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Search indexed NASA NTRS and DOE OSTI research on propulsion, heat transfer, battery materials and energy systems. Follow report and document links to the original sources.

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NASA NTRS2003

Oscillatory shear stress stimulates endothelial production of O2- from p47phox-dependent NAD(P)H oxidases, leading to monocyte adhesion

Arterial regions exposed to oscillatory shear (OS) in branched arteries are lesion-prone sites of atherosclerosis, whereas those of laminar shear (LS) are relatively well protected. Here, we examined the hypothesis that OS and LS differentially regulate production of O2- from the endothelial NAD(P)H oxidase, which, in turn, is responsible for their opposite effects on a critical atherogenic event, monocyte adhesion. We used aortic endothelial cells obtained from C57BL/6 (MAE-C57) and p47phox-/- (MAE-p47-/-) mice, which lack a component of NAD(P)H oxidase. O2- production was determined by dihydroethidium staining and an electron spin resonance using an electron spin trap methoxycarbonyl-2,2,5,5-tetramethyl-pyrrolidine. Chronic exposure (18 h) to an arterial level of OS (+/- 5 dynes/cm2) increased O2- (2-fold) and monocyte adhesion (3-fold) in MAE-C57 cells, whereas chronic LS (15 dynes/cm2, 18 h) significantly decreased both monocyte adhesion and O2- compared with static conditions. In contrast, neither LS nor OS were able to induce O2- production and monocyte adhesion to MAE-p47-/-. Treating MAE-C57 with a cell-permeable superoxide dismutase compound, polyethylene glycol-superoxide dismutase, also inhibited OS-induced monocyte adhesion. In addition, over-expressing p47phox in MAE-p47-/- restored OS-induced O2- production and monocyte adhesion. These results suggest that chronic exposure of endothelial cells to OS stimulates O2- and/or its derivatives produced from p47phox-dependent NAD(P)H oxidase, which, in turn, leads to monocyte adhesion, an early and critical atherogenic event.

NASA Program Fundamental Space Biology↗

NASA NTRS1998

Milk and other dietary influences on coronary heart disease

While dietary links to ischemic heart disease (IHD) and coronary heart disease (CHD) mortality have been studied for many years, the correlation has not clearly been resolved, especially for older populations. In this paper, a multi-country statistical approach involving 32 countries is used to find dietary links to IHD and CHD for various age groups aged 35+. For IHD, milk carbohydrates were found to have the highest statistical association for males aged 35+ and females aged 65+, while for females aged 35-64, sugar was found to have the highest association. In the case of CHD, non-fat milk was found to have the highest association for males aged 45+ and females aged 75+, while for females 65-74, milk carbohydrates and sugar had the highest associations, and for females aged 45-64, sugar had the highest association. A number of mechanisms have been proposed in the literature that might explain the milk carbohydrate or non-fat milk association. One of the most prominent theories is that animal proteins contribute to homocysteine (Hcy) production; however, milk more than meat lacks adequate B vitamins to convert Hcy to useful products. Lactose and calcium in conjunction with Hcy from consumption of non-fat milk may also contribute to calcification of the arteries.

Coronary Disease/etiology↗

NASA NTRS1988

Serotonin, atherosclerosis, and collateral vessel spasm

Studies on animal models demonstrate that platelet products contribute to vascular spasm in ischemic syndromes and that this is reversible with administration of ketanserin and thromboxane synthesis inhibitors. Laboratory animals (dogs, rabbits, and rats) that had femoral artery ligations exhibited supersensitivity to serotonin within days in their collateral blood vessels. This supersensitivity lasted at least 6 months. The response to serotonin was reversed by ketanserin, but not by 5HT-1 antagonists. Supersensitivity does not extend to norepinephrine, and alpha blockers do not influence the response to serotonin. It appears that platelet activation by endothelial injury contributes to ischemia through blood vessel occlusion and vascular spasm. When platelet activation occurs in vivo, blood vessel occlusion and vascular spasm are reversible in part by using ketanserin or agents that block thromboxane synthesis or its action. Combining both classes of agents reverses spasm completely. These findings support existing evidence that platelet products contribute to vascular disease, and provide an approach to improved management with currently available pharmacologic agents.

Review, Tutorial↗