Prolonged bed rest in the treatment of the dilated heart.
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Cardiomegaly↗
Biomedical subjects
V J Ferrans
Publications and source records attributed to V J Ferrans.
Optical methods for the nondestructive evaluation of collagen morphology in bioprosthetic heart valves.
The aim of the present study was to assess the suitability of nondestructive optical methods as a means of evaluating collagen morphology in bioprosthetic heart valve leaflets. The results of this study demonstrate that transmitted polarized light and incident polarized light optics facilitate the imaging of the inherent birefringence of valvular collagen fibers. Polarized light optics readily document the different patterns of collagen orientation and configuration in porcine aortic valvular (PAV) and bovine pericardial valvular (BPV) bioprostheses. Incident polarized light optics also provide information on leaflet surface morphology. Verification that the birefringence observed by polarized ligh optics represents leaflet collagen was provided by conventional histologic and transmission electron microscopic methods. Quantitative determinations of the spacing of collagen bundle waves gave similar values in intact and in sectioned BPV leaflets. Potential applications of polarized light optics in the assessment of bioprosthetic valve collagen are as follows: the selection of the desired orientation of collagen bundles within pericardium intended to be configured into bioprosthetic leaflets; evaluation of the effects of mechanical stresses and leaflet motion on collagen morphology in bioprosthetic valve leaflets; and initial screening of leaflet specimens and selection of the desired collagen orientation for embedding and sectioning of samples for conventional morphologic studies.
Animals↗
Etiologic factors and pathologic alterations in selenium-vitamin E deficiency and excess in animals and humans.
The etiology of selenium-vitamin E (Se-E) deficiency diseases may be complex. Many of the syndromes involve combined deficiency of selenium and vitamin E. Selenium moves into the animal and human food chain from soil and plants, which may contain inadequate amounts of the nutrient in many areas of the world. Vitamin E may be in low concentration in many animal feeds unless supplements are added. Some syndromes, such as steatitis in cats, result from an increased requirement of vitamin E in diets that contain large amounts of polyunsaturated fatty acids, and these diseases will only respond to vitamin E administration. Deficiency syndromes in animals owing to pure Se deficiency are infrequent and have been produced mainly by laboratory studies utilizing extreme deficiency conditions. Other factors that may affect the occurrence of these deficiency diseases are concurrent dietary deficiency of S-containing amino acids, bioavailability of different forms of dietary Se, intake of compounds that antagonize Se (e.g., silver salts), and exposure to various prooxidant substances (e.g., iron compounds, oxygen, ozone, and various drugs).
Animals↗
Ultrastructural features of hypertrophied human ventricular myocardium.
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Adult↗
Interleukin-1 alpha reduces the severity of the vascular leak syndrome produced by interleukin-2 and interleukin-2 plus interferon-alpha.
Histological and ultrastructural changes were investigated in lung, liver, and heart of mice given interleukin-2 (IL-2), either alone or in combination with other cytokines. IL-2 induced a vascular leak syndrome (VLS) of a moderate degree with infiltration of lymphoid cells, moderate endothelial damage, mild hepatic parenchymal damage, and minimal myocardial alterations. Interferon-alpha (IFN-alpha) produced infiltration mainly of monocytes/macrophages in liver and heart; endothelial cell damage was absent in lung and heart and minimal in liver. Interleukin-1 alpha (IL-1 alpha) caused an increased number of neutrophils in liver and lung; VLS and parenchymal cell and endothelial damage were not found. The VLS and the cellular damage caused by the combination of IL-2 and IFN were much more severe than those produced by IL-2 alone. In animals treated with IL-2, IFN-alpha, and IL-1 alpha, VLS was minimal and parenchymal and endothelial cell damage were less severe than after IL-2 alone or IL-2 plus IFN-alpha. Taken together, these observations show that IL-1 alpha reduces ultrastructural changes produced by IL-2 and IFN-alpha. This reduction may be clinically useful in the treatment of neoplasms.
Animals↗
Characterization of the pulmonary lesions induced in rats by human recombinant interleukin-2.
Histologic, electron microscopic, and immunohistochemical studies were made to analyze the structural features and the cellular composition of the pulmonary lesions produced in rats by the administration of interleukin-2 (IL-2). This agent induced pulmonary edema; thickening of alveolar septa; damage to endothelial cells in capillaries and venules, marked interstitial infiltration by cytotoxic T lymphocytes, lymphokine-activated killer (LAK) cells, macrophages, and dendritic cells (as demonstrated by cell counting in preparations stained immunohistochemically with peroxidase- and fluorochrome-labeled antibodies); and injury to bronchiolar and alveolar epithelial cells. Granular and agranular lymphocytes often were closely apposed to endothelial cells in capillaries and venules. Contacts between lymphocytes and type II alveolar epithelial cells also were observed. Damaged type II alveolar epithelial cells showed nuclear and cytoplasmic features that are considered indicative of apoptosis (confirmed by nick end labeling). Phagocytosis of apoptotic bodies by macrophages was occasionally found. These results support the concept that IL-2 induces cytotoxic vascular and parenchymal cell damage that is mediated by LAK cells and cytotoxic T lymphocytes, which make contacts with endothelial cells and type II alveolar epithelial cells. This damage appears to be exacerbated by the secondary release of a variety of vasoactive agents and inflammatory mediators.
Animals↗
Morphological aspects of the myocarditis and myositis in Calomys callosus experimentally infected with Trypanosoma cruzi: fibrogenesis and spontaneous regression of fibrosis.
Calomys callosus a wild rodent, is a natural host of Trypanosoma cruzi. Twelve C. callosus were infected with 10(5) trypomastigotes of the F strain (a myotropic strain) of T. cruzi. Parasitemia decreased on the 21st day becoming negative around the 40th day of infection. All animals survived but had positive parasitological tests, until the end of the experiment. The infected animals developed severe inflammation in the myocardium and skeletal muscle. This process was pronounced from the 26th to the 30th day and gradually subsided from the 50th day becoming absent or residual on the 64th day after infection. Collagen was identified by the picro Sirius red method. Fibrogenesis developed early, but regression of fibrosis occurred between the 50th and 64th day. Ultrastructural study disclosed a predominance of macrophages and fibroblasts in the inflammatory infiltrates, with small numbers of lymphocytes. Macrophages had active phagocytosis and showed points of contact with altered muscle cells. Different degrees of matrix expansion were present, with granular and fibrillar deposits and collagen bundles. These alterations subsided by the 64th days. Macrophages seem to be the main immune effector cell in the C. callosus model of infection with T. cruzi. The mechanisms involved in the rapid fibrogenesis and its regression deserve further investigation.
Animals↗
[Complications of heart valve prostheses].
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Heart Valve Prosthesis↗
Ultrastructural aspects of contractile proteins in cardiac hypertrophy and failure.
A review is presented in this chapter of morphological changes in contractile elements of cardiac muscle cells in hypertrophy and failure, with emphasis on alterations occurring in human hearts in the late stages of hypertrophy. The formation of new sarcomeres involves the synthesis of a variety of different proteins, their aggregation into filaments, and the organization of filaments into specific tridimensional arrays. Z-line material appears to play an organizer role in the formation of new sarcomeres. The ultrastructural appearance of contractile elements in hypertrophied muscle cells varies according to the cause and the stage of the hypertrophy. Myofibrillar lysis, with preferential loss of thick myofilaments, occurs in the late stages of hypertrophy in association with degenerative changes, including dissociation of intercellular junctions, proliferation of sarcoplasmic reticulum, cellular atrophy, and interstitial fibrosis.
Adult↗
Characterization of myosin from patients with asymmetric septal hypertrophy.
Human cardiac myosin isolated from operatively obtained samples of ventricular septum and left ventricular free wall of patients with asymmetric septal hypertrophy (ASH) was compared, with respect to structural and enzymatic properties, to myosin isolated from hearts of patients 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 SDS-polyacrylamide 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 patients with ASH and from patients without heart disease. Thus, the genetic defect present in patients with ASH is not expressed in the particular structural and functional characteristics of myosin evaluated in this study.
Actomyosin↗
Tissue-derived biomaterials and their use in cardiovascular prosthetic devices.
A variety of tissues and tissue components, ranging from allograft and xenograft tissues to albumin- and collagen-coated synthetic materials, have been used to fabricate cardiovascular prosthetic devices. Tissue-derived biomaterials include both viable and non-viable tissues as well as individual tissue components which have undergone some degree of preimplantation processing. A review of the biochemistry, immunogenicity, mechanical properties, physicochemical properties, preimplantation processing and the morphology of the following cardiovascular prostheses are discussed: heart valve bioprostheses and allografts; blood vessel allografts; biologic vascular grafts; and, protein-coated vascular prostheses. This review focuses on the generic aspects of prosthetic device fabrication using tissue-derived biomaterials, realizing that specific differences between various commercially available prostheses may exist.
Animals↗
The effects of anticalcification treatments on bioprosthetic heart valves implanted in sheep.
Several preimplantation processes have been shown to inhibit the calcification of pieces of porcine aortic valves and of bovine parietal pericardium implanted subcutaneously in rats. To investigate the effectiveness of these processes in modifying the calcification of bioprosthetic valves implanted in an intracardiac position, mitral and tricuspid valve replacements were performed in young sheep. Bioprosthetic valves treated with the following preimplantation processes were studied: 1) surfactants, including sodium dodecyl sulfate, polysorbate-80, Triton X-100 and N-lauryl sarcosine; 2) covalently bound aminohydroxypropane diphosphonic acid; 3) toluidine blue; and 4) incorporation of polyacrylamide into valvular tissues. Quantitative calcium analyses showed that only the surfactants substantially reduced calcification of bioprostheses implanted in intracardiac positions. This effect was evident only in porcine aortic valvular bioprostheses, and not in pericardial bioprostheses. Triton X-100 and N-lauryl sarcosine not only reduced calcification but also induced alterations that decreased the durability of the valves. Toluidine blue decreased calcification to a degree that was statistically significant but not biologically important, while polyacrylamide incorporation and diphosphonate binding increased calcification. Thus, data regarding anticalcification treatments obtained from subcutaneous implantation studies in small animal models should be interpreted cautiously and validated by studies with intracardiac valvular implantation in large animals.
Animals↗
Ultrastructural alterations in gizzard smooth muscle of selenium-vitamin-E-deficient ducklings.
Lesions of gizzard smooth muscle were studied by light and electron microscopy in newly hatched ducklings fed a selenium-vitamin-E-deficient diet for 13-21 days. Histopathologic alterations included initial hyaline change in damaged smooth-muscle cells, subsequent mineralization of sarcoplasmic debris in necrotic smooth-muscle cells, macrophagic invasion and phagocytosis of sarcoplasmic debris, and eventual fibroblastic proliferation and scarring of damaged areas in the gizzard wall. Ultrastructurally, mild damage in smooth-muscle cells was manifested by altered mitochondria with matrical densities and disrupted membranes and dilated elements of sarcoplasmic reticulum. In smooth-muscle cells with severe injury, the alterations of mitochondria and sarcoplasmic reticulum were accompanied by myofibrillar lysis and disruption of plasma membranes and external laminae. Expanding zones of mineralization of sarcoplasmic debris in necrotic smooth muscle cells were present at dense masses of lysed myofilaments that surrounded mineralized and disrupted mitochondria. Numerous macrophages infiltrated the areas of necrosis of smooth muscle and phagocytosed sarcoplasmic debris.
Animals↗
Evaluation of vitamin E and selenium protection against chronic adriamycin toxicity in rabbits.
Chronic Adriamycin (ADR) toxicity was produced in 50 weanling rabbits by weekly injections of 2.4 mg of ADR/kg of body weight for up to 17 weeks. An evaluation was made of the protective value of weekly injected supplements, given 24 hours before each ADR injection, which included: (a) low-dose vitamin E (alpha-tocopherol acetate, 17 mg/kg) (b) high-dose vitamin E (alpha-tocopherol acetate, 170 mg/kg); (c) selenium (as sodium selenite, 0.06 mg/kg); and (d) combined low-dose vitamin E and selenium. The incidence of cardiomyopathy was high in both supplemented and unsupplemented rabbits. Mean cardiomyopathy scores were low in the unsupplemented rabbits and moderatey high in the supplemented rabbits (that survived longer), but were lower in rabbits given high-dose vitamin E than in the other supplemented groups. Supplements of vitamin E, selenium, or both prolonged survival of animals treated continuously with ADR, but only supplements of large amounts of vitamin E provided any evidence of even partial protection against chronic cardiotoxicity.
Animals↗