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At least 595 records · Page 33Linked to original sources
PubMed1985

Improvement of the nicotinic acid test in the diagnosis of Gilbert's syndrome by pretreatment with indomethacin.

The hyperbilirubinemia induced by nicotinic acid (NA) is well correlated to 14C-bilirubin clearance, and is utilized to diagnose Gilbert's syndrome (GS). However, NA produces a number of vascular prostaglandin-mediated side effects. In an attempt to improve the NA test we evaluated the influence of pretreatment with Indomethacin, a PG-synthetase inhibitor, both on side effects and hyperbilirubinemia. NA (5.9 mumoles/kg of body weight i.v.) was administered on two separate occasions, before and one hour after i.m. injection of 100 mg Indomethacin in 11 GS males and 11 controls matched for sex and age (age range 18.34 years). The hyperbilirubinemic effect of NA was not modified by Indomethacin in any subject; the side effects were either significantly reduced or completely abolished. We suggest that patients undergoing the NA test for the diagnosis of GS be pretreated with Indomethacin.

Adolescent↗
PubMed1981

Nicotinic acid test in the diagnosis of Gilbert's syndrome: correlation with bilirubin clearance.

A provocation test with nicotinic acid (50 mg intravenously) was performed in 13 patients with Gilbert's syndrome and seven healthy volunteers to investigate the diagnostic value of several test parameters and to correlate them with the bilirubin clearance. The maximal increment of unconjugated serum bilirubin, the retention at four hours, and the area under the bilirubin concentration time curve. (AUC) were measured. Significant differences between patients and controls were found with regard to the AUC (7.95 +/- SD, 3.29 mmol/min/l vs. 3.08 +/- 0.57; P less than 0.001), the increment of unconjugated bilirubin (24.1 +/- 7.1 mumol/l vs. 10.2 +/- 3.2; P less than 0.001) and the retention (77.7 +/- 8.9% vs. 45.8 +/- 27.4%; P less than 0.02). Of those, the AUC discriminated best between patients and controls. Five patients with Gilbert's syndrome had normal serum bilirubin concentrations (less than 17.1 mumol/l = 1 mg%) at the time of the study, but abnormal AUC and bilirubin increment. A significant correlation was found between the bilirubin clearance and the retention (r = -0.96; P less than 0.001) as well as the AUC (r = -0.82; P less than 0.05) but not with the bilirubin increment. This simple test may be used to assess the disturbance of bilirubin clearance in Gilbert's syndrome.

Adult↗
PubMed1980

Inhibition of lipolysis by nicotinic acid and by acipimox.

Acipimox (5-methylpyrazinecarboxylic acid 4-oxide) is a new lipolysis inhibitor that has a distant chemical relationship with nicotinic acid (NA). The tritiated compound (100 mg) is rapidly absorbed, peak plasma radioactivity being reached after 2 hr, with an almost total elimination unchanged in urine. A comparison of th antilipolytic activity of three doses of acipimox and three doses of NA showed acipimox to be 20 times as potent as NA. There was a correlation between intensity and duration of effect for acipimox, but not for NA. Plasma acipimox levels correlated with inhibition of lipolysis. In consideration of the very good subjective tolerability of acipimox at all doses tested, this drug may be suitable for control of lipolysis in hyperlipidemias.

Adult↗
PubMed2000

Calcium release from the endoplasmic reticulum of higher plants elicited by the NADP metabolite nicotinic acid adenine dinucleotide phosphate.

Higher plants share with animals a responsiveness to the Ca(2+) mobilizing agents inositol 1,4,5-trisphosphate (InsP(3)) and cyclic ADP-ribose (cADPR). In this study, by using a vesicular (45)Ca(2+) flux assay, we demonstrate that microsomal vesicles from red beet and cauliflower also respond to nicotinic acid adenine dinucleotide phosphate (NAADP), a Ca(2+)-releasing molecule recently described in marine invertebrates. NAADP potently mobilizes Ca(2+) with a K(1/2) = 96 nM from microsomes of nonvacuolar origin in red beet. Analysis of sucrose gradient-separated cauliflower microsomes revealed that the NAADP-sensitive Ca(2+) pool was derived from the endoplasmic reticulum. This exclusively nonvacuolar location of the NAADP-sensitive Ca(2+) pathway distinguishes it from the InsP(3)- and cADPR-gated pathways. Desensitization experiments revealed that homogenates derived from cauliflower tissue contained low levels of NAADP (125 pmol/mg) and were competent in NAADP synthesis when provided with the substrates NADP and nicotinic acid. NAADP-induced Ca(2+) release is insensitive to heparin and 8-NH(2)-cADPR, specific inhibitors of the InsP(3)- and cADPR-controlled mechanisms, respectively. However, NAADP-induced Ca(2+) release could be blocked by pretreatment with a subthreshold dose of NAADP, as previously observed in sea urchin eggs. Furthermore, the NAADP-gated Ca(2+) release pathway is independent of cytosolic free Ca(2+) and therefore incapable of operating Ca(2+)-induced Ca(2+) release. In contrast to the sea urchin system, the NAADP-gated Ca(2+) release pathway in plants is not blocked by L-type channel antagonists. The existence of multiple Ca(2+) mobilization pathways and Ca(2+) release sites might contribute to the generation of stimulus-specific Ca(2+) signals in plant cells.

Brassica↗
PubMed1984

[Therapeutic and prophylactic action of monensin and nicotinic acid in cows with subclinical ketosis].

Experiments were carried out with sheep and cows on the basis of a limited feed ration--the giving of concentrates was discontinued, and the ration of alfalfa hay was replaced with meadow hay and a monensine supplement (at the rate of 20-25 mg for sheep and 250 mg for cows, daily), and nicotinic acid (at 0.8 g and 6.0 g, respectively). Observations revealed that in the course of 6-7 weeks in succession the drop of blood sugar was reduced, and monensine led to a rise of the alkali reserves of the blood by 27 to 41 per cent. Cows with ketonuria (from ++ up to + positive results with the nitroprusside tests) and hydroglycaemia (blood sugar up to 30 mg) were treated with monensine at the rate of 125 mg, in the morning and in the evening or with nicotinic acid at 3 g and the same frequency for 6-7 consecutive days. The symptoms receded to a greater extent (12.1 to 60 per cent) as compared to the process of self-healing for the same time period. In this respect the effect of monensine was better manifested. It was demonstrated that the prophylactic use of these drugs inhibited to a minimum the manifestation of hypoglycaemia and ketonuria.

Acidosis↗
PubMed1994

Simultaneous measurement of nicotinic acid and its major metabolite, nicotinuric acid in urine using high-performance liquid chromatography: application of solid-liquid extraction.

The concentrations of nicotinic acid (NiAc) and nicotinuric acid (NiUAc), a major metabolite of NiAc, were simultaneously determined in urine using solid-phase extraction (cation-exchange extraction) and reversed-phase high-performance liquid chromatography with ultraviolet detection. The intra- and inter-day precision studies showed good reproducibilities: the coefficients of variations were less than 8.1% for NiAc and 8.8% for NiUAc. The calibration curves were linear (r2 > 0.9934) in the concentration range 10-1000 micrograms/ml. The removal of endogenous interferences in urine by solid-phase extraction presented here is superior to the pretreatment protocols reported previously by other workers. The method was used in a preliminary pharmacokinetic study in rats after intravenous administration of NiAc (5 and 15 mg/kg).

Animals↗
PubMed1981

Effect of nicotinic acid on microbial protein synthesis in vitro and on dairy cattle growth and milk production.

The effect of nicotinic acid (niacin) on microbial fermentation was tested in vitro. Microbial protein synthesis was greater with niacin and soybean meal than with niacin and urea. Otherwise, in most instances niacin decreased synthesis with urea. These responses to niacin with soybean meal occurred regardless of roughage type or ratio of roughage to concentration, except when the substrate contained 50% roughage from alfalfa; then the opposite was true. Adding niacin to urea-containing rations of heifers weighing 375 or 114 g failed to improve the heifers' weight gain or feed efficiency. In one of two lactation studies with cows in midlactation fed urea-containing rations, a slight increase in milk production was attributable to niacin; in the other, a slight improvement in milk protein production was attributable to niacin. In a third lactation study, but with fresh cows, milk production increased in cows receiving niacin and soybean meal but not in those receiving niacin and urea. In a fourth lactation study with fresh cows fed soybean meal, cows receiving niacin gave slightly more milk than did those receiving none. Response to niacin is greater in fresh cows than in those in midlactation and is greater in cows fed natural protein than in those fed urea.

Animal Feed↗
PubMed1989

[Determination of nicotinic acid in injections by high-performance liquid chromatography].

A high-performance liquid chromatographic method for determination of nicotinic acid (NA) in commercial injections was established. NA was determined by high-performance liquid chromatography on an Inertsil ODS column (4.6 x 150 mm) using a mixture of 0.05M monobasic sodium phosphate solution (pH 3) and methanol (80:20) containing 1.5 mM sodium 1-octanesulfonate as the mobile phase at 35 degrees C and the detection wavelength at 260 nm. The working curve for 0 to 120 micrograms nicotinic acid/ml against 100 micrograms caffeine/ml as internal standard passed through the origin and was linear. On comparing the analytical data obtained by this method and those by the colorimetric method, both data were in good agreement.

Chromatography, High Pressure Liquid↗
PubMedDate not supplied

[Removal of nicotinic acid 7-14C from the body of rats on a varying supply of vitamin PP].

Dynamic was studied for nicotinic acid (NA-7-14C) and its total metabolites excretion with area of animals under different physiological states (standard PP-avitaminosis). Various "efficiency" is shown for systems regulating homeostasis of this vitamin. When it is administered both in the amount close to the physiological dose (50 mg per 1 kg of weight) and exceeding the dose (500 mg per 1 kg of weight). The data obtained make it possible to draw a conclusion that the biological halflife period of Na-7-14C administered in excess of a physiological dose depends mainly on the rate of the unchanged vitamin PP excretion with urea and when it is administered in the physiological amount the period depends on the rate of the acid-metabolic transformations in the organism.

Animals↗
PubMedDate not supplied

[Effect of nicotinic acid and nicotinamide on the activity of NADPH- and NADH-dependent redox chains in rat liver endoplasmic reticulum].

Nicotinic acid and nicotinamide injected to rats subcutaneously in a dose of 100 mg/kg produce after 4 hours an inhibition in liver microsomes of N-demethylation of amidopyrine, NADPH.H-ferricytochromo-c-, NAD.H-ferricytochromo-b5-oxidoreductases and NAD.H-oxidase. After 12 hours they stimulate p-hydroxylation of aniline, NADP.H-ferricytochromo-c-oxidoreductase, NADP.H-oxidase, NAD.H-ferricyanide- and NAD.H-ferricytochromo-b5-oxidoreductases. The content of cytochrome P450 and activity of NADP.H-nitrotetrasolium-reductase were decreased by that time.

Aminopyrine↗
PubMed1992

Low-dose, time-release nicotinic acid: effects in selected patients with low concentrations of high-density lipoprotein cholesterol.

In a retrospective analysis, 63 participants in a cardiac rehabilitation-preventive cardiology program were identified as having low blood concentrations (mean, 34 mg/dl) of high-density lipoprotein cholesterol (HDL-C) and a mean total cholesterol level of 223 mg/dl after 3 months of hygienic measures (aerobic exercise, avoidance of tobacco, diet, and weight loss) designed to increase the HDL-C level. These patients (treatment group) were treated with low-dose, time-release nicotinic acid (mean, 1,297 mg/day) for a mean duration of 7.4 months. All subjects were able to take the drug without intolerable side effects. Fifty-four patients similar to those in the treatment group participated in the same program but were not treated with nicotinic acid (control group). Exercise, diet, body weight, and smoking remained stable throughout the period of observation. For the treatment group, HDL-C levels increased a mean of 18% (+6 mg/dl), total cholesterol concentrations decreased 9% (-20 mg/dl), the ratio of total cholesterol to HDL-C decreased 25% (from 6.8 to 5.1), low-density lipoprotein cholesterol levels decreased 13% (-20 mg/dl), and triglyceride levels decreased 20% (from 165 mg/dl to 132 mg/dl). Aspartate aminotransferase and uric acid concentrations were minimally increased after treatment, and the blood glucose level was unchanged. In the control group, HDL-C levels increased a mean of 8% (+3 mg/dl) and the other blood lipid variables were not improved after a mean of 8.3 additional months of diet and exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Cholesterol, HDL↗
PubMed1995

Exacerbation of acetaminophen hepatotoxicity by thalidomide and protection by nicotinic acid amide.

1. The effects of racemic thalidomide (D[+]/L[-] alpha-phthalimido-glutarimide) on acetaminophen (AAP)-induced hepatitis were tested in male NMRI mice (n = 133) and quantified as serum activities of glutamate-oxaloacetate transaminase (GOT) and glutamate-pyruvate transaminase (GPT). 2. A 2.1-fold increase of GOT and a 1.9-fold increase of GPT activities (P < 0.001) were observed in mice treated perorally with 500 mg/kg of AAP plus 150 mg/kg of thalidomide (Thal). In the absence of AAP, Thal did not display any detectable hepatotoxic effects. 3. The Thal-induced exacerbation of AAP hepatotoxicity was completely inhibited by nicotinic acid amide, a selective inhibitor of poly(ADP-ribose) polymerase (PARP) (P < 0.0001), suggesting a possible influence of Thal on the hepatic metabolism of NAD-adenoribosylation. 4. We see the main application of nicotinic acid amide as for the combinational use in pharmaceutical preparations of AAP in order to avoid hepatic damage in patients treated with AAP and Thal.

Acetaminophen↗