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Biomedical subjects

V J Ferrans

Publications and source records attributed to V J Ferrans.

At least 343 records · Page 19Linked to original sources
PubMed1978

Discrete subaortic stenosis in Newfoundland dogs: association of infective endocarditis.

Necropsy findings are described in eight Newfoundland dogs from the same colony with discrete subaortic stenosis. Infective endocarditis involving the aortic valve occurred in four dogs and in each it proved fatal. Damage to the aortic valve cusps by the jet of blood ejected through the discretely narrowed left ventricular outflow tract predisposes to the development of infective endocarditis in both dogs and human beings with discrete subaortic stenosis. Severe abnormality of the intramural coronary arteries in the ventricular septum, which also occurs in patients with hypertrophic cardiomyopathy, was present in all eight dogs. Myocardial fiber disorganization and asymmetric septal hypertrophy, two other findings observed in patients with hypertrophic cardiomyopathy, were absent in each of the eight Newfoundland dogs with discrete subaortic stenosis.

Animals↗
PubMed1978

Structural changes in glutaraldehyde-treated porcine heterografts used as substitute cardiac valves. Transmission and scanning electron microscopic observations in 12 patients.

Scanning and transmission electron microscopic studies were made of (1) 12 glutaraldehyde-treated porcine valvular heterografts that had been implanted in patients for 2 days to 76 months; (2) 3 unimplanted commercially processed porcine aortic valves; and (3) 1 unprocessed porcine aortic valve. Comparison of unprocessed porcine valves and unimplanted commercially processed valves showed loss of endothelium and acid mucopolysaccharides during preimplantation processing. Short-term (less than 2 months) changes after implantation consisted of insudation of plasma proteins, penetration of erythrocytes into surface crevices, formation of a thin surface layer of fibrin, and deposition of macrophages, giant cells and a few platelets. Longer-term (more than 2 months) changes were proportional to the time interval after implantation and consisted of progressive disruption of collagen, erosion of the valve surfaces, formation of aggregates of platelets and accumulation of lipid. The surfaces of the leaflets did not become covered with endothelium or with a fibrous sheath. Calcific deposits were found in one valve and bacterial organisms in another. Thus, progressive breakdown of collagen appears to be a critical factor in determining the long-term durability of glutaraldehyde-treated porcine valvular heterografts.

Adult↗
PubMed1978

Cardiac lesions induced by chemicals.

Chemically induced cardiomyopathies are frequently the consequences of a cardiac metabolic imbalance brought about by exaggerated functional affects. The infarctlike lesions induced by adrenergic beta-receptor stimulants and the vasodilating antihypertensives serve as examples of this phenomenon. Direct cardiotoxic mechanisms not related to cardiovascular functional effects are responsible for another class of toxic cardiomyopathy. An example of this is the cardiomyopathy produced by the anthracycline antineoplastic agents. The pathogenesis, morphological changes and toxicologic features of these cardiomyopathies are described with particular reference to their detection in preclinical toxicity studies.

Acute Disease↗
PubMed1978

Ultrastructure of Hancock porcine valvular heterografts. Pre- and post-implantation changes.

Scanning and transmission electron microscopic studies were made of: 1) 15 glutaraldehyde-treated porcine valvular heterografts that had been implanted in patients for periods of time ranging from 2 days to 76 months; 2) unimplanted, commercially processed porcine aortic valves; and 3) unprocessed porcine aortic valves. Unimplanted, commercially processed valves showed loss of endothelium and acid mucopolysaccharides. Short-term (< 2 months) post-implantation changes consisted of insudation of plasma proteins, penetration of erythrocytes into surface crevices, formation of a thin surface layer of fibrin, and deposition of macrophages, giant cells and a few platelets. Longer term (> 2 months) changes consisted of progressive disruption of collagen, erosion of valvular surfaces, formation of aggregates of platelets, and accumulation of lipid. The surfaces of the leaflets did not become covered with endothelium or with a fibrous sheath. It is concluded that progressive breakdown of collagen is a critical factor in determining the long-term durability of glutaraldehyde-treated porcine valvular heterografts.

Animals↗
PubMed1978

Ultrastructure of the fibrous subaortic "ring" in dogs with discrete subaortic stenosis.

The subaortic fibrous "ring" in Newfoundland dogs with discrete subaortic stenosis is characterized by the presence of large, uni- and multinucleated, rounded connective tissue cells that resemble chondrocytes in several respects. Connective tissue adjacent to these cells is rich in acid mucopolysaccharides, small but cross-banded collagen fibrils, and small, poorly developed elastic fibers. The chondrocyte-like cells contain numerous cisternae of rough surfaced endoplasmic reticulum and prominent Golgi complexes, and they are surrounded by thick, concentrically arranged layers of basement membrane-like material. The differentiation of cellular and extracellular components of connective tissue in subaortic fibrous rings clearly differs in humans and in dogs with discrete subaortic stenosis.

Animals↗
PubMed1978

Overview of cardiac pathology in relation to anthracycline cardiotoxicity.

A review is presented of cardiac pathologic changes associated with acute and chronic toxicity of anthracyclines. These changes consist of cardiac dilatation, degeneration and atrophy of the muscle cells, and interstitial edema and fibrosis. The degeneration of cardiac muscle cells is a complex phenomenon that involves the myofibrils, the nucleus, the mitochondria and the membrane systems of the T-tubules, the sarcoplasmic reticulum, and the intercellular junctions. The pathogenesis of these alteration is discussed in terms of the biochemical effects of anthracyclines.

Animals↗
PubMed1978

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.

Animals↗
PubMed1978

Effect of selenium-vitamin E on adriamycin-induced cardiomyopathy in rabbits.

Administration of selenium-vitamin E (Se-E) to weanling rabbits chronically treated with adriamycin (ADR) resulted in decreased incidence and severity of cardiomyopathy and decreased cumulative mortality during a 10-week experiment. However, Se-E did not protect against extracardiac lesions or against a number of clinicopathologic alterations induced by chronic ADR toxicosis. Histopathologic alterations of ADR-induced cardiomyopathy were concentrated periarterially in the free and septal walls of the left ventricle. Initial vacuolar degeneration of injured cardiac muscle cells was followed by myofibrillar lysis and eventual cell death with subsequent interstitial fibrosis. Ultrastructurally, degenerated cardiac muscle cells had 3 prominent alterations: (1) sarcoplasmic vacuolization caused by distention of elements of sarcoplasmic reticulum and T-tubules, (2) degeneration of mitochondria forming large myelin figures from disrupted membranes, and (3) lysis of myofibrils producing granular sarcoplasmic masses. Severely injured fibers were necrotic and macrophages invaded to remove cellular debris. The interstitium was distended by edema and increased amounts of collagen. Extracardiac lesions in rabbits with chronic ADR toxicosis included the usually recognized alterations involving cell-renewal systems in kidney, testis, bone marrow, skin, and alimentary tract, as well as vacuolar degeneration of skeletal muscle and focal loss of pancreatic tissue, with ensuing pancreatic fibrosis and fat necrosis. Deaths in ADR-treated rabbits usually were precipitated by terminal septic embolism. The partial protection afforded by Se-E against ADR-induced cardiomyopathy may be associated with stabilization of the membranes of injured muscle cells or with prevention of ADR-induced inhibition of coenzyme Q10-dependent mitochondrial enzymes.

Alopecia↗
PubMed1978

Anchoring fibrils. A new connective tissue structure in fibrotic lung disease.

Electron microscopic studies of lung were made and compared in 17 patients with lung disease (10 with idiopathic pulmonary fibrosis, 3 with collagen--vascular diseases, 3 with sarcoidosis, and 1 with chronic eosinophilic pneumonia) and in 5 control patients. In control patients, the alveolar epithelial cells were normal, and no hemidesmosomes were present between the plasma membranes and the basal laminae. In comparison, cuboidal alveolar epithelial cells were present in 15 of the patients with fibrotic lung disease; in 9 of these the alveolar epithelial cells were multilayered. In 7 of the latter 9 patients (5 with idiopathic pulmonary fibrosis and 2 with collagen-vascular diseases), the basal laminae of the alveolar epithelial cells were attached to the plasma membranes by hemidesmosomes and to the underlying interstitial connective tissue by "anchoring fibrils." These fibrils measured from 4000 to 6000 A in length and from 200 to 600 A in width. One or both ends of the anchoring fibrils inserted into thebasal lamina, often forming arcs through which collagen fibrils and connective tissue microfibrils penetrated. Anchoring fibrils showed a complex pattern of transverse banding, which differed from that of collagen and appeared to be symmetric about the center of the fibril. These anchoring fibrils, which resemble those in normal skin and other tissues, were not found in lungs of control patients. In addition, there was a significant correlation between the severity of the pulmonary fibrosis and the presence of anchoring fibrils. These observations suggest that in severe fibrotic lung disease, anchoring fibrils reinforce the attachment of the basal lamina of multilayered alveolar epithelial cells to interstitial connective tissue.

Adult↗
PubMed1978

Ultrastructure of the fibrous ring in patient with discrete subaortic stenosis.

Histologic and ultrastructural studies disclosed the presence of five tissue layers in fibrous rings excised at operation from five patients with discrete subaortic stenosis. These layers were: (1) a surface monolayer of endothelial cells; (2) a subendothelial layer rich in acid mucopolysaccharides and basement membrane-like material; (3) a fibroelastic layer containing collagen and small (1 micrometer or less in diameter) elastic fibers; (4) a layer of smooth muscle cells with thickened basement membranes, and (5) a central fibrous layer with large amounts of collagen and small amounts of elastic fibers. The connective tissue layers in the rings frequently were discontinuous. The layered arrangement of these rings resembles that of normal endocardium in the left ventricular outflow tract.

Adolescent↗
PubMed1977

Ultrastructure of a cardiac rhabdomyoma.

Electron microscopic study of a cardiac rhabdomyoma removed at open heart operation revealed large rounded or polygonal cells that contained large amounts of monoparticulate glycogen. Myofibrils in these cells were few and located either subjacent to the plasma membranes or radiating from central areas. Leptofibrils and masses of anomalous Z band material were abundant. Shallow tubular sarcolemmal invaginations and elements of free and junctional sarcoplasmic reticulum were associated with the myofibrils. Desmosomes and nexuses were evident in intercellular junctions, which were extensive and randomly distributed throughout the cell surfaces. It is concluded that cardiac rhabdomyomas probably are hamartomas.

Cell Membrane↗
PubMed1977

Isolation and characterization of myosin from subjects with asymmetric septal hypertrophy.

Human cardiac myosin isolated from operatively obtained samples of ventricular septum and left ventricular free wall of subjects with asymmetric septal hypertrophy (ASH) was compared, with respect to structural and enzymatic properties, to myosin isolated from hearts of subjects without heart disease. The following parameters were studied: (1) activation of myosin ATPase activity by K+-EDTA and Ca2+, (2) molecular weight of the heavy and light chains of myosin as determined by electrophoretic migration in polyacrylamide-sodium dodecyl sulfate (SDS) gels and (3) ability to form bipolar aggregates at low ionic strength, as examined by electron microscopy. No difference was present in any of these parameters between human cardiac myosin from subjects with ASH and from subjects without heart disease. Thus, the genetic defect present in subjects with ASH is not expressed in the particular structural and functional characteristics of myosin evaluated in this study.

Adenosine Triphosphatases↗
PubMed1977

Left atrial ultrastructure in mitral valvular disease.

Light microscopic and ultrastructural observations were made on left atrial tissues obtained from 14 patients at the time of operation for correction of mitral valvular disease. Cardiac muscle cells varied in size but most frequently were hypertrophied. In fibrotic areas, present in all left atria, the muscle cells tended to be isolated from adjacent cells and exhibited degenerative changes of varying severity. These changes consisted or proliferation of Z-band material and cytoskeletal filaments, myofibrillar loss, proliferation of elements of free and extended junctional sarcoplasmic reticulum, variations in size and number of mitochondria, occurrence of abnormal mitochondria, dissociation of intercellular junctions, formation of spherical microparticles, and accumulation of lysosomal degradation products. Hypertrophy was considered to lead to cellular degeneration, with decrease or loss of contractile function. Atrial fibrillation was associated with severe cellular degeneration. The severity of degeneration was greater in patients with mitral regurgitation, with or without associated mitral stenosis, than in patients with pure mitral stenosis.

Adult↗