Document Detail

Influence of the terminal complement-complex on reperfusion injury, no-reflow and arrhythmias: a comparison between C6-competent and C6-deficient rabbits.
MedLine Citation:
PMID:  8796116     Owner:  NLM     Status:  MEDLINE    
OBJECTIVE: The complement system has been suggested to play a role in reperfusion injury which may result from an enhanced destruction of myocardial tissue or from an impairment of reflow. We investigated the influence of the C5b-9 complement complex on infarct size, reflow and arrhythmogenesis. METHODS: Twenty-eight C6-competent rabbits and 18 rabbits with congenital C6 deficiency were subjected to either 30 min or 2 h of coronary artery occlusion followed by reperfusion. C6 deficiency was confirmed by the complement titration test and immunohistology. The triphenyl tetrazolium chloride method was used to delineate infarct size. Reflow into infarcted areas was evaluated histologically after an in vivo injection of propidium iodide which served as an early fluorescence microscopic marker of damaged myocardium subjected to reflow. Continuous ECG monitoring allowed the recording of arrhythmias. RESULTS: After 30 min of coronary artery occlusion infarct size was significantly smaller in C6-deficient rabbits (5.0 +/- 2% of the risk region) as compared to C6-competent rabbits (28.4 +/- 8.5%, P = 0.0371). The extent of reflow into damaged myocardium was nearly the same in both animal groups at this time (38 +/- 9 vs. 39 +/- 7% of the risk region). After 2 h of coronary artery occlusion, infarct size was not different between both animal groups, but the extent of reflow into damaged myocardium was significantly smaller in C6-competent rabbits than in C6-deficient rabbits (25 +/- 4 vs. 40 +/- 4%; P = 0.0185). Two of the 18 C6-deficient rabbits had ventricular arrhythmias (Lown II-IV), none of which was fatal. Eleven of the 28 C6-competent animals had major ventricular arrhythmias which were fatal in 6 rabbits. CONCLUSIONS: These results suggest that the lytic C5b-9 complement complex leads to reperfusion injury in the early phase (30 min) of ischaemia, resulting in a larger infarct. After 2 h of ischaemia, complement activation enhances the no-reflow phenomenon but does not affect infarct size. Finally, the C6 status seems to influence the susceptibility to ventricular arrhythmias after coronary artery occlusion, independent of reperfusion.
W Ito; H J Schäfer; S Bhakdi; R Klask; S Hansen; S Schaarschmidt; J Schofer; F Hugo; T Hamdoch; D Mathey
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Cardiovascular research     Volume:  32     ISSN:  0008-6363     ISO Abbreviation:  Cardiovasc. Res.     Publication Date:  1996 Aug 
Date Detail:
Created Date:  1997-01-28     Completed Date:  1997-01-28     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0077427     Medline TA:  Cardiovasc Res     Country:  NETHERLANDS    
Other Details:
Languages:  eng     Pagination:  294-305     Citation Subset:  IM    
Department of Cardiology, University Hospital Eppendorf, Hamburg, Germany.
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MeSH Terms
Arrhythmias, Cardiac / immunology,  physiopathology
Complement Activation*
Complement C6 / deficiency*
Complement Membrane Attack Complex / analysis*
Myocardial Infarction / immunology*,  physiopathology
Myocardial Reperfusion Injury / immunology*,  physiopathology
Regional Blood Flow
Time Factors
Reg. No./Substance:
0/Complement C6; 0/Complement Membrane Attack Complex
Comment In:
Cardiovasc Res. 1997 Feb;33(2):495-6   [PMID:  9074715 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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