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The processes of distention and recoil have an essential role in the functions of arteries and lungs. In both organ systems, these processes involve to a great extent the connective tissues, in particular the manner in which the extracellular materials are arranged to afford such movements. This book concerns the microenvironment of the connective tissues in the walls of arteries and the stroma of lungs. Proteoglycans, collagen, and elastic fibers and their interrelationships are discussed by eight scientists who are established researchers in this area. Their reports include important findings on how this microenvironment is altered in diseases such as atherosclerosis, emphysema, and pulmonary fibrosis. The concepts developed result from studies at the biochemical, macromolecular, ultrastructural, and light microscopic levels. Taken col lectively, the reports focus attention upon the role of the connective tissues in arterial and lung distensibility and how alterations in the connective tissues result in the loss of this function. Medical researchers and physicians interested in arterial or lung functions or diseases will find the scientific approaches and findings of the authors innovative and provocative. Students of stereologic morphometry will be particularly interested in the quantitative studies of cells and fibers in arterial walls; histologists and pathologists will find the chapter on histochemical staining interesting from both a scientific and historic viewpoint.
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This volume is the product of a February 1982 conference, cosponsored by the American Heart Association, the National Institutes of Health, and the Bowman Gray School of Medicine, which examined techniques for delineating quantitatively the natural history of atherosclerosis. Against the background of current pathologic and clinical knowledge of atherosclerosis, invasive and noninvasive evaluative methods now in use and under development are surveyed in depth. Correlative clinicopathologic studies of atherosclerosis pose special questions with respect to both luminal and plaque characteristics that are addressed in this volume. An old observa tion, based on the examination of arterial casts, suggested that the so-called nodose lesion of atherosclerosis may be at first flattened into the wall of a weakened, dilated artery, rather than raised into the lumen. This is now fully confirmed in vivo by ultrasonic and other imaging techniques. The morbid anatomist is challenged anew to describe lesions as they are likely to occur in vivo. To achieve closer correlation with natural conditions, perfu sion fixation of arteries under arterial pressure is becoming more widely used and has already demonstrated more valid quantita tion of the composition and configuration of lesions. While the noninvasive methods of B-mode and Doppler ultrasound are suitable only for the clinical study of superficial arteries, such as the carotid or femoral, the new and relatively noninvasive procedure of intravenous digital subtraction angio graphy can be effectively used for the examination of deep systems, such as cerebral vessels.
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Two infonnal meetings of consultants expert in hemostatic phenomena and in atherogenesis were held in Bethesda, Maryland, in December 1975 and February 1976 by the National Heart, Lung, and Blood Institute. Their purpose was to discuss the current status of knowledge concerning the thrombotic process in the pathogenesis of atherosclerosis. It was readily agreed that thrombosis often played a major role in plaque building and in plaque complication. It was also commented, however, that the data were qualitative in nature and that quantitative infonnation was remarkably sparse. The term thromboatherogenesis was thought to be appropriate for those phenomena in which the full expression of the thrombotic process is manifest. At the same time, recent research was noted in which what appears to be an important pathway for the initiation of atherogenesis arises from the reaction of platelets with injured arterial endothelium and'Subendothelium without necessarily involving the complete classical thrombotic process. A name was not coined for this circumstance, but it was held that thromboatherogenesis was not a fully appropriate one.