic examination revealed degeneration of the neural processes in the ventral and lateral funiculi of all 6 horses. Myelin sheaths were dilated and vacuolated, and there were swollen, fragmented, or lysed axons. Neuronal degeneration, phagocytosis, and accumulation of periodic acid-Schiff-positive, xylol-insoluble lipopigment were observed in the affected neurons of the dorsal root ganglia. The plasma alpha-tocopherol values of 5 of the affected horses ranged from less than 0.03 to 0.08 (mean, 0.04 +/- 0.01) mg/dl. Seven clinically normal horses from the same herd had a range of less than 0.03 to 0.3 (mean, 0.11 +/- 0.02) mg/dl, which was low enough to be considered deficient.

Animal Population Groups↗

Osteomyelitis and neoplasia associated with use of the Jonas intramedullary splint in small animals.

In 11 cases (10 dogs, 1 cat) in which fractures were repaired with the Jonas intramedullary splint, osteomyelitis developed in 6 and tumors developed in 5. In each case, the tumor originated in close proximity to the splint, at the midshaft of the femur or radius. All implants had been in place for 6 months to 6 years in the case of tumors, and for 4 months to 6 years in the cases involving osteomyelitis. Corrosion was evident in all retrieved implants. The corrosion was attributed to fabrication of the devices with a corrosion-susceptible stainless steel, AISI type 304. The corrosion was believed to have been accelerated by stress effect due to differences in cold work of the sleeve and pin and the difference in composition between the sleeve and spring of the splint. It was concluded that fixation of fractures in small animals should not be performed with the Jonas intramedullary splint.

Animals↗

Effects of left atrial enlargement on atrial transmembrane potentials and structure in dogs with mitral valve fibrosis.

The effects of left atrial enlargement on atrial cell electrophysiology and structure were studied in dogs with mitral valve fibrosis. Thirteen dogs (Groups I) had left atrial enlargement and intermittent atrial arrhythmias; 10 dogs (Group II) had left atrial enlargement and chronic atrial fibrillation. The resting and action potentials of cells in isolated preparations from the enlarged left atrium were found not to differ from those in the nonenlarged right atrium or in the atrium of control dogs. The resting and action potentials of cells in Group II atria did not differ significantly from those in Group I atria. Some cells (15 percent of the total studied) in the atria of dogs in Groups I and II were inexcitable, but either superfusion with acetylcholine or norepinephrine restored excitability. The structural studies showed that the left atrium of the dogs in Groups I and II had a reduced number of muscle cell layers spanning the wall with an unusually large amount of connective tissue between greatly hypertrophied cells. Very few degenerating cells were seen. Dramatic abnormalities of cell electrophysiology may not be involved in the genesis of arrhythmias in the enlarged canine atrium, and the altered morphologic features of the atrium in these dogs may be important in the genesis of persistent atrial arrhythmias.

Acetylcholine↗

Feline hypertrophic cardiomyopathy: gross anatomic and quantitative histologic features.

Gross anatomic features and the pattern and extent of cardiac muscle cell disorganization were studied in the hearts of 51 with spontaneously occurring hypertrophic cardiomyopathy. Each cat had a hypertrophied, but nondilated, left ventricle. Ventricular septal disorganization was extensive, involving 5% or more of the relevant areas of the tissue section, in 14 (27%) of the 51 cats. Marked septal disorganization occurred only in those cats with asymmetric septal hypertrophy (ventricular septal to left ventricular free wall thickness ratio of greater than or equal to 1.1) Disorganization of cardiac muscle cells was uncommon and less extensive in the left ventricular free wall of the cats with hypertrophic cardiomyopathy. Disorganization involved the free wall of only 7 cats, each with asymmetric septal hypertrophy, and occupied greater than 5% of the free wall tissue sections in just 3. Hence, about one fourth of this population of cats had hypertrophic cardiomyopathy resembling the human form of this disease, with asymmetric left ventricular hypertrophy and marked disorganization of cardiac muscle cells in the ventricular septum. The majority of cats (about 75%), however, demonstrated a form of hypertrophic cardiomyopathy characterized by symmetric ventricular hypertrophy and normal arrangement of cardiac muscle cells.

Animals↗

Canine hypertrophic cardiomyopathy.

Necropsy findings in 10 dogs with naturally occurring cardiac disease closely resembled hypertrophic cardiomyopathy in human beings and cats. Each dog had marked cardiac hypertrophy, and 8 dogs had disproportionate thickening of the ventricular septum with respect to the left ventricular free wall (compared with dogs with normal hearts or with cardiac hypertrophy due to acquired or congenital heart disease). Ratios of septum to free wall thickness in the 10 dogs ranged from 1.1 to 1.5, and 6 had ratios greater than or equal to 1.3. Marked cardiac muscle cell disorganization in the ventricular septum, characteristic of human patients with hypertrophic cardiomyopathy, was found in only 2 of the 10 dogs. Death occurred while the dogs were under anesthesia during the course of operative procedures (5 dogs) or unexpectedly in animals without previous manifestations of cardiac disease (3 dogs). Four dogs had clinical signs of congestive heart failure, including 2 with marked cardiac decompensation. Two of these 4 dogs with heart failure and 1 dog that died during unrelated surgery, but without prior signs of heart disease, had electrocardiographic evidence of complete heart block.

Animals↗

Hypertrophic cardiomyopathy in the dog.

Clinical and necropsy findings in 10 dogs with a spontaneous primary hypertrophic cardiomyopathy are described. Each dog had marked cardiac hypertrophy, and 8 dogs had disproportionate thickening of the ventricular septum with respect to the left ventricular free wall (compared with dogs with normal hearts or with cardiac hypertrophy due to acquired or congenital heart disease). Septal:free wall thickness ratios in the 10 dogs ranged from 1.1 to 1.5; 6 had ratios greater than or equal to 1.3. However, marked cardiac muscle cell disorganization in the ventricular septum, characteristic of patients with hypertrophic cardiomyopathy, was present in only 2 of the 10 dogs. Death occurred most commonly while the dogs were under anesthesia during the course of operative procedures (5 dogs) or suddenly and unexpectedly in animals without previous symptomatic manifestations of cardiac disease (3 dogs). Four dogs had clinical signs of congestive heart failure, including 2 with marked cardiac decompensation. In addition, 2 of these 4 dogs with heart failure and 1 dog without previous symptoms (that died during a noncardiac operation) manifested complete heart block. It is conceivable that dogs with spontaneous hypertrophic cardiomyopathy may prove useful in the future investigations of the clinical, hemodynamic, and pathologic features of this disease in humans.

Animals↗

Atrioventricular bundle degeneration associated with sudden death in the dog.

Twelve dogs that were necropsied after sudden unexpected death, sudden episodes of viciousness, or seizure disorder were found to have degeneration of the atrioventricular bundle of the heart. In addition, hypoxic-type degeneration was found in the hippocampus and the dorsal one-half of the midportion of the cerebral cortex of the dogs.

Animals↗