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The protective effect of tetrahydrobiopterin on rat hearts during long‐term hypothermic preservation
Author(s) -
Zheng Mingzhi,
ZHU Li,
CHEN Yingying,
SHEN Yueliang
Publication year - 2009
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.23.1_supplement.939.9
Subject(s) - tetrahydrobiopterin , nitric oxide , formazan , chemistry , anesthesia , ultrastructure , medicine , nitric oxide synthase , pharmacology , biochemistry , anatomy
Objective To assess the protective effect of tetrahydrobiopterin (BH4) on rat hearts suffered from long‐term hypothermic preservation. Methods The Langendorff model of isolated rat heart was used. Forty SD rat hearts were divided randomly into five groups ( n =8): control group, hypothermic preservation groups (preserved in celsior solution for 6 or 12 h), BH4 groups (preserved in celsior solution containing 20 μmol/L of BH4 for 6 or 12 h). The myocardial contents of formazan, nitric monoxide (NO), and malonaldehyde (MDA) were measured. The myocardial ultrastructure was observed by transmission electron microscope. Results Compared with control group, hypothermic preservation of isolated hearts for 6 or 12 h could reduce the formazan and NO contents, and increase the MDA contents of myocardium. BH4 partly inhibited the hypothermic preservation‐induced decrease in formazan and NO contents, and enhancement of MDA content ( P <0.05). After hypothermic preserved rat hearts for 6 or 12 h, the myocardial ultrastructure was impaired. Treatment with BH4 resulted in improvement in myocardial ultrastructure in hypothermic preserved hearts. Conclusion BH4 could reduce rat myocardial injury that induced by long‐term hypothermic preservation. The mechanism might be through the enhancement of myocardial NO production and inhibition of the generation of reactive oxygen species.