ArticleThe Journal of pharmacology and experimental therapeutics2011
Reversal of isoflurane-induced depression of myocardial contraction by nitroxyl via myofilament sensitization to Ca2+.
Article in The Journal of pharmacology and experimental therapeutics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- Modulation of cardiac contractility and redox balance via cannabinoid type II receptor activation in healthy rats.Pflugers Archiv : European journal of physiology · 2025Article
- Cardiovascular Therapeutic Potential of the Redox Siblings, Nitric Oxide (NO•) and Nitroxyl (HNO), in the Setting of Reactive Oxygen Species Dysregulation.Handbook of experimental pharmacology · 2021Review
- Longitudinal impact on rat cardiac tissue transcriptomic profiles due to acute intratracheal inhalation exposures to isoflurane.PloS one · 2021Article
- The actin 'A-triad's' role in contractile regulation in health and disease.The Journal of physiology · 2020Review
- Anesthetic Agents Isoflurane and Propofol Decrease Maximal CaThe Journal of pharmacology and experimental therapeutics · 2019Article
- Intravenous Infusion of the Novel HNO Donor BMS-986231 Is Associated With Beneficial Inotropic, Lusitropic, and Vasodilatory Properties in 2 Canine Models of Heart Failure.JACC. Basic to translational science · 2018Article
- Fropofol decreases force development in cardiac muscle.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Nitric oxide signalling in cardiovascular health and disease.Nature reviews. Cardiology · 2018Review
- Therapeutic Potential of Nitroxyl (HNO) Donors in the Management of Acute Decompensated Heart Failure.Drugs · 2016Review
- Molecular mechanism of anesthetic-induced depression of myocardial contraction.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- Recent advances in the chemical biology of nitroxyl (HNO) detection and generation.Nitric oxide : biology and chemistry · 2016Review
- Molecular and Integrative Physiological Effects of Isoflurane Anesthesia: The Paradigm of Cardiovascular Studies in Rodents using Magnetic Resonance Imaging.Frontiers in cardiovascular medicine · 2016Review
- A change of heart: oxidative stress in governing muscle function?Biophysical reviews · 2015Article
- New acyloxy nitroso compounds with improved water solubility and nitroxyl (HNO) release kinetics and inhibitors of platelet aggregation.Bioorganic & medicinal chemistry · 2015Article
- Role for the propofol hydroxyl in anesthetic protein target molecular recognition.ACS chemical neuroscience · 2015Article
- The concomitant coronary vasodilator and positive inotropic actions of the nitroxyl donor Angeli's salt in the intact rat heart: contribution of soluble guanylyl cyclase-dependent and -independent mechanisms.British journal of pharmacology · 2014Article
- Effect of isoflurane on myocardial energetic and oxidative stress in cardiac muscle from Zucker diabetic fatty rat.The Journal of pharmacology and experimental therapeutics · 2014Article
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Authors and funding
8 authors at 6 institutions in 3 countries.
Funding
Abstract
Isoflurane (ISO) is known to depress cardiac contraction. Here, we hypothesized that decreasing myofilament Ca(2+) responsiveness is central to ISO-induced reduction in cardiac force development. Moreover, we also tested whether the nitroxyl (HNO) donor 1-nitrosocyclohexyl acetate (NCA), acting as a myofilament Ca(2+) sensitizer, restores force in the presence of ISO. Trabeculae from the right ventricles of LBN/F1 rats were superfused with Krebs-Henseleit solution at room temperature, and force and intracellular Ca(2+) ([Ca(2+)](i)) were measured. Steady-state activations were achieved by stimulating the muscles at 10 Hz in the presence of ryanodine. The same muscles were chemically skinned with 1% Triton X-100, and the force-Ca(2+) relation measurements were repeated. ISO depressed force in a dose-dependent manner without significantly altering [Ca(2+)](i). At 1.5%, force was reduced over 50%, whereas [Ca(2+)](i) remained unaffected. At 3%, contraction was decreased by ∼75% with [Ca(2+)](i) reduced by only 15%. During steady-state activation, 1.5% ISO depressed maximal Ca(2+)-activated force (F(max)) and increased the [Ca(2+)](i) required for 50% activation (Ca(50)) without affecting the Hill coefficient. After skinning, the same muscles showed similar decreases in F(max) and increases in Ca(50) in the presence of ISO. NCA restored force in the presence of ISO without affecting [Ca(2+)](i). These results show that 1) ISO depresses cardiac force development by decreasing myofilament Ca(2+) responsiveness, and 2) myofilament Ca(2+) sensitization by NCA can effectively restore force development without further increases in [Ca(2+)](i). The present findings have potential translational value because of the efficiency and efficacy of HNO on ISO-induced myocardial contractile dysfunction.
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