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Biomedical subjects

S Stender

Publications and source records attributed to S Stender.

At least 55 records · Page 3Linked to original sources
PubMed1995

Effect of oestrogen replacement therapy on development of experimental arteriosclerosis: a study in transplanted and balloon-injured rabbit aortas.

The mechanism underlying possible protection of oestrogen replacement therapy against cardiovascular disease appears to go beyond beneficial changes in plasma lipoproteins. A direct action of oestrogen on the metabolism of lipoproteins after entering the arterial wall may occur. The present study evaluated whether oestrogen replacement therapy affects the development of experimental arteriosclerosis in immunologically injured (experiment A + B) and balloon-injured (experiment B) aortas in ovariectomized rabbits maintained at a human level of plasma cholesterol; both models involve severe damage to the endothelium with resulting rapid accumulation of lipoproteins in the arterial intima and therefore appear suitable for studying factors directly affecting subendothelial lipoprotein metabolism. In experiment A, dietary cholesterol required to maintain a human level of plasma cholesterol was significantly higher for the oestrogen group than for the placebo group. Similarly, cholesterol accumulation in the aortic grafts was borderline higher for the oestrogen than the placebo group, whilst intimal hyperplasia was without difference between the groups. Due to a modified schedule of cholesterol feeding in experiment B, oestrogen and placebo groups received the same amount of dietary cholesterol, and cholesterol accumulation and intimal hyperplasia were similar in immunologically injured and balloon-injured parts of the aorta in both groups. These results suggest that in the female rabbit maintained at a human level of plasma cholesterol, oestrogen replacement therapy has no direct action on the development of experimental arteriosclerosis when induced by immunological or mechanical injury to the endothelium.

Animals↗
PubMed1995

Effect of the antioxidant probucol on transplant arteriosclerosis in aorta-allografted rabbits.

The attenuation of atherogenesis by oral probucol treatment, demonstrated in several animal studies, has been attributed to the antioxidative property of probucol. It is thought that probucol, by inhibiting oxidation of low density lipoproteins (LDL) decreases the uptake of LDL into monocytes, and thereby reduces the development of foam cells and fatty streaks. Also, the neointimal proliferation seen after balloon injury has been attenuated by treatment with probucol. Since foam cells and neointimal proliferation are both important elements of transplant arteriosclerosis, we have investigated whether probucol might also retard the development of experimental transplant arteriosclerosis. The thoracic aorta from one rabbit was transplanted as a bypass graft onto the abdominal aorta of another rabbit. Nine rabbits were treated with 1 g probucol per day and seven animals were treated with vehicle. After a recovery period of 2 weeks, all rabbits were clamped at a human level of plasma cholesterol (6 to 7 mmol/l) for a period of 3 weeks. The amount of dietary cholesterol necessary for this clamping tended to be higher in probucol treated than in vehicle-treated rabbits. The distribution of plasma cholesterol between lipoprotein classes was similar in the two groups, except for the concentration of high density lipoproteins (HDL), which was significantly lowered by probucol. Probucol markedly decreased the susceptibility of LDL and intermediate density lipoprotein plus very low density lipoprotein (IDL + VLDL) particles to oxidation, as measured by the production of conjugated dienes when adding Cu2+. Despite this, the development of transplant arteriosclerosis as well as the number of macrophages in the neointima were not significantly different in the aortic allografts from the two groups. These results suggest that antioxidative agents do not retard the development of experimental transplant arteriosclerosis.

Animals↗
PubMed1995

The influence of trans fatty acids on health: a report from the Danish Nutrition Council.

Trans fatty acids constitute 0-30% of the fat in Danish margarines, most in industry and bakery margarines and usually less in table margarine. The trans fatty acids make margarines more solid at room temperature and therefore provide an economical storage advantage. In British and U.S. reports from 1984-1989, the trans fatty acids were more or less acquitted of unhealthy effects. During the last 5-6 years, however, a series of new studies has been published regarding both the connection between the consumption of trans fatty acids and the occurrence of coronary heart disease and the impact on the lipoprotein level in plasma. Studies suggest that the consumption of trans fatty acids from margarine is equally, or perhaps more, responsible for the development of arteriosclerosis than saturated fatty acids. In addition, it is now clear that both the fetus and the breast-fed baby are exposed to trans fatty acids in relation to the mother's consumption. A couple of recent studies suggest a possible restrictive influence of the trans fatty acids on the weight of the fetus. The average consumption of trans fatty acids from margarine in Denmark in 1991 was approximately 2.5 g/day per person. For about 150,000 adult Danes, the consumption is assumed to be more than 5 g/day per person. On this basis, the Danish Nutrition Council recommend that the consumption of trans fatty acids is reduced as much as possible. This can be done by reducing the fat content in food and by reducing the trans fatty acid content in all Danish margarine products to 5% or less. Thereafter, the group of adult Danes, including pregnant and breast-feeding women, with a large consumption of margarine and margarine-containing products, will on average only consume 2 g of vegetable trans fatty acids/day. This corresponds to the consumption in the low-risk groups in the above-mentioned epidemiological studies. In addition, the Danish Nutrition Council encourage the producers of margarines to make products that can be marketed as 'free of trans fatty acids'.

Adult↗
PubMed1995

Replacement of dietary saturated fat with monounsaturated fat: effect on atherogenesis in cholesterol-fed rabbits clamped at the same plasma cholesterol level.

The aim was to compare the effect on atherogenesis of dietary monounsaturated and saturated fatty acids in cholesterol-clamped rabbits. To obtain an average plasma cholesterol concentration of 20 mmol/l in each rabbit during the 13-week cholesterol-feeding period, dietary cholesterol was adjusted weekly. The amount of fat fed daily was 10 g per rabbit in Expts A (n 23), C (n 36), and D (n 58) and 5 g per rabbit in Expt B (n 24). The source of monounsaturated fatty acids was olive oil in all four experiments. The source of saturated fatty acids was butter in Expt A, lard in Expt B, coconut oil in Expt C, and butter or lard in Expt D. Generally, olive oil-fed groups received more cholesterol and tended to have more cholesterol in VLDL and less in LDL compared with groups receiving saturated fat. Analysis of variance of the combined results of all four experiments showed that, in comparison with saturated fat, olive oil lowered aortic cholesterol by 13 (-9-30, 95% confidence interval) % in the aortic arch, and by 10 (-10-26) % in the thoracic aorta, which was not significant. In the comparison with olive oil, no differences in effects on aortic cholesterol content were detected between butter, lard and coconut oil. These findings do not support the view that replacement of dietary saturated fat with olive oil has a major impact on the development of atherosclerosis in addition to that accounted for by changes in plasma cholesterol levels.

Animals↗
PubMed1995

Transfer of lipoprotein(a) and LDL into aortic intima in normal and in cholesterol-fed rabbits.

To study the relative atherogenic potential of lipoprotein(a) [Lp(a)], the transfer of Lp(a) and LDL into the arterial wall was compared in normal rabbits, cholesterol-fed rabbits, and normal rabbits in which the plasma concentration of Lp(a) before injection of labeled lipoproteins was increased by an intravenous mass injection of 45 mg Lp(a). Aorta was removed either 60 minutes or 180 minutes after intravenous injection of a mixed preparation of human 125I-Lp(a) and 131I-LDL; intimal clearance was calculated as radioactivity in aortic intima/inner media divided by the average concentration of the appropriate radioactivity in plasma and by the length of the exposure time. The intimal clearance of labeled Lp(a) and LDL in the aortic arch after 60 minutes of exposure was 87 +/- 9 and 47 +/- 7 nL.cm-2.h-1 (n = 9) in normal rabbits and 82 +/- 14 and 62 +/- 10 nL.cm-2.h-1 (n = 10) in cholesterol-fed rabbits; after 180 minutes of exposure, the intimal clearance of labeled Lp(a) and LDL was 62 +/- 14 and 84 +/- 21 nL.cm-2.h-1 (n = 6) and 30 +/- 6 and 47 +/- 12 nL.cm-2.h-1 (n = 4) in cholesterol-fed and Lp(a)-injected rabbits, respectively. Linear regression analysis showed positive associations between intimal clearance of the two lipoproteins in all four groups of rabbits in the aortic arch, the thoracic aorta, and the abdominal aorta. Aortic immunoreactivity of human apolipoprotein(a) was detected in the intima in association with fatty streak lesions, predominantly within the cytoplasm of foam cells. These results suggest that Lp(a) is transferred into the aortic intima by a mechanism similar to that for LDL and that Lp(a) can be taken up by intimal foam cells; however, Lp(a) and LDL may be metabolized differently upon entrance into the arterial wall.

Animals↗
PubMed1994

[The effect on health of dietary antioxidants and antioxidant supplements].

Reactive free oxygen radicals are formed in the reactions involved in normal cell metabolism. This formation is closely regulated e.g. by dietary antioxidants. Present knowledge suggests that an imbalance, with surplus of free radicals, can play a role in the pathogenesis of certain types of cancer, atherosclerosis, and cataract. A number of epidemiological studies have demonstrated a reduced risk of developing these diseases in persons who consume a diet with a high content of vegetables and fruit, which contains large quantities of the antioxidants: beta-carotene, vitamins C and E. Intervention studies, using supplements of these antioxidants, have so far not been able to show a beneficial effect. The apparently protective effect of fruit and vegetables may be due to other active ingredients. In Denmark the average intake of vegetables and fruit is low, and it is estimated that an increased consumption of these foods could reduce the occurrence of certain cancer types and atherosclerosis. In contrast, there is no evidence that antioxidant supplements would provide protection against disease, and their safety remains to be established.

Antioxidants↗
PubMed1994

[Significance of trans-fatty acids for health].

Trans fatty acids make up 0-30% of the fatty acids in Danish margarines. The intake of trans fatty acids from margarine in Denmark was in 1991 on average about 2.5 gram/person/day, and for about 150,000 Danes more than 5 gram/person/day. Several recent case-control studies and a large cohort study as well as clinical ward studies suggest that the intake of trans fatty acids enhances atherogenesis to the same extent or possibly even more than saturated fatty acids. In addition a few studies suggest that the intake of trans fatty acids by the pregnant mother impairs growth of the human foetus. On this background it seems reasonable to reduce the intake of trans fatty acids as much as possible. This could be implemented by a reduction in the fat content of the diet together with a reduction of trans fatty acid content to less than 5% in all margarines. This would ensure that Danes--including pregnant and nursing women--with a high intake of margarine on average consume less than 2 gram of trans fatty acids of vegetables origin per day. This amount corresponds to intake in low risk groups in several studies.

Denmark↗
PubMed1994

Aortic permeability to LDL during estrogen therapy. A study in normocholesterolemic rabbits.

17 beta-Estradiol has recently been found to inhibit atherogenesis by mechanisms that are in part independent of the estrogenic action on plasma lipoprotein levels. Since aortic permeability to low-density lipoprotein (LDL) in normocholesterolemic rabbits is a strong predictor for subsequent atherosclerosis during hypercholesterolemia, the present study investigated a possible influence of 17 beta-estradiol on aortic permeability to LDL. Twenty rabbits were initially ovariectomized and then fed a nonatherogenic diet for 10 weeks. One group of rabbits (n = 10) received 4 mg of 17 beta-estradiol orally per day; the other group (n = 10) received placebo. Serum concentrations of very-low-density lipoprotein cholesterol and triglycerides increased significantly more in the placebo group than in the estrogen group (P < .03), whereas there were no statistically significant differences between groups in LDL, high-density lipoprotein, or total cholesterol. At the end of the experiment, 125I-LDL was injected intravenously into each rabbit. Aortas were removed 3 hours later, and the aortic permeability to LDL was calculated from the radioactivity in the plasma and the aortic intima/inner media. The aortic permeability to LDL was virtually identical in the 17 beta-estradiol (31.6 +/- 7.2 nL.cm-2.h-1) and the placebo (36.9 +/- 7.9 nL.cm-2.h-1) groups (mean +/- SEM). The aortic cholesterol content was also similar in the two groups. These data suggest that the plasma lipid-independent antiatherogenic effect of estradiol is not mediated through an effect on aortic permeability to LDL but rather is related to the metabolism of the lipoproteins after they have entered the arterial wall.

Animals↗
PubMed1994

Cyclosporin suppresses transplant arteriosclerosis in the aorta-allografted, cholesterol-clamped rabbit. Suppression preceded by decrease in arterial lipoprotein permeability.

The immunosuppressant cyclosporin has been suggested to aggravate as well as retard the development of transplant arteriosclerosis, the major long-term problem for patients with heart transplants. We examined the effect of human therapeutic levels of blood cyclosporin on the development of experimental transplant arteriosclerosis. The thoracic aorta from one rabbit was transplanted as an end-to-side bypass on the abdominal aorta of another rabbit, and plasma cholesterol was clamped at 5 to 7 mmol/L. Cyclosporin markedly suppressed the severity of transplant arteriosclerosis, judged both biochemically and histologically: cholesterol content in aortic transplants was reduced by 70% and 80% after 10 days and 20 days of cholesterol feeding, respectively (both comparisons, P < .01), and after 20 days of cholesterol feeding myointimal proliferation was totally inhibited in grafts from cyclosporin-treated animals, judged from maximal intimal thickness and intimal area on cross sections of grafts (both comparisons, P < .05). In another group of non-cholesterol-fed, aorta-transplanted rabbits, cyclosporin reduced by 90% (P < .01) an otherwise markedly increased permeability to low-density lipoprotein in transplanted aortas. These results suggest that cyclosporin causes a substantial decrease in the severity of transplant arteriosclerosis and that this effect is mediated at least partly via a large decrease in aortic lipoprotein permeability.

Animals↗
PubMed1994

Effect of angiotensin II and enalapril on transfer of low-density lipoprotein into aortic intima in rabbits.

To assess the mechanism behind a possible atherosclerosis-promoting effect of angiotensin II, the influence of angiotensin II, noradrenaline, and enalapril on transfer of low-density lipoprotein (LDL) into the arterial wall was investigated in conscious rabbits. Intravascular infusion of angiotensin II (1.4 micrograms/kg per minute) initially increased the mean blood pressure from 70 to 80 mm Hg to 125 to 150 mm Hg; this effect was transient, and the blood pressure returned to baseline values within 2 hours, despite continuous infusion of angiotensin II. The normalized influx of LDL into the aortic intima, determined after in vivo exposure to 125I-LDL for 1 hour, was 88 +/- 17 (n = 6), 12 +/- 12 (n = 5), and 28 +/- 6 (n = 5) nL/cm2 per hour (mean +/- SEM) during angiotensin II infusion at high blood pressure, during angiotensin II infusion after the blood pressure had been normalized, and during continuous saline infusions, respectively (P < .05 for high blood pressure versus low blood pressure and saline). When noradrenaline was used to increase blood pressure to a level similar to that induced by angiotensin II, the normalized influx of LDL in noradrenaline-treated rabbits was also increased markedly. Production of endogenous angiotensin II was inhibited with enalapril (2.9 mg/kg per day). Compared with placebo rabbits, enalapril-treated rabbits had a 92% lower plasma angiotensin-converting enzyme activity and a 23% lower blood pressure. The normalized influx of LDL, however, was similar in the two groups at 18 +/- 2 (n = 10) and 20 +/- 3 (n = 10) nL/cm2 per hour, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1993

Effect of testosterone on atherogenesis in cholesterol-fed rabbits with similar plasma cholesterol levels.

The aim was to examine the effect of testosterone on atherogenesis in cholesterol-fed, castrated male rabbits not mediated via different plasma cholesterol levels. The rabbits in the testosterone group (n = 19) and in the placebo group (n = 17) were injected intramuscularly twice weekly for 17 weeks with 25 mg testosterone enantate and placebo, respectively, reaching plasma testosterone levels of 50-150 nmol/l in the testosterone group. No effect of testosterone on liver function or body weight was detected, but at week 15 mean blood pressure was 75 +/- 2 mmHg (mean +/- S.E.) in the testosterone group compared with 69 +/- 2 mmHg in the placebo group (P < 0.05). To reduce variation in plasma cholesterol between the two groups, the amount of cholesterol fed to each rabbit was adjusted on the basis of weekly determinations of plasma cholesterol; the mean plasma cholesterol levels during the 17 weeks were 20.9 +/- 1.0 and 20.4 +/- 0.9 mmol/l for the placebo and testosterone groups. In the intima-inner medias of the aortic arch, the thoracic and the abdominal aorta there were no consistent significant differences in aortic cholesterol content, expressed either as nmol/cm2 or nmol/mg protein, between the two groups. However, the aortic cholesterol content tended to be lower in the testosterone group than in the placebo group. These findings suggest that in cholesterol-fed, castrated male rabbits, testosterone does not promote atherogenesis by an effect directly on the arterial wall.

Animals↗
PubMed1993

Effect of lovastatin on cholesterol absorption in cholesterol-fed rabbits.

The aim of the present study was to investigate the effect of the hydroxymethylglutaryl (HMG)-CoA reductase inhibitor lovastatin on some aspects of cholesterol metabolism in cholesterol-fed rabbits. The plasma cholesterol concentration was markedly lower in lovastatin-treated rabbits (6 mg/rabbit/day) compared to controls after 36 days of cholesterol-feeding (x +/- S.E.) (19 +/- 4 mmol/l, n = 9 versus 153 +/- 17 mmol/l, n = 7) (P < 0.00001). Intestinal absorption of cholesterol in such rabbits was reduced by 15% in lovastatin-treated rabbits (n = 21) compared to controls (n = 18) (P < 0.025). The results suggest that the hypocholesterolaemic effect of lovastatin in cholesterol-fed rabbits is associated with a decreased intestinal absorption of cholesterol.

Animals↗
PubMed1993

Increased urinary loss of high density lipoproteins in albuminuric insulin-dependent diabetic patients.

The pathophysiological mechanisms resulting in hyperlipidaemia in albuminuric insulin-dependent diabetic patients are largely unknown. Increased non-specific hepatic protein synthesis as a response to urinary protein loss, has been proposed. However in that case it is unexplained why the plasma concentration of the high density lipoprotein (HDL) subfraction, in contrast to all other lipoprotein subfractions, is normal or even reduced in albuminuric patients. We studied the urinary excretion of HDL-cholesterol in 26 insulin-dependent diabetic patients matched according to sex and age into three groups. I: normal urinary albumin excretion (< 30 mg 24 h-1; n = 8); II: incipient nephropathy (urinary albumin excretion in the range of 30-300 mg 24 h-1; n = 7); and III: clinical nephropathy (urinary albumin excretion > 300 mg 24 h-1; n = 11). Eight normal subjects served as controls. Lipoproteins in urine were separated by ultracentrifugation, and the daily urinary loss of HDL-cholesterol was 1.30 mumol (0.83-2.21) (median and range) in controls, 1.27 mumol (0.56-2.59) in group I, 1.39 mumol (0.55-1.97) in group II and 4.02 mumol (1.33-42.12) in group III (p < 0.01). More than 95% of cholesterol in urine was found in the HDL-fraction. The plasma concentrations of total cholesterol, very low density lipoprotein cholesterol, low density lipoprotein cholesterol and triglyceride were 21-94% higher in patients with clinical nephropathy compared with normal controls and group I.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Cholesterol-lowering diets may increase the food costs for Danish children. A cross-sectional study of food costs for Danish children with and without familial hypercholesterolaemia.

Food costs for 30 children under dietary treatment for familial hypercholesterolaemia were compared with those of 105 other Danish children. The daily intake of macronutrients and the daily cost of the diet for each child were calculated from dietary intakes and average prices of 365 different food items. The mean +/- SE percentages of energy (E%) from fat in the diet of children with and without known familial hypercholesterolaemia were 23.6 +/- 0.8 E+ and 34.5 +/- 0.5 E%, respectively (P < 0.001). The dietary costs per MJ in these two groups were 3.79 +/- 0.12 Danish crowns (DKr) and 3.34 +/- 0.05 DKr (P < 0.001), taking into account food wastage due to preparation and cooking. The cost per unit of energy increased with decreasing fat energy percentage of the diet for all children as one group (r = -0.37, P < 0.001), as well as for the group of children without familial hypercholesterolaemia (r = -0.35, P < 0.001). Stepwise multiple regression analysis showed that the differences in cost per MJ between the groups could be explained primarily by differences in percentage of energy from fat. We conclude that a reduction of dietary fat from 35 E% to 25 E% may increase food costs by 10-20% for Danish children.

Adolescent↗