title: [Effect of 17beta-estradiol on myocardial inducible NOS and endothelial NOS activities after ischemia-reperfusion in rat heart model].
abstract: OBJECTIVE
  To study the effect of 17beta-estradiol (E(2)) on myocardial inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS) activities of ischemia-reperfusion myocardium in rat model.
  
  
  METHODS
  40 Langendorff perfused hearts isolated from bilateral ovariectomy (OVX) rat were randomly divided into four groups: control group (Group C), in which hearts were reperfused ex vivo for 15 minutes before ischemia in rat; ischemia-reperfusion control (Group I-R), in which modified St. Thomas II cardioplegic solution was perfused to perform the ischemia-reperfusion; dissolved control group (Group D), in which 0.1% dimethyl sulfoxide (DMSO) was dissolved in cardioplegic solution; E(2) group (Group E), in which 0.1% DMSO and 5 micromol of E(2) were dissolved in cardioplegic solution. Myocardial iNOS and eNOS activities were detected before and after reperfusion. Creatine phosphokinase (CPK), lactic dehydrogenase (LDH) and nitric oxide (NO) of coronary flow were measured, and heart function was evaluated to observe the effect of E(2) on myocardial ischemia-reperfusion injury (MIRI).
  
  
  RESULTS
  Myocardial eNOS activity declined (P < 0.01) and iNOS activity increased after ischemia-reperfusion (8.87 +/- 3.74 nmol/min/g in Group C, 15.83 +/- 2.42 nmol/min/g in Group I-R, 17.60 +/- 5.21 nmol/min/g in Group E; P < 0.01), moreover, iNOS activity was much higher in Group E (25.85 +/- 5.21 nmol/min/g, P < 0.01). NO production was lower in Group I-R and Group D (P < 0.05), and higher in Group E (30.96 +/- 4.91 micromol/L in Group C, 33.16 +/- 5.57 micromol/L in Group E; P < 0.01). CPK and LDH were lower in Group E (P < 0.05). Recovery of heart function was better in Group E (P < 0.05).
  
  
  CONCLUSIONS
  E(2) can relieve the injury of MIRI and promote heart function recovery by increasing iNOS activity and NO production.
authors.affiliation: Department of Cardiothoracic Surgery, Aerospace Central Hospital, Beijing 100049, China.
authors.forename: Xu-dong
authors.initials: XD
authors.lastname: Wang
authors.forename: Zhan-ming
authors.initials: ZM
authors.lastname: Wang
authors.forename: Dong-lin
authors.initials: DL
authors.lastname: Jia
authors.forename: Peng
authors.initials: P
authors.lastname: Yu
mesh_terms: D000818:Animals; D003326:Coronary Circulation / Q000187:drug effects; D003402:Creatine Kinase / Q000378:metabolism; D004195:Disease Models, Animal; D004958:Estradiol / Q000494:pharmacology*; D005260:Female; D006321:Heart / Q000187:drug effects / Q000503:physiopathology; D066298:In Vitro Techniques; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology*; D009206:Myocardium / Q000201:enzymology / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism*; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar
chemical_list: D009569:Nitric Oxide; D004958:Estradiol; D007770:L-Lactate Dehydrogenase; D052247:Nitric Oxide Synthase Type II; D052250:Nitric Oxide Synthase Type III; D003402:Creatine Kinase