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Contribution of Hydrogen Sulfide to the Control of Coronary Blood Flow
Author(s) -
Casalini Eli D.,
Goodwill Adam G.,
Owen Meredith K.,
Moberly Steven P.,
Berwick Zachary C.,
Tune Johnathan D.
Publication year - 2014
Publication title -
microcirculation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.793
H-Index - 83
eISSN - 1549-8719
pISSN - 1073-9688
DOI - 10.1111/micc.12083
Subject(s) - coronary arteries , cardiology , medicine , coronary occlusion , blood flow , coronary circulation , in vivo , coronary vessel , ischemia , artery , biology , microbiology and biotechnology
Objective This study examined the mechanisms by which H 2 S modulates coronary microvascular resistance and myocardial perfusion at rest and in response to cardiac ischemia. Methods Experiments were conducted in isolated coronary arteries and in open‐chest anesthetized dogs. Results We found that the H 2 S substrate l ‐cysteine (1–10 mM ) did not alter coronary tone of isolated arteries in vitro or coronary blood flow in vivo . In contrast, intracoronary (ic) H 2 S (0.1–3 mM ) increased coronary flow from 0.49 ± 0.08 to 2.65 ± 0.13 mL /min/g ( p < 0.001). This increase in flow was unaffected by inhibition of K v channels with 4‐aminopyridine ( p = 0.127) but was attenuated (0.23 ± 0.02–1.13 ± 0.13 mL /min/g) by the K ATP channel antagonist glibenclamide ( p < 0.001). Inhibition of NO synthesis ( l ‐NAME) did not attenuate coronary responses to H 2 S. Immunohistochemistry revealed expression of CSE, an endogenous H 2 S enzyme, in myocardium. Inhibition of CSE with β‐cyano‐ l ‐alanine (10 μM) had no effect on baseline coronary flow or responses to a 15‐second coronary occlusion ( p = 0.82). Conclusions These findings demonstrate that exogenous H 2 S induces potent, endothelial‐independent dilation of the coronary microcirculation predominantly through the activation of K ATP channels, however, our data do not support a functional role for endogenous H 2 S in the regulation of coronary microvascular resistance.