Biomedical subjects

M Aviram

Publications and source records attributed to M Aviram.

At least 217 records · Page 12Linked to original sources

PubMed1986

Plasma lipoproteins and platelet aggregation during alimentary lipemia. Decreased atherogenic pattern in the elderly.

Ten healthy women in their tenth decade of life were compared with ten healthy women in their fourth decade of life regarding the response of plasma lipoproteins and platelet aggregation to one meal rich in saturated fats. In the elderly group, plasma cholesterol decreased in the postprandial state three hours after the meal in comparison to no significant changes in the younger group. This resulted from reduction in plasma lipoprotein cholesterol levels, except for the high-density lipoprotein (HDL) cholesterol, which was enhanced. A similar pattern was found for plasma lipoprotein levels. The increase in plasma triglyceride concentration in the elderly women was less than in the younger women, as fewer changes in their plasma triglyceride-rich lipoproteins (chylomicrons and very-low-density lipoprotein) were observed. Platelet aggregation in response to collagen was reduced in the elderly women, whereas in the younger group, increased platelet aggregation in the postprandial state was found. Our study thus demonstrates a clear advantage of the elderly women in comparison to the younger ones in reducing atherosclerosis and thrombotic risks. The elderly group responded to the saturated fat-rich meal by minimal plasma triglyceride elevation, an increase in HDL cholesterol concentration, and reduced platelet aggregation.

Adult↗

PubMed1986

Acute effects of dietary cod liver oil and cream on plasma lipoproteins.

Plasma lipoprotein concentration and composition of 6 healthy subjects were studied before and 3 h after a fatty meal (900 kcal) consisting of either cream (mainly saturated fatty acids) or cod liver oil (CLO; rich in n-3 polyunsaturated fatty acids). The plasma triglyceride concentration was increased after both meals. This was caused by an increase in both chylomicron and very-low-density lipoprotein (VLDL) triglycerides. Plasma total cholesterol was unchanged. The cholesterol content was also increased in low-density lipoproteins and in VLDL after cream intake, but was reduced in high-density lipoproteins (HDL), whereas no changes were observed in these fractions after CLO. The fatty acid composition of the diet was reflected in the plasma and in the chylomicron fraction. Both fatty meals reduced the relative concentration of plasma linoleic acid. Fatty acid composition in HDL suggested dietary fatty acid transfer from the chylomicrons and VLDL to the HDL after CLO, but not after the cream diet. The results suggest that in the postprandial state the fatty acid transfer between the triglyceride-rich lipoproteins and HDL depends on the quality of the fatty acids and that the n-3 polyunsaturated fatty acid may increase such transfer.

Animals↗

PubMed1986

Increased platelet aggregation during alimentary hyperlipemia in normal and hypertriglyceridemic subjects.

The influence of 2 different fatty meals, rich in either saturated or polyunsaturated fatty acids, on platelet aggregation in 7 normolipemic subjects and in 10 patients with phenotype IV hyperlipemia, was studied. 3 h after ingestion of a saturated- or polyunsaturated-fat-rich meal, plasma triglycerides were similarly increased in both groups. 5 h after ingestion of fat of either origin, the plasma triglyceride level in normal subjects returned almost to the fasting level, whereas in patients with hypertriglyceridemia it was still elevated. Platelet aggregation induced by ADP in platelet-rich plasma significantly increased in the normal group 3 h after both meals, whereas in the patient group it increased only after the saturated-fat-rich meal. These results were not changed 5 h after the meals. Postprandial elevated platelet activity was not correlated with increased plasma triglyceride concentration. No changes were found in washed-platelet aggregation in normal subjects, whereas the patient-derived washed platelets showed increased aggregation after the saturated-fat-rich meal. Plasma chylomicrons prepared from both groups during alimentary hyperlipemia inhibited ADP-induced platelet aggregation as well as thrombin-induced platelet 14C-serotonin release. This study indicates that the intake of fatty meals induces acute disturbance in platelet aggregation, favoring thrombosis. These changes are more comprehensive in hyperlipemic patients and after a saturated-fat-rich meal.

Adult↗

PubMed1986

Enhanced in vitro platelet aggregation in hemodialysis patients.

Hemodialysis patients suffer from premature atherosclerosis and various thrombotic and thromboembolic phenomena. Despite enhanced in vivo platelet activity, it is unclear whether in vitro platelet aggregation is increased or reduced in this population. We studied platelet aggregation in response to adenosine diphosphate and to epinephrine in 20 chronic hemodialysis patients and 21 controls. In the patient group the in vitro platelet aggregation was significantly enhanced in response to both aggregating agents. Our study demonstrated that in vitro platelet aggregation is enhanced in patients with chronic renal failure undergoing hemodialysis.

Adenosine Diphosphate↗

PubMed1986

Postprandial plasma lipoproteins in normal and hypertriglyceridaemic subjects and their in vitro effect on platelet activity: differences between saturated and polyunsaturated fats.

The postprandial plasma lipoprotein pattern was studied in 10 normal and 10 hypertriglyceridaemic subjects after consumption of either a saturated or a polyunsaturated fat-rich meal. Plasma triglycerides increased in both groups 3 h after the meal, and this was followed after 5 h by a dramatic reduction in the normal subjects only; the reduction was less after the saturated fat meal than after the polyunsaturated fat meal. This plasma triglyceride pattern was a consequence of changes in the chylomicron and very-low-density lipoprotein (VLDL) fractions. No significant changes were found in high-density lipoprotein (HDL)- and low-density lipoprotein (LDL)-cholesterol, triglycerides or protein concentration. Plasma cholesterol and apolipoproteins (apo) A-I and B were not significantly altered. The VLDL-apo C-III/apo C-II ratio increased 3 h after the saturated fat-rich meal, but decreased after the polyunsaturated fat-rich meal in normals, but not in the patient group. The effect of these postprandial lipoproteins on platelet function was studied by incubating normal washed platelets with the lipoprotein and then determining aggregation and [14C]serotonin release. All chylomicron fractions decreased platelet activity, whereas postprandial VLDL increased platelet activity. Five hours after the meals, the effect of VLDL on platelet activation was reduced in normal subjects only. The effect of postprandial LDL and HDL on platelet function differed little from that of the fasting lipoproteins.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1985

Chylomicron-like particles in severe hypertriglyceridemia.

Plasma lipoproteins in a diabetic patient with severe hypertriglyceridemia and turbid, milky plasma were studied and compared with those found in three primary type V hyperlipoproteinemic and in three normal subjects after a fatty meal. All subjects had normal post-heparin lipolytic activity. Lipoprotein electrophoresis of the patient's plasma revealed no chylomicron band, and upon short-time ultracentrifugation the patient's supernatant showed most lipid staining in the pre-beta-lipoprotein region. This supernatant, which in type V hyperlipoproteinemia as well as in normal subjects after a fatty meal, contains a large proportion of apolipoprotein B-48 (of intestinal origin), was found in our patient to contain mostly apolipoprotein B-100 (of liver origin). Upon incubation of normal washed platelets with chylomicrons derived either from type V hyperlipoproteinemic or from normal subjects after a fatty meal, platelet aggregation was decreased, whereas the chylomicron-like particles from the patient increased platelet activity. It is, thus, suggested that the triglyceride-rich, cholesterol-poor lipoproteins are of liver and not of intestinal origin.

Adult↗

PubMed1985

Plasma lipoproteins affect platelet malondialdehyde and thromboxane B2 production.

Platelet interaction with plasma lipoproteins was studied using gel-filtered platelets free of plasma constituents and purified lipoproteins. On incubation of gel-filtered platelets with plasma lipoproteins at 30 degrees C for 30 min, 100 micrograms of protein/ml of very-low as well as low-density lipoprotein caused 10% increment in platelet aggregation and [14C]serotonin release in parallel to elevation of around 15% of malondialdehyde and thromboxane B2 production. High-density lipoprotein showed the opposite effect and reduced platelet aggregation as well as thromboxane B2 synthesis by 17 and 32%, respectively. Lipoprotein-deficient plasma enhanced platelet function. Preincubation of the platelet suspension with prostacyclin did not prevent the effect of the lipoproteins on the in vitro platelet response as well as on the platelet prostaglandin pathway. Our results suggest that the formation of thromboxane B2 and malondialdehyde is influenced by plasma lipoproteins and that these, in turn, affect platelet aggregation and the release reaction. The possible significance of these results to platelet function in hyperlipidemic patients is discussed.

Blood Platelets↗

PubMed1985

Chylomicrons from patients with type V hyperlipoproteinemia inhibit platelet function.

Platelet aggregation and [14C]serotonin release induced by collagen and also by ADP and thrombin were significantly decreased in patients with primary Type V hyperlipoproteinemia. Platelets derived from these patients lost their hyporesponsiveness to thrombin and ADP (but not to collagen) after washings and isolation from their plasma environment. On incubation of platelets derived from normolipidemic controls with plasma derived from patients, platelet aggregation and [14C]serotonin release were lowered by 20% and 30%, respectively. On incubation of these platelets with 100 mg/dl of chylomicron triglyceride, a 40% reduction in both platelet aggregation and [14C]serotonin release was observed. The inhibition of platelet activity was positively correlated with chylomicron concentration up to a concentration of 225 mg/dl by chylomicron triglyceride. In 2 patients, bezafibrate administration (600 mg/day) resulted in marked reduction of plasma triglyceride concentration and a parallel improvement in platelet function. The platelet hyporesponsiveness in patients with Type V hyperlipoproteinemia appears to be a consequence of platelet-chylomicron interaction. This depressed platelet function may be responsible for the absence of overt atherosclerosis noted in these patients.

Adenosine Diphosphate↗

PubMed1985

Platelet function in a case with abetalipoproteinemia.

Platelet aggregation, [14C]serotonin release and platelet malondialdehyde production were determined in a patient with abetalipoproteinemia (ABL) and found to be normal. The patient demonstrated complete absence of apolipoprotein (apo) B and decreased apo A-I concentration in plasma. The high density lipoprotein (HDL) composition of plasma was abnormal, with an increased cholesterol/protein ratio, increased apo E levels and reduced apo C concentration. The patient's platelets, like platelets derived from a normolipidemic control, possessed receptors capable of binding lipoproteins. On incubating washed platelets derived from a control subject with HDL obtained from the ABL patient, an enhancement in platelet function was observed. A similar concentration of HDL derived from the control had the opposite effect, a depression of platelet function. Lipoprotein-deficient plasma (LPDP) derived from the patient, on the other hand, decreased platelet aggregation and [14C]serotonin release in comparison to the LPDP obtained from the control. The normal platelet function observed in the patient appears to be the result of the platelet-enhancing effect of an abnormal HDL, thus compensating for the absence of low and very low density lipoproteins from the patient's plasma which, when present, stimulate platelet function.

Abetalipoproteinemia↗

PubMed1985

Hypocholesterolaemia and abnormal high-density lipoprotein in rheumatoid arthritis.

Plasma lipid and lipoprotein patterns were determined in 54 female patients with rheumatoid arthritis (RA). The patients were divided into four groups, on the basis of the treatment that was being administered (gold, penicillamine, hydroxychloroquine and nonsteroidal anti-inflammatory drugs). Plasma cholesterol levels were significantly reduced in all groups. The reduced plasma cholesterol level was a result of 26% and 36% reductions in low- and high-density lipoproteins (LDL and HDL), respectively. Very-low-density lipoprotein cholesterol was reduced only in the group receiving hydroxychloroquine, and this was associated with decreased plasma triglycerides in this group. Plasma apolipoprotein (apo) B, the LDL protein moiety, demonstrated a pattern similar to that shown for LDL cholesterol. Plasma apo A-I, the major HDL protein, was, however, in the normal range, suggesting an abnormal HDL fraction. Even though reduced HDL cholesterol was found in RA patients, the HDL/LDL ratio was normal and the apo A-I/apo B ratio was increased, suggesting that these patients are not at increased risk for atherosclerosis.

Anti-Inflammatory Agents↗

PubMed1985

Differential effect of platelet inhibitors in normal and in hypercholesterolaemic subjects.

Dibutyryl cyclic AMP, forskolin, dipyridamole and butyl imidazole inhibited platelet aggregation (induced by ADP or collagen) in washed platelets more than in platelet-rich plasma preparations. Aspirin, indomethacin and epoprostenol (prostacyclin, PGI2) showed no preferential inhibition of these platelet preparations. When platelet-rich plasma from either normal or familial hypercholesterolaemic (FH) subjects was used, aspirin, indomethacin and dipyridamole (but not forskolin) inhibited platelet aggregation in normal subjects more than in FH patients. When low doses of aspirin (75 mg daily for 7 days) or dipyridamole (250 mg, single dose) were administered in vivo, platelet aggregation was inhibited more in the normal subjects in comparison to the patient group.

Adult↗

PubMed1985

Serum immunoglobulin-lipid complexes in plasma cell dyscrasia.

Immunoglobulin-lipid complexes (SILC) are found in the serum of all patients with monoclonal gammopathy. Fractionation by density gradient ultracentrifugation, Sephadex G-200 chromatography and Sepharose protein A affinity, followed by extensive immunoassaying for immunoglobulins and lipoproteins, does not confirm the accepted assumption that SILC are immune complexes between monoclonal immunoglobulins and lipoproteins. Lipid extraction of monoclonal fractions isolated on protein A columns followed by thin-layer chromatography shows a lipid pattern characteristic of the one found in cellular membranes. It is proposed that SILC are hydrophobic complexes between immunoglobulins and lipids, as described in membranes of B lymphocytes.

Chromatography, Gel↗

PubMed1985

Chylomicronaemia in multiple myeloma.

A patient with multiple myeloma presented with an accumulation of chylomicron-like particles. This rare finding resembled that of the type V hyperlipoproteinaemia phenotype. The lipid and lipoprotein concentration and composition were compared with values obtained from other patients with multiple myeloma, patients with the type V hyperlipoproteinaemia phenotype (accumulation of chylomicrons and very low density lipoproteins), and normal subjects. An immunoglobulin-lipid complex was demonstrated in our patient. This complex was found not to be associated with the chylomicrons and was detected only in the lipoprotein-deficient plasma. Lipid and lipoprotein concentration and composition differed from the other groups. Very low density lipoprotein concentration was reduced, and there was thus a marked difference from the type V phenotype. The chylomicrons derived from this patient were also richer in apolipoprotein C compared to chylomicrons derived from the patients with type V hypolipoproteinaemia. It appears that the abnormal composition of the triglyceride-rich lipoproteins observed in this patient renders her refractory to the normal pathways of metabolism.

Cholesterol↗

PubMed1985

Increased plasma triglycerides, cholesterol and apolipoprotein E during prolonged fasting in normal subjects.

Plasma lipid and high density lipoprotein (HDL) levels were studied in 20 normal, healthy, non-obese males while fasting (150 kcal/d with free intake of water) for 6 d in a hunger strike. Plasma triglyceride and cholesterol levels were increased by 18% after 6 d of fasting. HDL-cholesterol concentration was not significantly changed for 4 d, but decreased by 22% after 6 d. Platelet aggregation induced by adenosine diphosphate (ADP) or collagen after 6 d of fasting was in the normal range. In 3 subjects fasted for 9 d, a complete plasma lipoprotein analysis was done. Very low and low density lipoprotein (VLDL and LDL) levels were elevated, whereas HDL was reduced after 9 d of fasting. On isoelectric focusing analysis, a marked reduction in apolipoprotein (apo) E concentration in both VLDL and HDL was noted. Liver function tests showed a reduction in hepatic enzyme activity; and since apo E is of hepatic origin also, we suggest that long fasting inhibits liver function in normal subjects.

Adult↗

PubMed1985

Platelet adhesion in hyperlipidemic and hypertensive patients.

Platelet adhesion was studied in whole blood using a simple stagnation flow method in patients at high risk for the development of atherosclerosis. Fourteen patients with hypercholesterolemia, 26 with hypertriglyceridemia and 25 normolipidemic hypertensive subjects were compared with 75 normal (normotensive and normolipidemic) subjects. Increased platelet adhesion was found in hypercholesterolemic (but not hypertriglyceridemic) patients only when native blood with no anticoagulants was used. In hypertensive patients, platelet adhesion was significantly elevated, but remarkably reduced by beta-blocker drugs. Propranolol and atenolol significantly reduced platelet adhesion, but this effect was found to take a longer time than that required for significant blood pressure reduction.

Adult↗

PubMed1985

Increased platelet aggregation following splenectomy in patients with myeloproliferative disease.

In 30 patients with myeloproliferative disorders, decreased platelet aggregation in response to both ADP and collagen was demonstrated. The hypoaggregability was more drastic in patients with large spleens. Patients who had had splenectomy in the past showed normal platelet aggregation. In order to understand the role of the spleen in platelet function, platelet aggregation was studied in three patients with myeloproliferative disorders during the week following splenectomy and was compared to platelet aggregation in three control patients undergoing orthopedic operations. After splenectomy, platelet aggregation significantly increased, reaching a maximum after 3 to 4 days, but returned to presplenectomy values after 1 week. This is in contrast to the control patients, in whom no significant changes in platelet aggregation were observed. Our results suggest that the spleen retains or catabolizes the most hemostatically effective platelets.

Adult↗

PubMed1985

Plasma lipoprotein pattern and decreased platelet function in type V hyperlipoproteinemia.

Plasma lipid and lipoprotein pattern as well as platelet aggregation and [14C]serotonin release were studied in five male patients with primary Type V hyperlipoproteinemia and in age-matched healthy control subjects. Plasma very-low-density lipoprotein (VLDL) cholesterol, triglycerides (TG) and protein were significantly elevated in the patients, and this resulted in 54% and 32% increments in cholesterol:protein and TG:protein ratios, respectively. In both low-and high-density lipoproteins (LDL and HDL), the cholesterol:protein ratio was normal, but the TG:protein ratio increased threefold. In the patient VLDL, apolipoprotein (apo) E and the sialyzed apo C-III (C-III2) were elevated, but apo C-III0 was decreased; whereas in the patient HDL, sialyzed apo C-IIIs were lower than in the normal HDL. Platelet function was found to be decreased in our patients in comparison with the normal group. Upon incubation of plasma lipoproteins derived from both groups with normal washed platelets, all patient plasma lipoproteins caused decreased platelet function in comparison with the normal lipoproteins. This study indicates plasma lipoprotein abnormalities in Type V hyperlipoproteinemia and may suggest that depressed platelet aggregation and release in these patients are a result of this normal lipoprotein pattern.

Adult↗

PubMed1984

Native and modified low-density-lipoprotein interaction with human platelets in normal and homozygous familial-hypercholesterolaemic subjects.

The binding of low-density lipoproteins (LDL) as well as LDL modified by cyclohexanedione (CHD-LDL) to gel-filtered platelets (GFP) and its effect on platelet function were studied in normal and in homozygous familial hypercholesterolaemic (HFH) subjects. Only normal-derived LDL could significantly compete with normal 125I-labelled LDL for binding to normal platelets. When GFP from normal subjects were incubated with normal LDL at concentrations of 25-200 micrograms of protein/ml, platelet aggregation in the presence of thrombin (0.5 i.u./ml) was increased by 65-186%. CHD-LDL, at similar concentrations, caused the opposite effect and decreased platelet aggregation by 26-47%. Both LDL and CHD-LDL (100 micrograms/ml) from HFH patients, when incubated with normal GFP, caused a significant reduction in platelet aggregation (33 and 50% respectively). When HFH-derived platelets were used, both patient LDL and CHD-LDL (but not the normal lipoprotein) could markedly compete with the patient 125I-labelled LDL for binding to the platelets. LDL and CHD-LDL (100 micrograms/ml) from normal subjects decreased aggregation of HFH-platelets by 52 and 85% respectively, while corresponding concentrations of LDL derived from HFH subjects (HFH-LDL) and CHD-LDL derived from HFH subjects (CHD-HFH-LDL) increased platelet aggregation by 165 and 65% respectively. The present results support the following conclusions: platelet activation by LDL in normal subjects is through the arginine-rich apoprotein-binding site; more than one binding site for LDL exists on platelets; under certain circumstances, LDL binding can cause a reduction in platelet activity; specificity for LDL binding to the platelets resides in different regions of the lipoprotein in HFH and in normal subjects. We have thus suggested a model for LDL-platelet interaction in normal and in HFH subjects.

Adult↗