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Results for “NICOTINIC ACID”

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At least 649 records · Page 36Linked to original sources
PubMed1987

The effect of nicotinic acid on the depressant action of ethanol and pentobarbital.

The effect of nicotinic acid (NA) on sleeping time induced by a single dose of ethanol or pentobarbital was studied in rats. It was found that sleeping time was markedly reduced by NA in a dose-dependent manner. The effect was observed when NA was administered 10 min before or after ethanol or pentobarbital, but not when given 60 min in advance. NA did not affect the rate of ethanol elimination measured up to 5 hr after ethanol administration. Rats pretreated with NA 60 min before ethanol slept longer than controls. This latter effect was not observed with pentobarbital. These observations, together with the known lack of effect of high liver NAD+ levels on ethanol metabolism and the rather stable NAD+ concentration in brain cells, suggest that the effect of NA on sleeping time is not mediated by an increase in ethanol metabolism in liver or by NAD+ or NAD+-dependent reactions in brain. Our results are consistent with a direct action of NA, or some rapidly formed derivative, on a structure or process associated with brain cell functions or membranes.

Animals↗
PubMedDate not supplied

[Use of nicotinamide for correcting the disordered nicotinic acid allowance of patients with noncoronarogenic heart diseases].

A study was made of the effects of different doses of nicotinamide (NA) on the nicotinic acid supply in 37 patients with rheumocarditis of varying severity without circulation failure, in 5 patients with infectious-allergic myocarditis, and in 10 patients with tonzilogenous myocardiodystrophy. Twenty-eight patients with analogous diseases given unified therapy without NA and 70 healthy subjects were examined for control purposes. The rate of vitamin PP supply was evaluated from the content of NAD and NADP in red cells, from that of N'-methylnicotinamide in the blood and its excretion with urine. Administration of NA in a dose of 50 mg a day for 2 weeks to patients with tonsilogenous myocardiodystrophy made the indicators under consideration return to normal. The attainment of complete correction of abnormal vitamin PP supply in patients with rheumocarditis and infectious-allergic myocarditis demands a 2-time increase of the drug dose.

Adult↗
PubMed1988

Infusion of nicotinic acid stimulates leucine oxidation and inhibits protein synthesis in pigs before and during a meal.

Leucine metabolism was measured isotopically in immature female pigs to assess the effect of acute infusions of nicotinic acid (NA) on leucine kinetics in both the fed and fasting states. After an overnight fast, immature pigs were infused with 3H-alpha-ketoisocaproate (KIC) and 14C-leucine. After a 2-hour equilibration period, an infusion of either saline or 0.4 mg/kg.min of NA was begun. NA caused a decrease in plasma glucose and an increase in plasma glucagon. During the fasting period, NA increased KIC oxidation 2-fold over controls. After feeding, plasma free fatty acids (FFA) in both groups were equivalent, but KIC oxidation was still approximately 80% higher in NA-infused animals. In addition, NA stimulated proteolysis and inhibited protein synthesis during the meal. Because plasma FFA concentrations were equal during the fed period, it is unlikely that changes in FFA concentrations are responsible for the changes in leucine metabolism observal during NA infusion.

Animals↗
PubMed1979

[Influence of phenobarbital on hyperbilirubinemia caused by nicotinic acid and rifamycin--SV in healthy subjects].

Ten healthy subjects have been given before and after treatment with phenobarbital the following intravenous charges: a) nicotinic acid; b) rifamicyn-SV; c) simultaneous administration of the two drugs. Along with confirmatory evidence of the wellknown increase in bilirubinaemia (prevalently unconjugated), we have observed phenobarbital to attempts partially yet significantly that effect. On the base of direct experience on rat liver, we hypothise phenobarbital to increase the pool of the Y protein carrying cholephilic organic anions into the hepatocytes.

Adult↗
PubMed1997

Esterase-like activity of human serum albumin toward prodrug esters of nicotinic acid.

The esterase-like activity of human serum albumin (HSA) toward esters of nicotinic acid was investigated under a variety of conditions such as protein concentration, temperature, pH, ionic strength, nature of buffers, and presence of organic solvents. Initial rate constants of hydrolysis of 18 nicotinates in the presence of 50 microM HSA were measured at pH 7.4 and 37 degrees C. The substrates displayed half-lifes ranging from less than 15 min (2-butoxyethyl nicotinate) to more than 95 hr (methyl nicotinate). The hydrolysis of tert-butyl nicotinate was too slow to be measurable, whereas 1-carbamoylethyl nicotinate was stabilized against hydrolysis by the presence of HSA. The rate constants of HSA-catalyzed hydrolysis were well correlated (r2 = 0.85; N = 12) with previously published data obtained in human plasma, indicating similar substrate specificities in the two biological preparations. All evidence points to serum albumin as the possible major catalyst of hydrolysis of nicotinate esters in human plasma.

Esterases↗
PubMed1994

Enhancement of myocardial [fluorine-18]fluorodeoxyglucose uptake by a nicotinic acid derivative.

UNLABELLED: Recently, the euglycemic hyperinsulinemic clamp technique was shown to give excellent image quality during metabolic steady-state conditions. Acipimox is a new potent nicotinic acid derivative that rapidly reduces serum free fatty acid (FFA) levels by inhibiting lipolysis in peripheral tissue. METHODS: To compare the effects of acipimox administration and insulin clamp on [18F]fluorodeoxyglucose ([18F]FDG) uptake and myocardial glucose utilization, five nondiabetic and seven type II diabetic patients who had had previous myocardial infarctions were studied twice: once during a clamp study and once after the administration of acipimox (2 x 250 mg orally). All patients also underwent resting SPECT perfusion imaging prior to PET scans. RESULTS: The patients tolerated acipimox well. Although fasting plasma glucose levels were higher in diabetic patients (9.2 +/- 3.4 versus 5.5 +/- 0.3 mM, p = 0.03), they were decreased both during clamping and after acipimox; during imaging, no significant differences between the groups and approaches were detected. By visual analysis, the image quality and myocardial [18F]FDG uptake patterns were similar during clamping and after acipimox. Compared with the relative [18F]FDG uptake values obtained during clamping, acipimox yielded similar results in normal, mismatch and scar segments (r = 0.88, p = 0.0001). Similar rMGU values were also obtained during both approaches. CONCLUSION: Thus, PET imaging with [18F]FDG after the administration of acipimox is a simple and feasible method for clinical viability studies both in nondiabetic and diabetic patients. It results in excellent image quality and gives rMGU levels similar to the insulin clamp technique.

Adult↗
PubMed1975

Control of ventricular arrhythmias during myocardial infarction by antilipolytic treatment using a nicotinic-acid analogue.

The effect of lowering raised plasma-free-fatty acids (F.F.A.) on the incidence of serious ventricular arrhythmias after myocardial infarction was assessed by a double-blind trial in eighty-one patients. A nicotinic-acid analogue (N.A.A.) with very slight haemodynamic effects was given within 12 hours of the onset of myocardial infarction to lower plasma-F.F.A. When treatment with N.A.A. was started within 5 hours of the onset of symptoms, the numbers of patients with ventricular symptoms, the numbers of patients with ventricular tachycardia were significantly reduced, provided elevated plasma-F.F.A. levels were rapidly lowered and maintained in the normal range throughout the treatment period. The incidence of R-on-apex T ventricular premature beats and beats in which the ectopic R wave interrupted the apex of the T wave of a previous ventricular premature beat was also reduced in patients receiving N.A.A within 5 hours of the onset of symptoms. Plasma-total-catecholamines and serum-creatine-kinase levels were similar in the N.A.A.-treated and placebo groups. N.A.A. rarely caused skin flushing, but vomiting occurred in some patients after many hours of treatment. These findings suggest that treatment directed towards stabilsing the matabolism of the ischaemic myocardium can be of therapeutic value and lead to fewer serious ventricular arrhythmias.

Arrhythmias, Cardiac↗