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Mechanism of cardioprotective effects of S‐nitrosothiols in rat hearts
Author(s) -
Novalija Enis,
Broniowska Katarzyna,
Novalija Jutta,
Hogg Neil
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a451
Subject(s) - chemistry , ischemia , pharmacology , mechanism of action , necrosis , free radical scavenger , scavenger , biochemistry , antioxidant , medicine , biology , in vitro
Low molecular weight S‐nitrosothiols (RSNO) have been observed in many biological systems and as a posttranslational event may be an important cellular regulatory mechanism. 1 We investigated whether exposure to RSNO may attenuate postischemic contractile dysfunction and limit necrosis after 30 min of global, no‐flow ischemia, and if the action of amino acid transport system L (L‐AT) is required. 2 Isolated (9–12 weeks‐old Wistar male) rat hearts ( n = 40) were exposed to S‐nitrosocysteine (CysNO, 10 μM) for 30 minutes with/without AT‐L competitor L‐leucine (L‐Leu, 1 mM) or NO scavenger oxyhemoglobin (oxyHb, 20 μM) prior to prolonged ischemia. Cardiac function was assessed during 120 min of reperfusion using the Langendorff model. We found that functional recovery (rate‐pressure product, mmHg/min) was significantly improved in CysNO ± oxyHb groups compared to hearts in CysNO + L‐Leu and control groups ( P < 0.05). Necrosis, measured by triphenyltetrazolium chloride staining, was significantly reduced in CysNO ± oxyHb hearts ( P < 0.05). This study demonstrated that exposure to RSNO before ischemia improves postischemic contractile dysfunction and attenuates necrosis. Mechanism of cardioprotective effects of S‐nitrosothiols requires the action of L‐AT. Supported in part by grant No. PO1GM066730 (EN) and GM55792 (NH) from the National Institutes of Health.