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Results for “NICOTINIC ACID”

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PubMed1984

Enhancement of metabolic coronary vasodilatation by nicotinic acid or amide.

Cardiostimulation produced by noradrenaline, glucagon, or tachycardia on the isolated perfused rat heart produced a metabolic coronary dilatation that was potentiated by nicotinic acid or its amide [NIC; 0.05-1.0 mM] without affecting the cardiostimulation. Reactive hyperaemia to brief coronary occlusion was unaffected by NIC, thus confirming that its vasodilator mechanism is of a different nature than that leading to metabolic coronary dilatation. It is suggested that NIC may be of significance as an adjuvant in the treatment of certain types of coronary insufficiencies.

Animals↗
PubMed1996

Impact of nicotinic acid treatment on insulin secretion and insulin sensitivity in low and high insulin responders.

The aim of the study was to evaluate the effect of nicotinic acid (NA) on glucose tolerance, insulin secretion and sensitivity in relation to perturbations of non-esterified fatty acids (NEFA) and previously characterized insulin responses. Healthy subjects (n = 12) were treated for 14 days with incremental doses of NA reaching 2 g day-1. Before NA and on day 14 a hyperglycaemic clamp (11 mmol l-1) was performed with arginine (5 g i.v.) stimulation before and during the clamp. Fasting serum levels of NEFA were evanescently decreased on day 3 (-38%; p < 0.01) and day 7 (-33%; p < 0.05), but not on day 14 (-14%; NS). NA treatment did not significantly affect levels of fasting blood glucose, insulin, C-peptide, proinsulin or glucagon. NA treatment lowered the amount of infused glucose necessary to achieve clamp levels 48 (8) vs. 61 (10) mumol kg-1 min-1 (p < 0.01). Incremental increases in fasting NEFA levels correlated (r = -0.72) with decreased insulin sensitivity as reflected by M/I ratios (the amount of glucose infused, minus glucosuria, divided by the mean insulin level) (p < 0.01). Insulin and glucagon responses to arginine and glucose were similar before and after NA in subgroups with initially low and high insulin responses to glucose. NA-induced insulin resistance in this study is (a) less than previously reported; (b) not associated with changes in insulin secretory responsiveness, but is (c) influenced by an individually variable NA effect on fasting NEFA levels. Our results do not indicate that NA treatment can be used to test the capacity of B cells to cope with insulin resistance.

Adult↗
PubMed1984

[Treatment of primary neuritis of the facial nerve with compresses of dimexide and nicotinic acid].

The author describes a method of treating Bell's palsy by compresses of the following composition: 10 ml dimexide (DMCO), a 1% solution of nicotinic acid (5 ml) and physiological saline (5 ml). Compresses are applied onto the area of the papillary process of the involved side. A course of treatment consisted of 10-12 sessions. Sixty-five patients with Bell's palsy were treated using this method. The therapeutic efficacy was compared with the results of the conventional treatment of Bell's palsy in the control group. The new method of treatment was associated with a statistically significant increase in the rate of those cured and a decrease in the therapy duration.

Administration, Topical↗
PubMed2005

Separation of nicotinic acid and its structural isomers using 1-ethyl-3-methylimidazolium ionic liquid as a buffer additive by capillary electrophoresis.

The growing interest in application of ionic liquids (ILs) in analytical chemistry has been observed. The aim of presented investigation was to verify whether ILs would be a suitable modifier of the background electrolyte (BGE) for pharmaceutical analysis of the closely related drug analogues. The study demonstrates the use of 1-ethyl-3-methylimidazolium tetrafluoroborate (1E-3MI-TFB) ionic liquid as modifiers in the separation of nicotinic acid and its structural isomers by capillary electrophoresis. Dependences of the ionic liquid concentration in a BGE on the separation parameters like migration time, resolution factor and width at peak's baseline have been compared. The separation mechanism involves the free imidazolium ions, which can interact with inner surface of the capillary wall. Increased 1E-3MI-TFB concentration to 150 mmol/L caused decrease of migration times of analytes, improve peaks shape and increase of separation performances. At this ionic liquid concentration in a BGE resolution factor between nicotinic and isonicotinic acids increased to 1.86. The proposed CE separation procedure is highly reproducible and can be applied in qualitative and quantitative analysis of carboxylic acids.

Buffers↗
PubMed2004

[Exercise and nicotinic acid delayed action drug Enduracin: application in outpatient rehabilitation of patients with ischemic heart disease].

AIM: To evaluate efficacy of combined use of moderate exercise and nicotinic acid drug enduracin in patients with coronary heart disease (CHD) with moderate dyslipidemia (DE). MATERIAL AND METHODS: The effects of exercise therapy alone, enduracin alone and their combination on physical performance (PP), hemodynamics, blood lipid spectrum and clinical course of CHD were studied in 93 CHD patients with moderate DE. The results were evaluated clinically after 1-year treatment. RESULTS: Combined used of exercise and enduracin in CHD patients showed its efficacy manifesting in improvement of PP, hemodynamics at rest and exercise test, left ventricular systolic function, clinical course, reduction of DE. Enduracin + exercise appeared more efficient than their use in monotherapy. Enduracin monotherapy had a positive action on PP, arterial pressure and anginal attacks frequency. CONCLUSION: Enduracin is recommended as monotherapy and in combination with moderate exercise in outpatient rehabilitation and secondary prophylaxis of CHD patients with moderate dyslipidemia and angina pectoris to relieve myocardial ischemia under exercise, to raise PP, improve lipid composition of blood and prevent maladaptive left ventricular remodeling.

Ambulatory Care↗
PubMed2003

Antiproteinuric effect of niceritrol, a nicotinic acid derivative, in chronic renal disease with hyperlipidemia: a randomized trial.

PURPOSE: Lipoprotein (a) [Lp(a)] levels increase in patients with renal disease. We administered niceritrol, a nicotinic acid derivative, to patients with chronic renal disease and a high serum Lp(a) level, and studied its effects on lipid metabolism, proteinuria, and renal function. METHODS: Thirty-three patients with chronic renal disease whose serum Lp(a) levels were > or = 15 mg/dL were randomly (but not blindly) assigned to treatment with niceritrol (n = 16) or to an untreated control group (n = 17). Parameters of lipid metabolism, excretion of urinary protein, and renal function were examined for 12 months. RESULTS: Changes in urinary protein excretion, as well as Lp(a) levels, differed significantly between the two groups. The mean (+/- SD) change from baseline in excretion of urinary protein was 0.77 +/- 1.23 g/d in the control group compared with -1.41 +/- 2.26 g/d in the niceritrol group at 12 months (P =0.003). Mean Lp(a) levels increased by 3 +/- 10 mg/dL in the control group compared with a decrease of 10 +/- 13 mg/dL in the niceritrol group at 12 months (P =0.004). The mean creatinine clearance declined by 10 +/- 12 mL/min in the control group, compared with 1 +/- 13 mL/min in the niceritrol group at 12 months (P =0.06). CONCLUSION: Lipid levels improved with niceritrol treatment, whereas the excretion of urinary protein decreased, perhaps slowing the rate of loss of renal function in chronic renal disease.

Chronic Disease↗