Related Experiment Video
Updated: May 13, 2026

Confirmation of Myocardial Ischemia and Reperfusion Injury in Mice Using Surface Pad Electrocardiography
Published on: November 24, 2016
Early accumulation of the terminal complement-complex in the ischaemic myocardium after reperfusion
D Mathey1, J Schofer, H J Schäfer
1Department of Cardiology, University Hospital Eppendorf, Hamburg, Germany.
Insights
Complement complex C5b-9 accumulates late in infarcted myocardium without reperfusion. With reperfusion, C5b-9 deposition occurs rapidly, suggesting a role in myocardial reperfusion injury.
Area of Science:
- Cardiovascular Research
- Immunology
- Pathology
Background:
- The terminal complement complex C5b-9 (also known as the membrane attack complex) is implicated in tissue damage.
- Its accumulation in infarcted myocardium suggests a role in myocardial infarction pathogenesis.
Purpose of the Study:
- To investigate the time course of C5b-9 deposition in experimental myocardial infarction.
- To determine the influence of reperfusion on C5b-9 accumulation in the infarcted heart.
Main Methods:
- Experimental myocardial infarction was induced in rabbits by coronary artery occlusion.
- Groups were subjected to either prolonged occlusion without reperfusion or shorter occlusion followed by reperfusion.
- C5b-9 deposition was quantified using immunohistochemistry and ELISA on myocardial biopsies.
Main Results:
- In the absence of reperfusion, C5b-9 accumulation was a late event, observed after 5-6 hours of ischemia.
- In the presence of reperfusion, significant C5b-9 deposition was detected as early as 30 minutes after ischemia onset.
- This indicates reperfusion accelerates C5b-9 deposition in ischemic myocardium.
Conclusions:
- C5b-9 accumulation occurs late in myocardial infarction when tissue is largely necrotic if reperfusion is absent.
- Rapid C5b-9 deposition during ischemia-reperfusion suggests the complement system activation plays a significant role in reperfusion injury.
- These findings highlight the complement system's involvement in the pathophysiology of myocardial infarction and reperfusion injury.
Abstract:
The terminal, membrane-damaging complement complex C5b-9 accumulates in the infarcted myocardium. In experimental myocardial infarction, we investigated the time course of C5b-9 deposition and the influence of reperfusion. In a group of 17 rabbits (group 1), the circumflex coronary artery was occluded for different time periods ranging from 0.5 to 29 h without subsequent reperfusion. A second group of 23 rabbits (group 2) underwent coronary artery occlusion for periods ranging from 0.5 to 6 h followed by reperfusion. C5b-9 was determined in transmural myocardial biopsies by immunohistochemistry and by ELISA. In group 1, C5b-9 accumulation in the ischaemic myocardium was found only after 5 to 6 h of coronary artery occlusion. In group 2 (ischaemia and reperfusion), significant C5b-9 deposition was already observed after 30 min of myocardial ischaemia. We conclude that in the absence of reperfusion C5b-9 accumulation occurs as a late event when most of the jeopardized myocardium has probably already become necrotic. In the presence of reperfusion, however, the complement system is activated rapidly and this could play a role in the pathogenesis of reperfusion injury.
More Related Videos
06:38Simultaneous 3D Analysis of Cardiac Damage and Immune Response in Reperfused Acute Myocardial Infarction Using Light Sheet Fluorescence Microscopy
Published on: September 26, 2025
11:17A Microscopic 2,3,5-Triphenyltetrazolium Chloride Assay for Accurate and Reliable Analysis of Myocardial Injury
Published on: November 28, 2025
Related Concept Videos
Formation of the Platelet Plug
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
Blood Studies for Cardiovascular System I: Cardiac Biomarkers
The essential diagnostic tools for detecting myocardial necrosis and monitoring individuals suspected of having acute coronary syndrome (ACS) include:
Troponins
Troponins, particularly cardiac troponins I and T, are the most precise and sensitive markers of myocardial injury. They are detectable within 4-6 hours of myocardial injury and remain...
Myocarditis I: Introduction
Acute Coronary Syndrome I: Introduction
Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations
Acute Coronary Syndrome III: Diagnostic Studies