ArticleMicrocirculation (New York, N.Y. : 1994)2014
Contribution of hydrogen sulfide to the control of coronary blood flow.
Article in Microcirculation (New York, N.Y. : 1994), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed, 21 citations in OpenAlex.
- The Role of Hydrogen Sulfide in Peripheral Nervous System Modulation.Handbook of experimental pharmacology · 2026Review
- Inhibition of the voltage-gated potassium channel Kv1.5 by hydrogen sulfide attenuates remodeling through S-nitrosylation-mediated signaling.Communications biology · 2023Article
- Hydrogen Sulfide Modulates Endothelial-Mesenchymal Transition in Heart Failure.Circulation research · 2023Article
- ATP- and voltage-dependent electro-metabolic signaling regulates blood flow in heart.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Erucin exhibits vasorelaxing effects and antihypertensive activity by HBritish journal of pharmacology · 2020Article
- Elastase-triggered HChemical communications (Cambridge, England) · 2020Article
- Sulfur-containing gaseous signal molecules, ion channels and cardiovascular diseases.British journal of pharmacology · 2018Review
- Cardiovascular disease and resuscitated septic shock lead to the downregulation of the HIntensive care medicine experimental · 2017Article
- Smooth Muscle Ion Channels and Regulation of Vascular Tone in Resistance Arteries and Arterioles.Comprehensive Physiology · 2017Review
- MPST but not CSE is the primary regulator of hydrogen sulfide production and function in the coronary artery.American journal of physiology. Heart and circulatory physiology · 2016Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveThis study examined the mechanisms by which H2 S modulates coronary microvascular resistance and myocardial perfusion at rest and in response to cardiac ischemia.
methodsExperiments were conducted in isolated coronary arteries and in open-chest anesthetized dogs.
resultsWe found that the H2 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) H2 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 Kv channels with 4-aminopyridine (p = 0.127) but was attenuated (0.23 ± 0.02-1.13 ± 0.13 mL/min/g) by the KATP channel antagonist glibenclamide (p < 0.001). Inhibition of NO synthesis (l-NAME) did not attenuate coronary responses to H2 S. Immunohistochemistry revealed expression of CSE, an endogenous H2 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).
conclusionsThese findings demonstrate that exogenous H2 S induces potent, endothelial-independent dilation of the coronary microcirculation predominantly through the activation of KATP channels, however, our data do not support a functional role for endogenous H2 S in the regulation of coronary microvascular resistance.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.