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Biomedical subjects

D Vesselinovitch

Publications and source records attributed to D Vesselinovitch.

At least 37 records · Page 2Linked to original sources
PubMed1984

Histochemical detection and quantification of macrophages in rhesus and cynomolgus monkey atherosclerotic lesions.

A detailed histochemical study of the macrophage involvement during experimental atherogenesis in rhesus and cynomolgus monkeys was performed. Aortic, carotid, and femoral artery lesions were examined in both species after 4, 8, and 12 months of atherogenic diet feeding. Macrophages were identified and quantified in the atherosclerotic lesions using acid lipase, acid esterase, beta-galactosidase, and cytochrome oxidase histochemical procedures. Morphometric quantitation revealed that the cynomolgus monkey arterial lesions were larger and consistently demonstrated a greater number of cells with characteristics of macrophages in the intimal, medial, and adventitial portion of the arteries when compared to the primarily intimal rhesus monkey lesions. Biochemical assays of aortic samples for acid lipase and acid esterase activity also showed consistently higher activities in the cynomolgus samples when compared to the rhesus samples. Average serum cholesterol levels were higher in the cynomolgus monkeys than in the rhesus monkeys, but the differences in the arterial lesions still existed when animals with overlapping cholesterol levels were compared. Macrophages and their associated activities predominated in experimental cynomolgus monkey atherosclerosis when it was compared to the rhesus disease process, which may be an explanation for some of the differences in atherogenesis reported in these two species.

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PubMed1983

The effect of estradiol on the proliferation of rabbit aortic medial tissue culture cells induced by hyperlipemic serum.

The outgrowths of medial explants of thoracic aorta from New Zealand rabbits were used to study the influence of estrogen on cell proliferation. After 5-6 weeks of rapid growth in Basal Eagle Medium (BME) supplemented with 10% normal rabbit serum, such cultures reached a stationary phase during which they showed little mitotic activity and little further increase in surface area. Replacement of 5% of the normal serum with hyperlipemic rabbit serum resulted in a stimulation of these stationary cultures into a phase of renewed proliferation, which was measured directly as increase in cell culture size and by [3H]thymidine incorporation visualized by autoradiography. The addition of estrogen (estradiol, Progynon, Schering Corp.) in a concentration of 0.02 microgram/ml to the culture medium inhibited the proliferative effect induced by the hyperlipemic serum. On the other hand it had no effect on the growth rate of such explant cultures during their rapid growth phase if added at the time of explantation for 6 weeks. This would indicate that the inhibition of the hyperlipemic serum-induced proliferation by estrogen is not due to a toxic effect on mitosis in general. Cells exposed to estrogen tended to have larger amounts of intracellular lipid as visualized by oil red O staining. Moreover, prolonged exposure to estrogen resulted in a significant decrease in stainable collagen and elastin in these cultures.

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PubMed1983

Arterial lesions and blood lipids in rhesus monkeys fed human diets.

The results of three consecutive experiments are reported in which atherosclerotic lesions of adult male rhesus monkeys produced by a ration relatively rich in calories, cholesterol, and saturated fats and resembling the "average American" table-prepared fare were compared with the atherosclerotic lesions in similar monkeys fed a low-fat, low-cholesterol, and low-calorie, so-called "prudent" table-prepared ration. Each experiment lasted 2 years. The frequency and severity of gross and microscopic aortic atheromatous disease and microscopic coronary artery disease were compared. In addition, the qualitative features of the lesions, several types of analyses of blood lipids, and the reactions of aortic cells to in vivo deposited interstitial aortic deposits of lipoprotein fractions prepared from these animals are described. In general, the animals fed the average American ration had serum cholesterols that were consistently higher (383 +/- 35 mg%) than animals fed the prudent ration (199 +/- 13 mg%). The contrasts in lesion involvement varied from about 6:1 in severity for both aortic and coronary lesions to approximately 3:1 or 4:1 in frequency. The aortic gross surface area involvement at autopsy was 46% for monkeys fed the average American ration compared to 7% for the prudent diet group. In lesions of animals fed the average American ration much of the lipid was extracellular and both cell proliferation and fiber protein deposition were prominent. The small lesions in the animals fed the prudent ration were much more likely to be composed mostly of "foam cell" intimal thickenings. The lesions seen in the animals fed the average American ration resemble those seen in autopsies of many young Americans whose lesions have been studied recently and who demonstrate raised lesions in their coronary arteries and aortas in the third decade.

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PubMed1983

The complementary interaction of epidemiological and experimental animal studies: a key foundation of the preventive effort.

This overview will examine the contributions made by animal models of atherosclerosis to our understanding of its pathogenesis and will describe the principles for prevention of this disease process. In addition, some of the recent biochemical and cell biological discoveries, many utilizing animal cells and animal lipoproteins, will be discussed. Further, the increasing knowledge brought to worldwide efforts for the prevention and regression of atherosclerosis by the aforementioned research approaches will be reviewed. The results of some of the most promising animal studies of advanced atherosclerotic plaque regression will be briefly summarized, emphasizing the quantitation of changes. The prospects for verifying some of these findings in quantitative studies of human atherosclerosis will be presented along with some of the obstacles to be overcome.

Animals↗
PubMed1983

Combined effects of cholestyramine and probucol on regression of atherosclerosis in rhesus monkey aortas.

Adult male rhesus monkeys were fed a high fat, high cholesterol diet for 13 months. During the subsequent 12 months this diet was continued, but the animals were also treated with cholestyramine and/or probucol. The combined drug treatment caused lowering of blood cholesterol without a change in HDL-cholesterol. Regression of plaques was more marked than in animals treated with either drug alone. Animals remained in good health during the treatment period.

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PubMed1983

An ultrastructural comparison of diet-induced atherosclerosis of arteries supplying the central nervous system in cynomolgus and rhesus monkeys.

The carotid lesions of cynomolgus and rhesus monkeys fed an 8- to 12-months atherogenic diet are very severe. However, the basilar, vertebral and middle cerebral arteries of the same atherosclerotic monkeys look instead, at SEM examination, similar to the control ones. At TEM examination, these arteries of the atherosclerotic monkeys show only minimal lesions in the subendothelial space ('edema' and presence of fragments of basilar membrane) and sometimes necrobiosis of endothelial cells. The smooth muscle cells, which are also present in the controls in these arteries in the subendothelial space, are sometimes surrounded by a nest of basement membrane beads and do not contain lipid droplets.

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PubMed1980

A comparison of the turnover and metabolism cholesterol in normal and atherosclerotic monkey aortas.

Rhesus monkeys were fed high cholesterol and cholesterol-free diets for 21-24 months. The animals were then given isotopic cholesterol intravenously and autopsied from 1 to 51 weeks later. The plasma and aortic cholesterol contents were 633 +/- 130 mg/dl and 35.6 +/- 11.4 mg/g dried tissue (45.5% in ester form) for atherosclerotic monkeys and 135 +/- 25 mg/dl and 9.9 +/- 3.6 mg/g (15.0% in ester form) for control monkeys, respectively. The minimal influx rate of cholesterol from plasma into the aorta was much greater for atherosclerotic animals, 0.470 +/- 0.20 mg/g per day versus 0.088 +/- 0.031 for control monkeys. There was a rapid turnover of both free and esterified cholesterol in the atherosclerotic aortas, greater than for normal aortas. These studies of cholesteryl ester metabolism indicated a likely origin of aortic cholesteryl ester from the plasma cholesteryl esters. Our data indicated a dynamic cholesterol metabolism and turnover in the aorta during atherogenesis.

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PubMed1979

The effect of various dietary regimens and cholestyramine on aortic glycosaminoglycans during regression of atherosclerotic lesions in rhesus monkeys.

The effect of various diets on the aortic glycosaminoglycan (GAG) composition was studied in rhesus monkeys. Aortas were obtained from monkeys fed diets containing cholesterol and comparative fats including coconut oil--butter and peanut oil and with and without cholestyramine. Additional groups in each experiment were placed on regression diets of low-fat, low-cholesterol with and without cholestyramine. Further, an atherogenic diet of coconut oil--butter was alternated every 2 months with a diet enriched with corn oil. GAG isolated from intima and media--adventitia indicated slight variations in the concentration of total GAG among different dietary groups but major differences in the concentration of individual GAG. The concentrations of hyaluronic acid and heparan sulfate were generally greater in aortas of monkeys fed corn oil diets than in those fed coconut oil--butter or peanut oil diets. The concentration of dermatan suulfate generally decreased during regression of lesions induced by the saturated fat--cholesterol diet. Furthermore, the aortas of monkeys with lesions from feeding peanut oil showed higher levels of dermatan sulfate and lower levels of chondroitin 4-sulfate than the saturated fat-fed groups. The addition of cholestyramine enhanced the effects of regression. These observations show that the composition of GAG of the arterial wall can be influenced by various dietary programs and that GAG play a role in induction and regression of experimental atherosclerotic lesions.

Animals↗
PubMed1977

Regression of arteriosclerotic lesions in rhesus monkey aortas after regression diet. Scanning and transmission electron microscope observations of the endothelium.

Scanning and transmission microscopy were used to study aortic intima atherosclerotic lesions in Rhesus monkeys during both progression and regression phases. Scanning micrographs of severely atherosclerotic lesions showed areas of disjunctive endothelium and discontinuous basement membranes, frequently accompanied by red blood cells and other circulating elements adhering to the surface. Transmission micrographs also showed occasional areas of endothelial cell damage and loss with lipid-laden smooth muscle cells and foam cells beneath. Regressed lesions (affected by low-fat, low-cholesterol diet with or without cholestyramine) showed endothelial changes suggestive of reparative processes. Scanning micrographs showed flattened residual lesions with continous endothelial lining, while transmission microscopy disclosed interdigitated intercellular tight junctions and frequently reduplicated basement membranes.

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PubMed1976

Studies of regression of advanced atherosclerosis in experimental animals and man.

In general, the results to date in humans and experimental animals seem to indicate that substantial regression of advanced atherosclerosis is possible. The results also indicate that the advanced atherosclerotic lesions are much more likely to respond favorably if the serum cholesterol concentrations are reduced to the minimum that prevails in animals or people who consume a low-fat low-cholesterol diet. In human subjects and in rhesus monkeys, this value appears to be about 150 mg%. Under these circumstances, much of the lipid disappears from the plaques, and the remaining fibrous tissue and cells appear to condense and undergo remodeling, as they do in fracture or wound healing. Additional effort will be required to ascertain how rapidly and how much of the fiber proteins and calcium can be removed from the advanced plaques and to work out methods that will consistently produce regression of advanced atherosclerotic lesions in human subjects. This goal would appear to be worth working toward. Interruption of progression of atherosclerosis appears to be more easily achieved, and it also would appear to be a worthwhile goal. The diagram that is reproduced as FIGURE 2 presents the multiple methods of intervention in atherosclerosis that are now available to the physician and to the patient. To those of us who look on atherosclerosis as an almost completely preventable disease and one that is largely reversible, the following quotation from the perceptive essay by Lewis Thomas seems to be prophetic and most appropriate. An extremely complex and costly technology for the management of coronary heart disease has evolved, involving specialized ambulances and hospital units, all kinds of electronic gadgetry and whole platoons of new professional personnel to deal with the end results of coronary thrombosis. Almost everything offered today for the treatment of heat disease is at this level of technology, with the transplatned and artificial hearts as ultimate examples. When enough has been learned for us to know what really goes wrong in heart disease, we ought to be in a position to figure out ways to prevent or reverse the process; and when this happens, the current elaborate technology will be set to one side.

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