title: CD59 prevents human complement-mediated injuries in isolated guinea pig hearts.
abstract: OBJECTIVE
  To assess complement-mediated myocardial injury on isolated guinea pig working hearts and cardioprotective effects of CD59.
  
  
  METHODS
  Using a modified Langendorff apparatus, isolated guinea-pig working hearts were perfused with a modified Krebs Henseleit buffer containing 3% heat-inactivated human plasma and zymosan (IPZ) (control) (n = 10), 3% normal human plasma and zymosan (NPZ) (n = 10), or 3% normal human plasma and zymosan and 1.5 microg/ml CD59 (NPZC) (n = 10), respectively. Epicardial electrocardiogram (ECG), cardiac output (CO), coronary arterial flow (CF), maximum left ventricular developed pressure (LVP(max)), maximum left ventricular developed pressure increase rate (+ dp/dt(max)), maximum left ventricular developed pressure decrease rate (- dp/dt(max)) and heart rate (HR) were recorded at 0, 15, 30, 45 and 60 min of treatment. After the experiment, immunohistochemical examination was performed to detect the presence of C3a or C5b-9 in the myocardium of the isolated hearts.
  
  
  RESULTS
  Compared the IPZ group, hearts treated with NPZ showed a slight depression on ST segments of epicardial ECG at 15 min, a significant elevation between 30 min to 60 min, a decrease in CF, CO, LVP(max), + dp/dt(max) and - dp/dt(max), and an increase in HR at 15 min. The observed alterations in CF, CO, LVP(max), + dp/dt(max) and - dp/dt(max) remained decreased, while the HR remained increased until the end of the protocol. The all above parameters of hearts treated with NPZC were similar to the control group (IPZ) at any given time. Immunohistochemical examination showed positive signals of C3a and C5b-9 in the myocardium of hearts treated with NPZ. C3a was positive in NPZC, and C3a and C5b-9 were negative in IPZ.
  
  
  CONCLUSIONS
  Activated human complements directly damage isolated guinea pig working hearts, and CD59 offers a significant protection against the injuries.
authors.affiliation: Department of Cardiology, First Affiliated Hospital, Sun Yat-sen University of Medical Sciences (SUMS), Guangzhou 510080, China. wusuhua@163.net
authors.forename: Suhua
authors.initials: S
authors.lastname: Wu
authors.forename: Hong
authors.initials: H
authors.lastname: Ma
authors.forename: Shoujian
authors.initials: S
authors.lastname: Huang
authors.forename: Yigang
authors.initials: Y
authors.lastname: Dong
authors.forename: Chukuan
authors.initials: C
authors.lastname: Wu
authors.forename: Jiajing
authors.initials: J
authors.lastname: Shun
mesh_terms: D000818:Animals; D018957:CD59 Antigens / Q000494:pharmacology*; D015926:Complement C3a / Q000037:antagonists & inhibitors* / Q000378:metabolism; D003169:Complement Inactivator Proteins / Q000494:pharmacology*; D004562:Electrocardiography; D006168:Guinea Pigs; D006321:Heart / Q000187:drug effects* / Q000502:physiology; D007150:Immunohistochemistry; D066298:In Vitro Techniques; D008297:Male; D009206:Myocardium / Q000378:metabolism / Q000473:pathology*; D013997:Time Factors
chemical_list: D018957:CD59 Antigens; D003169:Complement Inactivator Proteins; D015926:Complement C3a