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Biomedical subjects

L P Tilley

Publications and source records attributed to L P Tilley.

At least 19 recordsLinked to original sources
PubMed1989

Cardiopulmonary disease in the geriatric dog and cat.

The incidence of cardiopulmonary disease increases with age. Degenerative valvular disease, chronic obstructive pulmonary disease, and arrhythmias are common in the geriatric dog. Chronic bronchial disease, pulmonary neoplasia, and arrhythmias occur in the geriatric cat. Systemic diseases in both species often show cardiopulmonary manifestations. Medical management to treat the underlying disease and to control clinical signs is complicated by altered absorption, metabolism, and elimination of drugs.

Aging↗
PubMed1986

Clinical and pathologic findings in dogs with atherosclerosis: 21 cases (1970-1983).

Atherosclerosis was diagnosed on necropsy in 21 dogs in a 14-year period. Nine dogs died and 12 were euthanatized because of complications associated with the disease. The mean age was 8.5 +/- 0.5 years; 18 dogs were male. Three breeds (Miniature Schnauzer, Doberman Pinscher, and Labrador Retriever) had a higher prevalence of the disease than other breeds in the canine necropsy population of The Animal Medical Center. Most common clinical signs were lethargy, anorexia, weakness, dyspnea, collapse, and vomiting. Hypercholesterolemia, lipidemia, and hypothyroidism were common in affected dogs tested, and protein electrophoresis revealed high values for alpha 2 and beta fractions in all dogs tested. Electrocardiography indicated conduction abnormalities and myocardial infarction in 3 of 7 dogs. Necropsy revealed that affected arteries (including coronary, myocardial, renal, carotid, thyroidal, intestinal, pancreatic, splenic, gastric, prostatic, cerebral, and mesenteric) were yellow-white, thick and nodular, and had narrow lumens. Myocardial fibrosis and infarction also were observed in the myocardium. Histologically, affected arterial walls contained foamy cells or vacuoles, cystic spaces, mineralized material, debris with or without eroded intima, and degenerated muscle cells.

Animals↗
PubMed1985

Ventricular preexcitation in seven dogs and nine cats.

Ventricular preexcitation was diagnosed in 6 dogs and 7 cats examined because of weakness, syncope, or congestive heart failure, and as an incidental finding in 1 dog and 2 cats. Reciprocating tachycardias were documented in 8 of the cases. Six of the cats had a pathologic diagnosis of primary cardiomyopathy. Two of the dogs had an associated congenital heart defect. Reciprocating tachycardias were controlled in 4 cases with digoxin, in 2 cases with propranolol, and in 1 case with quinidine. Conduction through the accessory pathway was altered by quinidine (2 cases), digoxin, and propranolol (1 case each), resulting in a lengthened P-R interval and more normal QRS complex configuration.

Animals↗
PubMed1984

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↗
PubMed1982

Excessive moderator bands in the left ventricle of 21 cats.

Excessive numbers of moderator bands bridging the left ventricular septum and free wall and entangling papillary muscles were associated with heart failure and death in 21 cats. Clinical findings included dyspnea, anorexia, hypothermia, cardiomegaly, pleural effusion, plumonary edema, heart murmurs, gallop rhythm, electrocardiographic abnormalities (especially conduction disturbances), increased left ventricular end-diastolic pressure, angiocardiographic evidence of left ventricular restriction, and aortic thromboembolism. Pathologic changes included a morphologically distinct network of abnormal numbers of moderator bands in the left ventricle, left ventricular hypertrophy (younger cats--mean age, 4 years) or dilatation (older cats--mean age, 8.7 years), left atrial enlargement and hypertrophy, and pulmonary edema with heart failure cells in the alveoli. Heart weights of affected cats were significantly less than those of cats with congestive, hypertrophic, and restrictive cardiomyopathy (endocardial fibrosis), but were not significantly less than heart weights of clinically normal cats. Pathologic changes were characteristic of the syndrome grossly and histologically, but clinical findings were not clearly definable.

Animals↗
PubMed1982

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↗
PubMed1982

Safety assessment of a new anticancer compound, mitoxantrone, in beagle dogs: comparison with doxorubicin. I. Clinical observations.

Twenty-four adult beagle dogs were divided into four groups of three males and three females and received iv infusions of doxorubicin (36.05 mg/m2), mitoxantrone (2.58 or 5.15 mg/m2), or the vehicle (0.9% normal saline). All animals were given a single dose once every 3 weeks. The duration of the study was 30 weeks. Animals were observed for toxicologic and cardiotoxic signs. The methods used to evaluate the cardiotoxic potential of both mitoxantrone and doxorubicin were sequential endomyocardial biopsies, ECGs, blood pressure, and serum levels of the cardiospecific isoenzyme CPK-MB (MB band of CPK). Animals given mitoxantrone had signs of gastrointestinal toxicity and fluctuating decreases in wbc counts. Animals given doxorubicin had signs of gastrointestinal toxicity and cardiotoxicity, as well as alopecia, fluctuating decreases in wbc counts, and diffuse erythema. All three male animals given doxorubicin died during the study from apparent congestive heart failure. All dogs treated with doxorubicin had positive CPK isoenzyme elevation, ECG changes, or progressive cardiomyopathy prior to administration of the last dose. None of these signs was observed in dogs treated with mitoxantrone. One male dog given mitoxantrone died during the course of the study.

Animals↗
PubMed1981

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↗