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Biomedical subjects

L A Carlson

Publications and source records attributed to L A Carlson.

At least 127 records · Page 7Linked to original sources
PubMed1979

Dissociation of the effects of nicotinic acid on vasodilatation and lipolysis by a prostaglandin synthesis inhibitor, indomethacin, in man.

The effects of nicotinic acid on plasma free fatty acid (FFA) concentration and forearm blood flow were studied in seven healthy fasting volunteers with and without pretreatment by indomethacin to see if some effects of nicotinic acid are mediated by release of endogenous prostaglandin. 1 g of nicotinic acid per os decreased plasma FFA concentration to a lowest value of 1/4 of initial level and increased forearm blood flow four times. When the same dose of nicotinic acid was given after pretreatment with indomethacin, the blood flow increase was only 1/3 of that without indomethacin. Indomethacin did not alter the rapid initial decrease in plasma FFA, although the period of low FFA concentration was shortened and the rebound to supranormal concentration was abolished. Thus the vasodilatory effect of nicotinic acid seems to be mediated by release of endogenous prostaglandin while the inhibition of lipolysis by the drug is mainly produced by other mechanisms.

Adult↗
PubMed1979

Change in myocardial metabolism in man by a new stimulator of carbohydrate oxidation.

The effect on human myocardial metabolism of (S)-4-hydroxyphenylglycine, a substance which in animal experiments has been shown to stimulate carbohydrate metabolism mainly by activation of pyruvate dehydrogenase was studied in five healthy volunteers by coronary sinus catheterization. 90 min after i.v. injection of the drug myocardial extraction of glucose and lactate was doubled, myocardial oxidation of plasma free fatty acids (FFA) significantly reduced and myocardial RQ increased accordingly. This a pronounce shift towards carbohydrate oxidation was achieved with a dose which gave no side effects.

Adult↗
PubMed1979

Risk factors for myocardial infarction in the Stockholm prospective study. A 14-year follow-up focussing on the role of plasma triglycerides and cholesterol.

A 14-year follow-up of the Stockholm prospective study is reported. A number of 130 new myocardial infarctions (MI) were found in a prospective group of men (n = 3189) and another 46, i.e. a total of 176 MI, in the total group (n = 3486). Different types of multivariate statistical analyses show that age, blood pressure, smoking, fasting plasma concentrations of cholesterol and triglycerides, ESR and Hb were independent risk factors for MI, while the weight/height index was not. Elevated BP became an important risk factor only after the age of 50. When only age, BP, smoking and the two plasma lipids were entered into the logistic multivariate analysis, plasma triglycerides were more important as a risk factor than cholesterol. Quintile analysis showed that the rate of new MIs increased more with increasing triglyceride than increasing cholesterol levels. In the prospective group, the average rate of new MIs for men below 60 years was 32 per 1000. In the bottom and top quintile these rates were 16 and 65 for plasma triglycerides and 27 and 47 for cholesterol. When the men were divided into 4 groups with regard to both plasma lipids, the rate of new MIs increased successively from group to group along this chain: both lipids normal, only cholesterol high, only triglycerides high and both plasma lipids high.

Adult↗
PubMed1978

Concentration and composition of human serum lipoproteins at birth.

By ultracentrifugation of sera from 69 cord bloods very low (VLDL), low (LDL) and high density lipoproteins (HDL) were obtained and analysed for triglycerides (TG) and cholesterol (CHOL). Electrophoresis in agarose gel was performed on serum, VLDL and LDL + HDL. VLDL lipids were present in all newborns. VLDL contained 30 and 5% of serum TG and CHOL. The range of TG in VLDL was wide (0.02-0.62 mmol/l), but there was a constant ratio between TG and CHOL. The electrophoretic mobility of VLDL was slower than in adults. LDL contained 50% of both serum TG and CHOL, and HDL contained 15 and 50% of these serum lipids. A published formula for calculating CHOL in VLDL and LDL from serum CHOL and TG and CHOL in HDL gave values for CHOL in LDL which corresponded well with the determined values. For VLDL, however, the calculated values were too high.

Cholesterol↗
PubMed1978

Relative increase in apolipoprotein CII content of VLDL and chylomicrons in a case with massive type V hyperlipoproteinaemia by nicotinic acid treatment.

VLDL of fasting serum was fractionated into 4 fractions of decreasing particle size by preparative ultracentrifugation in a density gradient from a patient with massive type V hyperlipoproteinaemia before and after treatment with 12 g daily of nicotinic acid. Serum triglycerides fell from 58 to 9 mmol/1 in response to treatment due particularly to reduction of larger VLDL particles. Total, insoluble (apoprotein B) and soluble protein of all VLDL fractions also fell but the ratio of these 3 protein fractions to triglyceride rose particularly in the smaller VLDL fractions. The relative amount of apolipoprotein CII increased in all fractions and the ratio apo CII to triglycerides increased by 60--90% in all VLDL fractions. The relative amounts of apo CI, apo CII-2 and apo E appeared also to increase. The results are consistent with the hypothesis that low amounts of apo CII may play a role for the development of hypertriglyceridaemia.

Apolipoproteins↗
PubMed1978

Acute effect of dietary therapy of type IV hyperlipoproteinaemia on the serum and lipoprotein concentrations and relative composition.

In a detailed study the acute effect of diet and hospital admission on the plasma and lipoprotein lipid concentrations and composition was studied in 28 patients with type IV hyperlipoproteinaemia. Within 6 days there were significant falls in the mean serum cholesterol and triglycerides, very low density lipoprotein (VLDL) cholesterol and triglycerides and in high density lipoprotein triglycerides. These changes were accompanied by a significant rise in the mean low density lipoprotein (LDL) cholesterol concentrations. Using multiple regession models highly significant predictions of the change in VLDL triglyceride (R2 = 0.71) and LDL cholesterol (R2 = 0.47) were obtained utilising the pre-treatment lipoprotein levels as independant variables. Since elevated LDL cholesterol concentations are associated with atherosclerotic disease such models may have important therapeutic applications.

Cholesterol↗
PubMed1978

Conversion of the electrophoretic pattern of type IV hyperlipidaemia to type III by intravenous heparin.

Heparin was given i.v. to subjects with type IV hyperlipoproteinaemia who had only ordinary pre-beta lipoproteins and no late pre-beta lipoproteins (LP-beta) in their very low density lipoproteins (VLDL, d less than 1.006) upon agarose gel lipoprotein electrophoresis. Within 15 min the electrophoretic pattern of VLDL had changed completely. The normal pre-beta lipoproteins had disappeared and a discrete LP-beta lipoprotein had appeared. This new electrophoretic pattern, induced 15 min after heparin, is similar to that diagnostic of type III hyperlipoproteinaemia. It is suggested that the LP-beta lipoproteins represent an end stage in the catabolism of VLDL.

Cholesterol↗
PubMed1978

The relation between carbohydrate extraction by the forearm and arterial free fatty acid concentration in man. I. Forearm work with nicotinic acid infusion.

To see if the magnitude of carbohydrate extraction by working skeletal muscle in man is inversely correlated with the arterial free fatty acid (FFA) concentration as in the heart, eighteen healthy men were studied during dynamic forearm work with and without nicotinic acid. The extraction or release of glucose, lactate and pyruvate was determined by the simultaneous sampling of blood from the brachial artery (a) and a deep vein (dv) of the active forearm. Nicotinic acid decreased the arterial FFA concentration from 498 +/- 53 to 134 +/- 12 mumol per litre plasma and this caused a decrease in calculated extraction of FFA. However, it did not affect the extraction of glucose, which was of a magnitude similar to one third of the oxidative metabolism in both situations. One of the possible reasons of this difference compared to the human heart muscle is that the exercising skeletal muscle may utilize stored substrate to a greater extent, which makes possible shifts in substrate utilized for oxidation without changes in substrate extraction. Another reason may be that FFA utilization covers a far smaller proportion of oxidative metabolism in skeletal than in heart muscle already before nicotinic acid.

Adult↗
PubMed1977

Heparin-induced release of lipase activity in the human forearm: an immunological study.

Low doses of heparin were injected into the brachial artery of three volunteers. The lipase activities in the deep vein of the same forearm, draining mainly muscle tissue, and in the artery were monitored over a 10-min period. Lipase activity, rapidly released by heparin in the deep vein, was immunologically similar to lipoprotein lipase (E.C. 3.1.1.3), i.e. (1) it did not react with antiserum against human post-heparin plasma hepatic lipase and (2) it was inhibited by an antiserum against bovine milk lipoprotein lipase, which cross reacts with human post-heparin plasma lipoprotein lipase. The evidence that human muscle contains lipoprotein lipase is discussed.

Adult↗