ArticlePflugers Archiv : European journal of physiology2003
Sepiapterin reduces postischemic injury in the rat heart.
Article in Pflugers Archiv : European journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 29 citations in OpenAlex.
- Nanomedicine-Based Therapeutics for Myocardial Ischemic/Reperfusion Injury.Advanced healthcare materials · 2023Review
- Multiple Shades of Gray-Macrophages in Acute Allograft Rejection.International journal of molecular sciences · 2023Review
- Endothelial cell-specific roles for tetrahydrobiopterin in myocardial function, cardiac hypertrophy, and response to myocardial ischemia-reperfusion injury.American journal of physiology. Heart and circulatory physiology · 2023Article
- L-sepiapterin restores SLE serum-induced markers of endothelial function in endothelial cells.Lupus science & medicine · 2019Article
- Reperfusion injury and reactive oxygen species: The evolution of a concept.Redox biology · 2015Review
- Liposomal tetrahydrobiopterin preserves eNOS coupling in the post-ischemic heart conferring in vivo cardioprotection.Journal of molecular and cellular cardiology · 2015Article
- Methylglyoxal modulates endothelial nitric oxide synthase-associated functions in EA.hy926 endothelial cells.Cardiovascular diabetology · 2013Article
- Novel strategies to ameliorate radiation injury: a possible role for tetrahydrobiopterin.Current drug targets · 2010Review
- Role of tetrahydrobiopterin in resistance to myocardial ischemia in Brown Norway and Dahl S rats.American journal of physiology. Heart and circulatory physiology · 2009Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A reduced availability of tetrahydrobiopterin (BH4), an essential cofactor for NO-synthesis, is causally involved in the development of endothelial dysfunction associated with ischemia/reperfusion. We, therefore, investigated the effect of sepiapterin, a substrate for BH4 synthesis, on postischemic injury in myocardial infarction and myocardial stunning. In rats, myocardial stunning was induced by repetitive ischemia (5 x 10-min ligature of the left coronary artery, 5 x 20-min reperfusion) and myocardial infarction by 50-min ligature and 60-min reperfusion. Myocardial blood flow was determined by H2-clearance, regional myocardial function by pulsed Doppler and infarct size by tetrazolium staining. Myeloperoxidase (MPO) activity was measured as a marker of neutrophil extravasation. cGMP was determined in rat serum as an indicator of increased NO synthesis. In animals treated with sepiapterin, regional myocardial function was significantly improved in both myocardial stunning and infarction and infarct size was significantly reduced. MPO activity decreased with sepiapterin treatment in both models. The systemic level of cGMP was reduced both following myocardial stunning and myocardial infarction in the control group. Pretreatment with sepiapterin induced a significant increase of cGMP level at the end of the protocol in both models. Substitution of sepiapterin reduces postischemic injury both in myocardial stunning and infarction apparently by ameliorating the availability of NO, thereby attenuating the activation of neutrophils in ischemia/reperfusion.
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