J Klar — Page 2 | PubMed Health

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Enhanced myocardial preservation by nicotinic acid, an antilipolytic compound: mechanism of action.

The cardioprotective effects of an antilipolytic compound, nicotinic acid, on arrested-reperfused myocardium were investigated in the isolated in situ pig heart preparation. Hearts were preperfused for 15 min in the presence of (5-3H)-glucose and (U-14C)-palmitic acid. Half of the hearts were then perfused with 0.08 mM nicotinic acid for an additional 15-min period, while the remaining control hearts received unmodified perfusion. Arrest was then induced in all animals for 2 h using hypothermic K+ cardioplegia, followed by 60 min of normothermic reperfusion. In control hearts, there were significantly greater levels of long-chain acyl Co-A and acyl carnitine and lower levels of membrane phospholipids than in the nicotinic acid group. While nicotinic acid inhibited beta-oxidation during pre-ischemia and reperfusion, it also prevented the degradation of membrane phospholipids. The net result was a reduction of free fatty acid accumulation during arrest and reperfusion in the nicotinic acid group. Glycolysis, as reflected in 3H2O production, was significantly increased by nicotinic acid administration. In the control heart as compared to the nicotinic acid group, the incorporation of 14C-label from palmitate into triglyceride and cholesterol during arrest was enhanced, while incorporation into phospholipids was depressed. The cardioprotective effects of nicotinic acid were demonstrated by decreased release of creatine kinase and improved coronary blood flow, and cardiac contractility in the reperfused myocardium supplemented with nicotinic acid compared to the control group. These results suggest that nicotinic acid significantly protects the arrested-reperfused myocardium by a) preventing elevation of myocardial fatty acid levels, b) stimulating glycolysis by limiting fatty acid oxidation, c) inhibiting degradation of membrane phospholipids, and d) preventing accumulation of fatty acid metabolites with harmful detergent properties.

Animals↗

PubMedDate not supplied

Heavy smoking among a sample of employed women.

Understanding the phenomenon of heavy smoking among women and factors related to it is of considerable public health importance. Whereas lighter smokers have been more successful in their cessation attempts, the percentage of smokers who smoke more than 25 cigarettes per day has increased in recent years. This article examines the hypothesis that, compared to lighter smokers, female heavy smokers will report more responsiveness to internal cues to smoke, less interest in quitting, more difficulty with previous cessation attempts, more uncertainty about cessation strategies, and more concern about weight gain as a result of quitting. We collected data in 1984 through a self-administered survey completed by 874 women employed as nurses in acute care, chronic care, and home care nursing in Worcester, Massachusetts; we base our analyses on data collected from 158 light and moderate smokers and 67 heavy smokers. Our findings suggest that, compared to lighter smokers, heavy smokers may depend more on nicotine and are likely to respond to a broader array of cues to smoke, factors that appear to contribute to heavy smokers' greater difficulties with quitting. These female heavy smokers are just as likely as lighter smokers to have made previous attempts to quit and want to quit just as much. Major barriers to quitting for female heavy smokers include a lack of confidence in their ability to quit, insufficient tools to succeed with cessation attempts, and fear that weight gain will accompany quitting.

Adult↗