scholarly journals Role of nitric oxide and NADPH oxidase-derived superoxide in regulating coronary blood flow and metabolism in cardio-metabolic diseases

2014 ◽  
Vol 9 (5-6) ◽  
pp. 255-255
Author(s):  
Akos Koller
1996 ◽  
Vol 27 (7) ◽  
pp. 1804-1812 ◽  
Author(s):  
Masafumi Kitakaze ◽  
Koichi Node ◽  
Tetsuo Minamino ◽  
Hiroaki Kosaka ◽  
Yoshiro Shinozaki ◽  
...  

Heart ◽  
2012 ◽  
Vol 98 (Suppl 1) ◽  
pp. A60.2-A61
Author(s):  
H Shabeeh ◽  
N Melikian ◽  
R Dworakowski ◽  
B Casadei ◽  
P Chowienczyk ◽  
...  

Circulation ◽  
2000 ◽  
Vol 101 (25) ◽  
pp. 2942-2948 ◽  
Author(s):  
Johnathan D. Tune ◽  
Keith Neu Richmond ◽  
Mark W. Gorman ◽  
Eric O. Feigl

2013 ◽  
Vol 304 (9) ◽  
pp. H1277-H1282 ◽  
Author(s):  
Husain Shabeeh ◽  
Narbeh Melikian ◽  
Rafal Dworakowski ◽  
Barbara Casadei ◽  
Phil Chowienczyk ◽  
...  

Endothelial nitric oxide synthase (eNOS) was assumed to be the only source of nitric oxide (NO) involved in the regulation of human coronary blood flow (CBF). However, our recent first-in-human study using the neuronal NOS (nNOS)-selective inhibitor S-methyl-L-thiocitrulline (SMTC) showed that nNOS-derived NO also plays a role. In this study, we investigated the relative contribution of nNOS and eNOS to the CBF response to a pacing-induced increase in cardiac workload. Incremental right atrial pacing was undertaken in patients with angiographically normal coronary arteries during intracoronary infusion of saline vehicle and then either SMTC or NG-monomethyl-l-arginine (l-NMMA; which inhibits both eNOS and nNOS). Intracoronary SMTC (0.625 μmol/min) and l-NMMA (25 μmol/min) reduced basal CBF to a similar extent (−19.2 ± 3.2% and 25.0 ± 2.7%, respectively; n = 10 per group). Pacing-induced increases in CBF were significantly blunted by l-NMMA (maximum CBF: 83.5 ± 14.2 ml/min during saline vs. 61.6 ± 9.5 ml/min during l-NMMA; P < 0.01). By contrast, intracoronary SMTC had no effect on the maximum CBF during pacing (98.5 ± 12.9 ml/min during saline vs. 102.1 ± 16.6 ml/min during SMTC; P = not significant). l-NMMA also blunted the pacing-induced increase in coronary artery diameter ( P < 0.001 vs. saline), whereas SMTC had no effect. Our results confirm a role of nNOS in the regulation of basal CBF in humans but show that coronary vasodilation in response to a pacing-induced increase in cardiac workload is exclusively mediated by eNOS-derived NO.


2001 ◽  
Vol 65 (9) ◽  
pp. 827-833 ◽  
Author(s):  
Hideo Tada ◽  
Kensuke Egashira ◽  
Mitsutaka Yamamoto ◽  
Makoto Usui ◽  
Yukinori Arai ◽  
...  

1996 ◽  
Vol 7 (2) ◽  
pp. 149-154 ◽  
Author(s):  
Magda Heras ◽  
Eulália Roig ◽  
Félix Pérez-Villa ◽  
Marco Paz ◽  
Gaspar Melis ◽  
...  

Hypertension ◽  
1995 ◽  
Vol 25 (3) ◽  
pp. 408-414 ◽  
Author(s):  
Francisco J. Fenoy ◽  
Paloma Ferrer ◽  
Luis Carbonell ◽  
Miguel García-Salom

Mathematics ◽  
2020 ◽  
Vol 8 (8) ◽  
pp. 1205
Author(s):  
Timur Gamilov ◽  
Philipp Kopylov ◽  
Maria Serova ◽  
Roman Syunyaev ◽  
Andrey Pikunov ◽  
...  

In this work we present a one-dimensional (1D) mathematical model of the coronary circulation and use it to study the effects of arrhythmias on coronary blood flow (CBF). Hydrodynamical models are rarely used to study arrhythmias’ effects on CBF. Our model accounts for action potential duration, which updates the length of systole depending on the heart rate. It also includes dependency of stroke volume on heart rate, which is based on clinical data. We apply the new methodology to the computational evaluation of CBF during interventricular asynchrony due to cardiac pacing and some types of arrhythmias including tachycardia, bradycardia, long QT syndrome and premature ventricular contraction (bigeminy, trigeminy, quadrigeminy). We find that CBF can be significantly affected by arrhythmias. CBF at rest (60 bpm) is 26% lower in LCA and 22% lower in RCA for long QT syndrome. During bigeminy, trigeminy and quadrigeminy, respectively, CBF decreases by 28%, 19% and 14% with respect to a healthy case.


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