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Biomedical subjects

F Kummerow

Publications and source records attributed to F Kummerow.

12 recordsLinked to original sources
PubMed2001

Oxidized low density lipoprotein inhibits prostacyclin generation by rat aorta in vitro: a key role of lysolecithin.

The objective of this study was to examine the effect of oxLDL on prostacyclin (PGI2) generation by rat aortic segments and to see whether the lipid fraction of oxLDL or its components are responsible for that effect. We also tested if antioxidants have any protective role. LDL oxidized by copper was characterized by higher TBARS, conjugated diene, lysophosphatidylcholine (lyso PC), oxysterols and less polyunsaturated fatty acids (PUFA) than nLDL. Preincubation of aortas with oxLDL caused a significant inhibition of PGI2 generation compared to aortas preincubated with nLDL or buffer only. The percent inhibition was dependent on the concentration of oxLDL. Most of the inhibitory effect of oxLDL resided in its lipid moiety while the lipid fraction of nLDL, as well as native LDL had no effect. Preincubation of aortas with 10 microg/ml of 7-ketocholesterol the major oxysterol in oxLDL reduced the amount of PGI2 generated by aorta at all times tested; however that decrease did not reach a significant level. Aortas preincubated with 10 microg/ml of lyso PC showed a 21-36% inhibition of PGI2 generation which was comparable to the inhibition produced by preincubating the aortas with 50 microg protein/ml of oxLDL (containing about 7.5 microg lyso PC). This indicated that most of the inhibitory effect of oxLDL was due to its lyso PC. The small molecular weight fraction (< 10 kDa) with a high level of TBARS (TBARS solution) also significantly decreased the PGI2 generation by aorta. Addition of superoxide dismutase (SOD) + catalase or vitamin E simultaneously with oxLDL or TBARS solution in the preincubation medium did not reverse their inhibitory effects. This indicated that oxygen free radicals are not a contributing factor to the inhibitory effect of oxLDL but lyso PC and the lipid peroxides and probably other components already present within oxLDL are the important inhibitors.

Animals↗
PubMed1990

26-hydroxycholesterol-stimulated DNA synthesis in smooth muscle cells and induction of endothelial injury using a coculture technique.

We investigated the effects of 0.5, 2.5, and 10 micrograms/ml of cholesterol or 26-hydroxycholesterol on bovine aortic ECs and SMCs. Suppression of viable cell density and cytotoxic changes in both cells were induced by 2.5 and 10 micrograms/ml 26-hydroxycholesterol. ECs were more severely damaged than SMCs in the presence of 26-hydroxycholesterol. Levels of up to 10 micrograms/ml cholesterol had no effect on ECs or SMCs growth or cytotoxicity. Confluent ECs exposed to 2.5 or 10 micrograms/ml of 26-hydroxycholesterol secreted significant amounts of 6-ketoprostaglandin F1 alpha after a 24-hr incubation. An equivalent concentration of cholesterol had no such effect. SMCs cocultured with ECs exposed to 10 micrograms/ml 26-hydroxycholesterol, when compared with an equivalent level of cholesterol, synthesized DNA in significantly greater amounts during a 24-hr incubation. The cocultured ECs incubated in the presence of 2.5 and 10 micrograms/ml 26-hydroxycholesterol were partially detached due to cell death. However, no difference was observed in the DNA content of SMCs cultured without ECs in the presence of cholesterol or 26-hydroxycholesterol. The results suggest that 26-hydroxycholesterol produced not only cytotoxicity to ECs and SMCs but also stimulated DNA synthesis in SMCs through endothelial injury.

Animals↗
PubMed1987

The effect of elastase on chickens with endogenous hyperlipidemia.

Elastase has been reported to have a multiplicity of activities which may be protective against atherosclerosis. The data reported here support those reports and show a clear antiatherosclerotic effect in hyperlipidemic chickens. We have shown here that a reduction in calcium and lipid accumulation in aortic tissue and possibly a plasma cholesterol lowering effect can be seen in the chicken when treated with elastase. The most important effect in this animal is probably to aid removal of lipid bound to elastin in the intima. This was achieved at a dose of only 600 U elastase while reductions in tissue calcium required 1800 U elastase.

Administration, Oral↗
PubMed1985

Angiotoxicity in swine of a moderate excess of dietary vitamin D3.

The effects of five different dietary levels of vitamin D3 on the coronary arteries of groups of 17-60 2-month old weanling Yorkshire swine were studied. Four groups were fed the following levels of vitamin D3 per ton of ration continuously for 4 months: group I--100,000 IU, group II--300,000 IU, group IV--2,000,000, and group V--4,000,000 IU. Swine in group III were fed the diet containing 100,000 IU of vitamin D3 per ton of ration for the first 2 months of the study after which they were fed a diet supplemented with 4,000,000 IU of vitamin D3 per ton of ration for the remaining 2 months of the study. The highest degree of intimal thickening of the coronary arteries was observed among group V. The thickened areas contained numerous lipid-containing cells and degenerate cells without stainable lipid. Electron microscopic examination revealed a greater frequency of degenerate cells without stainable lipid in the coronary arteries of groups III and IV than in groups I and II. These results suggest a possible link between excessive daily intake of vitamin D3 and the development of human coronary atherosclerosis.

Animals↗
PubMed1985

Ultrastructure of human umbilical artery and vein. Characterization and quantification of lipid laden cells.

Intimal thickening and lipid accumulation, which occur in atherosclerosis, were observed in fifteen human umbilical vessels. Quantification of lipid laden cells was done electron-microscopically. Within 1 month after birth, lipid laden cells originating from macrophages were observed in the umbilical artery, while those originating from smooth muscle cells were seen in the umbilical artery and vein. Lipid droplet formation appeared to be independent and different in macrophages and smooth muscle cells; the latter cells were stimulated to produce lipid droplets by hypoxia and the former cells by blood components.

Age Factors↗
PubMed1984

Ultrastructure of newly formed vessels in thrombi. Endothelium formation in human umbilical artery.

Thrombi with newly formed vessels in thirteen human umbilical arteries were studied. Red blood cells formed masses which were covered by fibrin within twelve hours after birth. By the second day, the intima including endothelial cells was denuded. In the junctional area between the thrombi and the original intima on the sixth day, red blood cells were surrounded by endothelial-like cells, which displayed junctional complexes and did not show any connection with intact endothelial cells. These cells also exhibited filaments with fusiform densities, suggesting a probable origin from vascular smooth muscle cells. Examination of older specimens indicated that these were precursor structures of functional capillaries found in mature thrombi.

Age Factors↗
PubMed1984

Ultrastructure of aging human umbilical artery and vein.

Qualitative and quantitative changes in the human umbilical artery and vein were observed in 15 human specimens at different stages of development. Features such as intimal thickening and cellular lipid accumulation were found in umbilical vasculature. Cellular origin and quantification of lipid-containing cells were determined by electron microscopy. Within 1 month after birth, lipid-containing cells originating from macrophages were observed in the umbilical artery, while those originating from smooth muscle cells were observed in both the umbilical artery and vein. Lipid droplet formation appeared to be independent and different in macrophages and smooth muscle cells; the former cells were stimulated to produce lipid droplets primarily by plasma insudation and the latter cells primarily by hypoxia. These findings indicate that ultrastructural changes observed in closing umbilical vasculature may closely parallel and serve as a model for atherosclerotic changes which occur in mature vessels.

Aging↗
PubMed1981

Vasculotoxic effects of dietary testosterone, estradiol, and cholesterol on chick artery.

Five-day-old female chicks were fed diets containing testosterone, estradiol, and cholesterol for 2 months. Cholesterol supplementation of 1 per cent. resulted in production of lipid vacuoles in the interlamellar connective tissue cells and to a lesser extent in the smooth muscle cells in the aorta; cholesterol had no effect on the coronary artery. The vasculo-toxic nature of estrogen was indicated when 0.05 per cent. dietary estradiol produced more accumulations of lipid vacuoles in smooth muscle cells, more extracellular lipid, and more smooth muscle cell death than cholesterol feeding. A dietary combination of cholesterol plus estradiol produced severe lipid deposition throughout the entire thickness of ascending aorta, and degenerative atherosclerotic changes in the coronary artery. Combined testosterone and estradiol supplementation resulted in peculiar dwarf chickens which exhibited increased vascular smooth muscle cell mitosis and degeneration.

Animals↗
PubMed1981

Angiotoxic effects of dietary 7-ketocholesterol in chick aorta.

Although dietary 1-ketocholesterol treatment had little effect on plasma and liver lipid metabolism, aortas from chickens treated with 7-ketocholesterol contained numerous dead and dying smooth muscle cells. Chicks receiving dietary cholesterol, in amounts equal to or greater than the amount of 7-ketocholesterol, did not demonstrate significant smooth muscle cell degeneration. After eight weeks, a combined diet of 1% cholesterol plus 10-20 mg/day 1-ketocholesterol produced no larger amounts of aortic lipid deposition, and no greater increases in smooth muscle cell degeneration than a comparable group receiving 7-ketocholesterol alone. The abdominal aorta was always more severely damaged than the ascending arch or thoracic aorta in chicks fed 7-ketocholesterol. The results demonstrate a potent angiotoxic effect of 7-ketocholesterol.

Animals↗
PubMed1980

Ultrastructure of developing human ductus arteriosus.

Histological and ultrastructural studies were made of 25 specimens of human ductus arteriosus obtained from abortion of autopsy, and ranging in age from 15 weeks of gestation to 7 years. Samples of ductus with normal muscular type structure exhibited active intimal thickening as early as 15 weeks' gestational age when the internal elastic lamina was found to be focally discontinuous. At the same time, intimal smooth muscle cells were closely arranged, and often intimately connected to cells of the tunica media. Ultrastructurally, both smooth muscle cells and endothelial cells at 15 weeks' gestational age contained abundant glycogen deposits. From 18-32 weeks' gestational age, glycogen deposits gradually disappeared, collagen fibres began to appear in the extracellular space and the first signs of smooth collagen fibres began to appear in the extracellular space and the first signs of smooth muscle cell degeneration became apparent. After birth, intimal thickening and degeneration of smooth muscle cells was much more pronounced. The ultrastructure of intimal smooth muscle cells indicated that intimal thickening was caused by smooth muscle cell migration as opposed to rapid proliferation; and both intracellular and extracellular membrane-bound lipid-filled vacuoles were commonly seen in the more advanced stages of degeneration. Of the ductus specimens examined, three were rich in elastic fibres. Two of these three specimens were from a group of 10 abortion cases, and the third was from a 2 weeks old full term infant who had been exposed to maternal rubella. The 2 weeks old infant had a widely patent ductus arteriosus; whether the two fetal specimens with ductus elastosis would have eventually developed into clinical patent ductus arteriosus was not clear.

Ductus Arteriosus↗