一氧化氮系统功能障碍与动脉粥样硬化

[1] Molecular therapies for vasculardiseases. Gibbons GH,Dzau VJ. Science . 1996

[2] Oxygen tension regulates the expression of the platelet-derivedgrowth factor-B chain gene in human endothelial cells. Kourembanas S,Hannan RL,Faller DV. The Journal of Clinical Investigation . 1990

[3] Mediators of leukocyteadhesion in rat mesenteric venules elicited by inhibition ofnitric odse synthesis. Arndt,Russell,Kurose,et al. Gastroenterology . 1993

[4] Physiologic consequences ofincreased vascular oxidant atresses in hyperc-holesterolemia and atherosclerosis implications for impaired vasomotion. Harrision DG,Ohara Y. The American Journal of Cardiology . 1995

[5] Hypercholesterolemia increases endothelial superoxide anionproduction. Ohara Y,Peterson TE,Harrison oo. The Journal of Clinical Investigation . 1993

[6] Generation of Superoxide by purified brain nitric oxide synthase. Pou S,Pou WS,Bredt DS,et al. Journal of Biolchemistics . 1992

[7] Cellular mechanism of atherogenesisand the effects of nitric okide. Cook JP,Tsao P. Current Opinion in Cardiology . 1992

[8] Nitric oxide regulates the expression of vasconstrictors andgrowth factors by vascular endothelium under both normoxin and hypoxia. Kourembanas S,Mcquillan LP,Leung CK,et al. The Journal of Clinical Investigation . 1993

[9] Nitric oxide, anendothelial cell relaxation factor, inhibits neutrophil suPerokide anion production via a direct action on NADPHoxidase. Clancy RM,Piziak JL,Abramson SB. The Journal of Clinical Investigation . 1992

[10] Peroxgnitriteipduced membrane lipid peroxidation the cytotoxic potenitial of superoxide and nitric oxide. Radi R,Bechman JS,Bush KM,et al. Archive of Biochemistry and Biophysics . 1991

[1] Molecular therapies for vasculardiseases. Gibbons GH,Dzau VJ. Science . 1996

[2] Oxygen tension regulates the expression of the platelet-derivedgrowth factor-B chain gene in human endothelial cells. Kourembanas S,Hannan RL,Faller DV. The Journal of Clinical Investigation . 1990

[3] Mediators of leukocyteadhesion in rat mesenteric venules elicited by inhibition ofnitric odse synthesis. Arndt,Russell,Kurose,et al. Gastroenterology . 1993

[4] Physiologic consequences ofincreased vascular oxidant atresses in hyperc-holesterolemia and atherosclerosis implications for impaired vasomotion. Harrision DG,Ohara Y. The American Journal of Cardiology . 1995

[5] Hypercholesterolemia increases endothelial superoxide anionproduction. Ohara Y,Peterson TE,Harrison oo. The Journal of Clinical Investigation . 1993

[6] Generation of Superoxide by purified brain nitric oxide synthase. Pou S,Pou WS,Bredt DS,et al. Journal of Biolchemistics . 1992

[7] Cellular mechanism of atherogenesisand the effects of nitric okide. Cook JP,Tsao P. Current Opinion in Cardiology . 1992

[8] Nitric oxide regulates the expression of vasconstrictors andgrowth factors by vascular endothelium under both normoxin and hypoxia. Kourembanas S,Mcquillan LP,Leung CK,et al. The Journal of Clinical Investigation . 1993

[9] Nitric oxide, anendothelial cell relaxation factor, inhibits neutrophil suPerokide anion production via a direct action on NADPHoxidase. Clancy RM,Piziak JL,Abramson SB. The Journal of Clinical Investigation . 1992

[10] Peroxgnitriteipduced membrane lipid peroxidation the cytotoxic potenitial of superoxide and nitric oxide. Radi R,Bechman JS,Bush KM,et al. Archive of Biochemistry and Biophysics . 1991