The fate and fibrogenic potential of subintimal implants of crystalline lipid in the canine aorta. Quantitative histological and autoradiographic studies.
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Biomedical subjects
Publications and source records attributed to B G Brown.
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More accurate characterization of coronary artery lesions is needed for evaluation of short and long-term interventions in coronary disease. A method of segmental artery analysis has been developed to maximize the information obtained from coronary arteriograms. Coronary lesions are traced from two projected, perpendicular, 35 mm cineangiographic views and transmetted, in digital form, to a PDP 11/45 computer. Magnification and distortion of the image are compensated for in order to determine the actual vessel profiles, using the catheter and its location as a scaling device. The two views are matched; a spatial representation of the vessel centerline is constructed mathematically; and orthogonal vessel diameters are computed at increments along this centerline. Assuming an elliptical lumen, the absolute and percentage reduction in diameter and cross-sectional area in the stenosis are computed. More complex functions (integrated atheroma mass, Poiseuille resistance, and orifice resistance) are then calculated. The accuracy and variability of the different steps involved in lesion analysis have been determined. Dimensional accuracies of +/- 150 microns (SD) are feasible. Examples are given of patients with Prinzmetal's angina and with progressive coronary disease.
Segmental ureteral replacement with free autogenous fibroelastic Dacron tube grafts in three dogs was unsuccessful during preliminary trials. However, a proliferation of urothelium, smooth muscle, and blood vessels throughout the length of the grafts was demonstrated, providing an encouraging potential for further investigations. Technical refinements are suggested that may provide for improved success with experimental ureteral replacement.
Smooth muscle cells (SMC) were grown from inner media explants of swine aorta and used as a model for studying the role of lipoproteins in atherogenesis. These cultured cells retain the characteristics of SMC through multiple passages. Cell growth curves, in time, were obtained by using standard counting techniques, SMC grew slowly (0.019 cycle/day) in modified Dulbecco-Vogt medium supplemented with 1.5% swine serum. Purified lipoproteins were prepared from three normolipidemic and two hyperlipidemic (cholesterol-fed) swine. When the medium of 84 growth experiments was supplemented with these lipoproteins, SMC growth rate increased linearly with lipoprotein cholesterol concentration up to 10 mg/dl. At 10 mg/dl of lipoprotein cholesterol, very low density lipoproteins (VLDL) increased growth rate 7.2-fold (P less than 0.01); low density lipoproteins (LDL) 5.7-fold (P less than 0.01); high density lipoproteins (HDL2) 3,4-fold (P less than 0.02); and HDLc, and lipoprotein appearing in the hyperlipidemic swine, 3.0-fold (P less than 0.01). Addition of 10% lipoprotein-free serum stimulated growth rate 6.0-fold (P less than 0.01). There was no difference between normo- and hyperlipidemic lipoproteins with respect to cell growth rate. Factors present in the ultracentrifugal bottom, and factors appearing during the platelet release reaction, were shown to contribute to the SMC growth response. Morphological alterations characteristic of intimal foam cells occurred in SMC grown in VLDL at triglyceride levels in excess of 15 mg per 100 ml. Thus there are distinct parallels between SMC response in this model in vitro and atherogenesis in vivo.
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