ArticleBritish journal of pharmacology2006
Positive inotropic effects of carbon monoxide-releasing molecules (CO-RMs) in the isolated perfused rat heart.
Article in British journal of pharmacology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 50 citations in OpenAlex.
- Cardiovascular Effects of Ruthenium Complexes: A Potential Therapeutic Tool in Hypertension and Myocardial Injury.Mini reviews in medicinal chemistry · 2025Review
- Review
- The carbon monoxide prodrug oCOm-21 increases CaPhysiological reports · 2024Article
- CORM-3 Inhibits the Inflammatory Response of Human Periodontal Ligament Fibroblasts Stimulated by LPS and High Glucose.Journal of inflammation research · 2024Article
- Carbon monoxide and a change of heart.Redox biology · 2021Review
- Carbon monoxide activates large-conductance calcium-activated potassium channels of human cardiac fibroblasts through various mechanisms.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2021Article
- A key role for peroxynitrite-mediated inhibition of cardiac ERG (Kv11.1) KFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- Heme Oxygenase-1 and Carbon Monoxide in the Heart: The Balancing Act Between Danger Signaling and Pro-Survival.Circulation research · 2016Review
- Carbon monoxide modulates electrical activity of murine myocardium via cGMP-dependent mechanisms.Journal of physiology and biochemistry · 2015Article
- Diverse mechanisms underlying the regulation of ion channels by carbon monoxide.British journal of pharmacology · 2015Review
- Modulation of sinoatrial node pacemaker activity by carbon monoxide and hydrogen sulfide.Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sections · 2013Article
- Use of carbon monoxide in minimizing ischemia/reperfusion injury in transplantation.Transplantation reviews (Orlando, Fla.) · 2012Review
- Therapeutic potential of carbon monoxide in multiple sclerosis.Clinical and experimental immunology · 2012Review
- Acute myocardial infarction in streptozotocin-induced hyperglycaemic rats: protection by a carbon monoxide-releasing molecule (CORM-3).Naunyn-Schmiedeberg's archives of pharmacology · 2012Article
- Modulation of ion channels and transporters by carbon monoxide: causes for concern?Frontiers in physiology · 2012Article
- Carbon monoxide affects electrical and contractile activity of rat myocardium.Journal of biomedical science · 2011Article
- Use of carbon monoxide as a therapeutic agent: promises and challenges.Intensive care medicine · 2008Review
- Changes in the electrical and contractile activities of rat atrial myocardium caused by carbon monoxide.Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sectionsArticle
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeCarbon monoxide (CO) generated by the enzyme haeme oxygenase-1 (HO-1) during the breakdown of haeme is known to mediate a number of biological effects. Here, we investigated whether CO liberated from two water soluble carbon monoxide-releasing molecules (CO-RMs) exerts inotropic effects on the myocardium. EXPERIMENTAL APPROACH: Rat isolated hearts perfused either at constant flow or constant pressure were used to test the effect of CO-RMs. KEY
resultsCORM-3, a fast CO releaser, produced a direct positive inotropic effect when cumulative doses (3, 10 and 30 microg min(-1)) or a single dose (5 microM) were infused at either constant coronary pressure (CCP) or constant coronary flow (CCF). The inotropic effect mediated by CORM-3 was abolished by blockade of soluble guanylate cyclase or Na(+)/H(+) exchanger, but not by inhibitors of L-type Ca(2+) channels and protein kinase C. CORM-3 also caused a slight reduction in heart rate but did not alter coronary flow. In contrast, the slow CO releaser CORM-A1 produced significant coronary vasodilatation when given at the highest concentration (30 mug min(-1)) but exerted no effect on myocardial contractility or heart rate. CONCLUSION AND IMPLICATIONS: A rapid CO release from CORM-3 exerts a direct positive inotropic effect on rat isolated perfused hearts, whereas CO slowly released by CORM-A1 had no effect on myocardial contractility but caused significant coronary vasodilatation. Both cGMP and Na(+)/H(+) exchange appear to be involved in this effect but further work is needed to determine the relative contribution of each pathway in CO-mediated inotropic effect.
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