scholarly journals Deficiency of Neuronal Nitric Oxide Synthase Increases Mortality and Cardiac Remodeling After Myocardial Infarction

Circulation ◽  
2005 ◽  
Vol 112 (22) ◽  
pp. 3415-3422 ◽  
Author(s):  
Roberto M. Saraiva ◽  
Khalid M. Minhas ◽  
Shubha V.Y. Raju ◽  
Lili A. Barouch ◽  
Eleanor Pitz ◽  
...  
Circulation ◽  
2004 ◽  
Vol 110 (16) ◽  
pp. 2368-2375 ◽  
Author(s):  
Jennifer K. Bendall ◽  
Thibaud Damy ◽  
Philippe Ratajczak ◽  
Xavier Loyer ◽  
Virginie Monceau ◽  
...  

2021 ◽  
Vol Volume 14 ◽  
pp. 3669-3676
Author(s):  
Otávio T Nóbrega ◽  
Alessandra M Campos-Staffico ◽  
Elayne Kelen Oliveira ◽  
Daniel B Munhoz ◽  
Filipe A Moura ◽  
...  

2021 ◽  
Author(s):  
Otávio T Nóbrega ◽  
Alessandra M. Campos-Staffico ◽  
Elayne Kelen Oliveira ◽  
Daniel B Munhoz ◽  
Filipe A. Moura ◽  
...  

Abstract Background: glycemia disorders are a strong predictor of mortality in ST-Elevation Myocardial Infarction (STEMI) patients. Disruption in nitric oxide (NO) production is associated with insulin-resistant states. We evaluated whether NO production in carriers of a defective allele of the neuronal nitric oxide synthase (nNOS or NOS1), whose in vivo expression is reduced by up to 50%, might influence the insulin response during acute phase of STEMI. Methods and Results: Consecutive patients with STEMI (n = 354) underwent clinical evaluations and genotyping for the promoter variation rs41279104. Blood tests were performed at admission (D1) and after five days (D5) of in-hospital follow up, with the disposition index assessed in the period. Flow-mediated dilation (FMD) was assessed by reactive hyperemia on the 30th day. Homozygotes for the defective allele (A) showed lower glycemia and insulin sensitivity at D1 while showing the highest b-cells function and no changes in the circulating NO pool, what is compatible with hyperresponsive b-cells to counteract the inherent glucose-resistant state of AA patients. At D5, glycemic scores shifted to indicate greater insulin sensitivity among A homozygotes, paralleled by a slight yet poor increase in NO bioavailability than that among G carriers. All in all, defective homozygotes showed greater insulin resistance expressed by the disposition index at admission, which was compensated 5 days after STEMI even though FMD of A carriers was lower compared to G homozygotes. Conclusion: a defective nNOS allele seems to elicit endocrine adaptation and to associate with insulin resistance during the acute phase of STEMI.


Circulation ◽  
2009 ◽  
Vol 120 (14) ◽  
pp. 1345-1354 ◽  
Author(s):  
Dylan E. Burger ◽  
Xiangru Lu ◽  
Ming Lei ◽  
Fu-Li Xiang ◽  
Lamis Hammoud ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document