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of 39
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Autor:
Adam G. Goodwill, Eli D. Casalini, Daniel J. Sassoon, Zachary C. Berwick, Gregory M. Dick, Lijuan Fu, Ghassan S. Kassab, Jillian N. Noblet, Johnathan D. Tune
Publikováno v:
American Journal of Physiology-Heart and Circulatory Physiology. 310:H693-H704
Hydrogen peroxide (H2O2) and voltage-dependent K+ (KV) channels play key roles in regulating coronary blood flow in response to metabolic, ischemic, and paracrine stimuli. The KV channels responsible have not been identified, but KV7 channels are pos
Autor:
Dirk J. Duncker, Daphne Merkus, Maaike Hoekstra, Vincent J. de Beer, Veemal Hemradj, Zhichao Zhou, Fen Gao
Publikováno v:
American Journal of Physiology-Heart and Circulatory Physiology, 302(8), H1747-H1755. American Physiological Society
Zhou Z, Hemradj V, de Beer VJ, Gao F, Hoekstra M, Merkus D, Duncker DJ. Cytochrome P-450 2C9 exerts a vasoconstrictor influence on coronary resistance vessels in swine at rest and during exercise. Am J Physiol Heart Circ Physiol 302: H1747-H1755, 201
Publikováno v:
American Journal of Physiology-Heart and Circulatory Physiology. 300:H109-H117
The extracellular K+ concentration ([K+]o) has been proposed to link cardiac metabolism with coronary perfusion and arrhythmogenesis, particularly during ischemia. Several animal studies have also supported K+ as an EDHF that activates Na+-K+-ATPase
Publikováno v:
American Journal of Physiology-Heart and Circulatory Physiology. 294:H145-H155
This study was designed to determine the effect of inhibitors of cyclooxygenase (COX)-1, COX-2, and the nonselective COX inhibitor naproxen on coronary vasoactivity and thrombogenicity under baseline and lipopolysaccharide (LPS)-induced inflammatory
Autor:
Paul A. Rogers, Gregory M. Dick, Albert N. Swafford, Shu Ichi Saitoh, Jarrod D. Knudson, William M. Chilian, Marta Focardi, Ian N. Bratz, Johnathan D. Tune
Publikováno v:
American Journal of Physiology-Heart and Circulatory Physiology. 291:H2473-H2482
Hydrogen peroxide (H2O2) is a proposed endothelium-derived hyperpolarizing factor and metabolic vasodilator of the coronary circulation, but its mechanisms of action on vascular smooth muscle remain unclear. Voltage-dependent K+(KV) channels sensitiv
Autor:
Jurgen W. G. E. VanTeeffelen, Jos A. E. Spaan, Hans Vink, Dirk S. Fokkema, Simone Dekker, Maria Siebes
Publikováno v:
American journal of physiology. Heart and circulatory physiology, 289(6), H2508-H2513. American Physiological Society
Because adenosine is commonly used for inducing maximal coronary hyperemia in the clinic, it is imperative that adenosine-induced hyperemia (AH) resembles coronary hyperemia that can be attained by endogenous stimuli. In the present study we hypothes
Autor:
George A. Beller, Timothy L. Macdonald, David K. Glover, Mirta Ruiz, Jayson M. Rieger, Denny D. Watson, Gail W. Sullivan, Laurent Riou, Joel Linden
Publikováno v:
American Journal of Physiology-Heart and Circulatory Physiology. 288:H1851-H1858
Adenosine and adenosine A2Areceptor agonists have been shown to limit myocardial infarct size when given at vasodilatory doses during reperfusion. This beneficial effect is thought to be due, in part, to stimulation of adenosine A2Areceptors on infla
Publikováno v:
Journal of Applied Physiology. 97:404-415
At rest the myocardium extracts ∼75% of the oxygen delivered by coronary blood flow. Thus there is little extraction reserve when myocardial oxygen consumption is augmented severalfold during exercise. There are local metabolic feedback and sympath
Publikováno v:
American Journal of Physiology-Heart and Circulatory Physiology. 282:H696-H703
This study was designed to test if nitric oxide (NO) contributes to norepinephrine-induced right coronary vasodilation and if NO blunts the norepinephrine-induced increase in myocardial oxygen consumption (MV˙o2) in the right ventricle. In five anes
Autor:
Kensuke Egashira, Akira Takeshita, Ken-ichi Arimura, Hiroaki Shimokawa, Ryo Nakamura, Hiroyuki Tsutsui, Tomomi Ide, Youji Machida
Publikováno v:
American Journal of Physiology-Heart and Circulatory Physiology. 281:H2619-H2625
Recent evidence suggests that increased inactivation of endothelium-derived nitric oxide (NO) by oxygen free radical (OFR) formation is involved in the pathogenesis of endothelial dysfunction in heart failure (HF). However, it is unclear whether incr