ArticleSultan Qaboos University medical journal2011
Effects of hydrogen sulphide on the isolated perfused rat heart.
Article in Sultan Qaboos University medical journal, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed, 3 citations in OpenAlex.
- The effects of hydrogen sulfide under sevoflurane administration against ischemia and reperfusion injury in isolated rat heart.Korean journal of anesthesiology · 2012Article
- Hydrogen Sulphide and Nitric Oxide Cooperate in Cardioprotection Against Ischemia/Reperfusion Injury in Isolated Rat Heart.In vivo (Athens, Greece)Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesHydrogen sulphide has been identified as a gas signalling molecule in the body, and has previously been shown to have vasorelaxant properties. The aim of the study was to investigate the effects of sodium hydrosulphide (NaHS), a hydrogen sulphide donor, on heart rate (HR), left ventricular developed pressure (LVDP) and coronary flow (CF) in the isolated perfused rat heart.
methodsA Langendorff isolated heart preparation was used to investigate the effect of a dose range of sodium hydrosulphide, in the presence and absence of inhibitors, on heart rate, left ventricular developed pressure and coronary flow.
resultsSodium hydrosulphide caused a significant decrease in heart rate at a concentration of 10-3 M (P <0.001). This decrease was partially inhibited by glibenclamide, a K(ATP) channel blocker (P <0.05); L-NAME, a nitric oxide synthase inhibitor (P <0.001), and methylene blue (P <0.001), but not by H-89, a protein kinase A inhibitor. Sodium hydrosulphide significantly increased coronary flow at concentrations of 10-4 - 10-3M (P <0.05). This response was significantly increased in the presence of L-NAME (P <0.001) and methylene blue (P <0.001), whereas H-89 inhibited the increase in coronary flow due to sodium hydrosulphide (P <0.001). Sodium hydrosulphide significantly decreased LVDP at all concentrations (P <0.001). In the presence of glibenclamide and H-89, the time period of the decrease in LVDP due to sodium hydrosulphide was extended (P <0.001), whereas methylene blue and L-NAME caused a significant reduction in the response to sodium hydrosulphide (P <0.05, P <0.01 respectively).
conclusionSodium hydrosulphide reduced heart rate and LVDP, and increased coronary flow in the isolated perfused rat heart; however, the mechanisms of action could not be fully elucidated.
Indexed as
Identifiers
21969896PMC3121029W48027523What OpenQuestion holds
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