In a controlled study comprising 176 patients, quinidine in the form of Kinidin Durules was found to reduced significantly the recurrence of the atrial fibrillation during a 1-year follow-up period after successful electric shock conversion. After one year, 51 per cent (52/101) of the patients in the quinidine group, and 28 per cent (21/75) in the control group remained in sinus rhythm (P smaller than 0.001). No less than 43 per cent of the patients converted to sinus rhythm during treatment with maintenance doses of quinidine sulphate before intended DC conversion. Gastrointestinal side-effects were not uncommon, and caused interruption of quinidine treatment in some cases.
Eleven patients with uncomplicated ischemic cardiovascular diseases and moderate hyperlipoproteinemia were studied for 6 hours after the administration of one gram of placebo and two days later one gram of nicotinic acid.
Plasma levels of free fatty acids were significantly depressed by nicotinic acid as compared to the control study during the first three hours after administration. Then, however, there was a pronounced rebound of FFA. The concentration of glycerol in plasma followed the same pattern as the free fatty acids.
The values for cholesterol in plasma remained unchanged during the six‐hour period in both the placebo and the nicotinic acid study. While the level of triglycerides as well was unchanged in the placebo study, the concentration of triglycerides decreased significantly 4 and 6 hours after the administration of nicotinic acid.
The concentration of blood glucose was not significantly different in the two groups during the study.
The concentration of free nicotinic acid in plasma reached a peak value 30 to 60 minutes after nicotinic acid was taken by mouth. At 5–6 hours the level had returned to pretreatment values. The values for the plasma levels of free nicotinic acid and free fatty acids indicated that a concentration of nicotinic acid above 1 μg/ml plasma is needed to maintain low free fatty acid levels.
The interrelation between free fatty acids, triglycerides and cholesterol in plasma is discussed. The results from these studies are compatible with the hypothesis that acute inhibition of FFA mobilization reduces the concentration of plasma triglycerides but not plasma cholesterol. They do not explain the mechanism behind the cholesterol‐lowering effect of nicotinic acid seen after chronic administration.
Bergström, S., L. A. Carlson, L. G. Ekelund and L. Orö. Cardiovascular and metabolic response to infusions of prostaglandin E1 and to simultaneous infusions of noradrenaline and prostaglandin E1 in man. Acta physiol. scand. 1965. 64. 332–339. – Prostaglandin E1 (PGE1) was infused at a rate of 0.1–0.2 μg/kg/min into 3 healthy, fasting male subjects for 20 min. No consistent changes in arterial pressures occurred. The heart rate increased about 20 beats/min. The concentration of free fatty acids (FFA) and of glycerol in plasma increased. A slight increase in oxygen consumption was observed. PGE1 infused simultaneously with noradrenaline to 2 healthy, fasting male subjects reduced the increase in arterial pressures seen when only noradrenaline was infused to these subjects. Furthermore, PGE1 completely inhibited the noradrenaline induced bradycardia. The increase in the concentration of FFA and glycerol in plasma caused by noradrenaline was only slightly reduced by PGE1. PGE1 had no effect on the calorigenic effect of noradrenaline.
A B STRACT 33 male volunteers were studied in the morning after fasting overnight. 11 (the control group) were allowed to sit comfortably for three consecutive 2-hr periods, no stressors or treatment being introduced. The remaining 22 were divided into two groups, each being exposed to standardized, emotional stressors during the second of the three 2-hr periods. The subjects in one of these groups were each given a total dose of 3 g of nicotinic acid during the first 3 hr of the experiment, whereas the other group received no treatment.Stress was accompanied and followed by increased levels of free fatty acids and triglycerides in arterial plasma, by an increase in catecholamine excretion, and a rise in heart rate and systolic and diastolic blood pressure. No such increases were seen in the control group.The stress-induced rise in free fatty acids was inhibited by nicotinic acid, and 'the triglyceride rise was turned into a fall. The stressor-induced increase in catecholamine excretion was not significantly affected by nicotinic acid, neither were the increases in heart rate and blood pressure. The hypothesis is discussed, from a qualitative as well as a quantitative viewpoint, that there is a direct relationship between the increased concentration of free fatty acids accompanying emotional
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