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We assessed the short and long-term efficacy and safety of the lipid lowering drugs, nicotinic acid, and the HMG-CoA reductase inhibitor, lovastatin, in combination with cholestyramine in four renal transplant patients. Combination therapy with cholestyramine failed to lower the TC and LDL to the levels recommended by the NCEP guidelines.
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A system has been developed for the determination of quinolinate phosphoribosyltransferase (QPRT) activity in liver and kidney homogenates using HPLC. A product, nicotinic acid mononucleotide (NaMN), is separated by reversed-phase chromatography (a Tosoh ODS 80TS was used as an analytical column) using a mixture of 10 mM KH2PO4-K2HPO4 buffer (pH 7.0) containing 1.48 g/l tetra-n-butylammonium bromide-acetonitrile (9:1, v/v) as a mobile phase. The flow-rate was 1.0 ml/min, the detection wavelength was 265 nm. The column temperature was maintained at 40 degrees C. Under these conditions, NaMN was eluted at about 8.1 min. Sample preparation was very straightforward. The reaction mixture of QPRT assay was stopped by immersing the tube into a boiling water bath, the resulting supernatant was filtered, and the filtrate was directly injected into a HPLC system. The total HPLC analysis time was approximately 20 min.
3-Pyridine-carboxaldehyde and 3-pyridine-aldoxime were effective and specific inhibitors of the uptake of both nicotinic acid (NA) and nicotinamide (ND) by Bordetella pertussis, although neither compound inhibited the growth of the bacteria in liquid medium or the oxidation of glutamate by washed suspensions. In contrast, the following pyridine derivatives did not inhibit uptake of NA or ND: iso-NA, iso-ND, isoniazid, 6-amino-NA and 6-amino-ND, 3-acetyl-pyridine, 3-pyridyl-acetic acid, N,N-diethyl-ND and 3-pyridine-sulphonic acid. 3- Pyridyl-carbinol was inhibitory, but less so than the first listed compounds.
The present work is divided into two parts: clinical observations and experimental investigations. The endogenic formation of nicotinic acid was decreased in all patients with ischaemic heart disease, and we have found an increased accumulation of kynurenine in blood serum after tryptophan loading in many cases - a clear indication of pyridoxal-5-phosphate (P-5-P) deficiency in the organism. The results of experimental investigations showed that L-kynurenine sulphate initiates cardiac dysrhythmias as well as dystrophic changes in cardiomyocytes. Both the clinical observations and experimental investigations point out a previously unknown pathogenetic mechanism for the ischaemic heart disease, and for bradyarrhythmia as well as myocardial cell failure, caused by P-5-P deficiency in the organism.
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Our objective was to examine very low density lipoprotein-triglyceride (VLDL-TG) kinetics after chronic and acute administration of nicotinic acid (NA). Incorporation of [1,2,3,4-(13)C(4)]palmitate and [2-(13)C(1)]glycerol into VLDL-TG was measured in five healthy, normolipidemic women. Each subject was studied twice; the 4-day hospital stays were separated by 1 mo, during which time doses of NA were increased to 2 g/day (500 mg, 4 times/day). During posttreatment study, 500 mg of NA were administered acutely at 0800. Under baseline postabsorptive conditions, incorporation curves from (13)C-labeled free fatty acid (FFA) and (13)C-labeled glycerol were superimposable, and VLDL-TG kinetics were in agreement (t(1/2) = 1.4 +/- 0.3 and 1.3 +/- 0.3 h, and production rates = 27.2 +/- 6.1 and 28.5 +/- 5.3 g/day, respectively). In the postabsorptive state after chronic NA therapy, VLDL-TG concentrations and production rates were lower despite a trend toward elevated plasma FFA concentrations and fluxes. After the acute dose of NA, plasma FFA concentrations and flux fell dramatically, and there was a virtual halt to VLDL-TG production, which continued throughout the 6-h period after NA, despite a marked rebound overshoot in serum FFA concentrations and flux after hour 2. Plasma homocysteine concentrations increased 68% (P < 0.001) in the NA phase, consistent with chronic increased transmethylation demand. We conclude that 1) NA acutely and chronically decreases VLDL-TG production rate in normal women; 2) the acute effect on VLDL-TG production is associated with an initial suppression of lipolysis but persists for several hours after the antilipolytic action of NA has abated and is observed in the basal postabsorptive state, when lipolytic rates are not reduced; and 3) the effect of NA on VLDL-TG production, therefore, cannot be completely explained by its antilipolytic actions.