Acipimox (5-methylpyrazine carboxylic acid 4-oxide) is a new inhibitor of lipolysis with long-lasting activity, whose plasma lipid lowering potential was demonstrated in early clinical trials. The hypolipidemic effect of acipimox was investigated in two double-blind cross-over trials versus placebo. The first trial, carried out in 12 type IV patients, showed a significant triglyceride lowering effect (-35%) following 4 weeks of drug administration at a 250 tid dose. The same regimen, maintained for 9 weeks in 18 type IIA patients, failed to induce a significant reduction of total cholesterolemia. However, in 10 subjects, in whom lipoprotein cholesterol fractionation was carried out, a significant reduction of low density and highly significant increase in high density lipoprotein cholesterol levels (respectively -11% and +20%) were observed.

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Distribution of 14C-labelled 2-[p-(1-oxo-2-isoindolinyl)phenyl]butyric acid, (indobufen or K 3920) in blood, platelets and platelet components.

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Clinical pharmacology studies with indobufen (K 3920): inhibitor of platelet aggregation.

When given to 12 subjects at single oral doses of 100 and 300 mg, indobufen caused clear-cut, dose-dependent, reversible inhibition of epinephrine- and collagen-induced platelet aggregation. Platelet factor 3 availability and platelet factor 4 release were not affected by the lower dose but were markedly reduced by the 300-mg dose. Bleeding time was slightly influenced by 100 mg, and 300 mg had a more pronounced effect. Indobufen 300 mg was also intravenously injected to five subjects. When washed platelets obtained before indobufen were resuspended in plasma obtained after indobufen, aggregation was inhibited. This was not the case when washed platelets obtained after indobufen were resuspended in plasma obtained before indobufen. These experiments indicate tha indobufen causes reversible inhibition of platelet functions unlike the effect of acetylsalicylic acid.

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Physiological effects of intravenous fructose 1.6-diphosphate on diaphragmatic function in malnourished patients with COPD.

BACKGROUND: A low body mass index is one of the strongest predictors of mortality in Chronic Obstructive Pulmonary Disease (COPD) patients. Under-nutrition is often associated with skeletal muscle wasting and hypophosphatemia. AIM AND METHODS: In a pilot, randomised, double-blind placebo-controlled study, we assessed the physiological effects of phosphorous administration in 17 stable undernourished COPD patients, on diaphragmatic function, breathing pattern, neuromuscular drive (P0.1) and dyspnea score. Fructose 1.6-diphosphate (FDP) or placebo was administered i.v. for 7 consecutive days. RESULTS: FDP administration was associated with a marked increase in inspiratory time (Ti) that induced a significant rise (p < 0.05) in the Pressure Time Product of the diaphragm per breath (PTPdi/b). However, since breathing frequency also decreased, the Pressure Time Product per minute of the diaphragm (PTPdi/min), index of diaphragmatic energy expenditure was markedly reduced. The efficiency of the respiratory pump in clearing CO2 was also improved, although not significantly, in the FDP group (p = 0.09) as well as the maximal transdiaphragmatic pressure during the sniff manoeuvre (Pdi,sniff). CONCLUSIONS: This pilot physiological study showed that phosphorus replacement in undernourished, stable COPD patients, may be associated with a complex modification in respiratory pattern and diaphragmatic functions, leading to a marked although not significant reduction in PTPdi/min.

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