Related Experiment Video
Updated: Jan 24, 2026
Myocardial Infarction and Functional Outcome Assessment in Pigs
Published on: April 25, 2014
[Dynamics of brain CD68+ and stabilin-1+ macrophage infiltration in patients with myocardial infarction]
M S Rebenkova1, A E Gombozhapova1, Yu V Rogovskaya1
1Tomsk National Research Medical Center of the Russian Academy of Science; National Research Tomsk State University.
Insights
Brain macrophage infiltration increases significantly within 72 hours of myocardial infarction (MI). CD68+ macrophage levels in the brain correlate with those in the heart, but M2-like stabilin-1+ macrophages do not change.
Area of Science:
- Neuroimmunology
- Cardiovascular Pathology
- Inflammatory Response
Background:
- Myocardial infarction (MI) is a critical cardiovascular event.
- The role of brain immune cell dynamics in MI pathogenesis is not fully understood.
- Macrophage infiltration in the brain may influence outcomes post-MI.
Purpose of the Study:
- To investigate the temporal changes in brain macrophage populations following fatal Type 1 MI.
- To differentiate between general macrophage markers (CD68+) and M2-like macrophages (stabilin-1+) in the brain post-MI.
- To explore correlations between brain and myocardial macrophage infiltration.
Main Methods:
- Immunohistochemical analysis of brain tissue from 31 fatal MI patients and 10 controls.
- Patients were grouped based on time of death: within 72 hours (Group 1) or 4-28 days (Group 2) post-MI.
- CD68 used as a pan-macrophage marker; stabilin-1 as an M2-like macrophage marker.
Main Results:
- CD68+ macrophage infiltration in the brain was significantly elevated in Group 1 compared to controls.
- Brain CD68+ cells were lower in Group 2 than Group 1 but higher than controls.
- Stabilin-1+ macrophages showed minimal presence and no significant difference between MI groups and controls.
- Positive correlation found between CD68+ macrophages in the brain and myocardium.
Conclusions:
- Brain CD68+ macrophage numbers significantly increase within the initial 72 hours of Type 1 MI.
- Stabilin-1+ macrophage levels in the brain remain unchanged and do not differ from controls.
- A direct correlation exists between CD68+ macrophage infiltration in the brain and myocardium post-MI.
Abstract:
Te aim of the study was to evaluate the temporal dynamics of brain CD68+ and stabilin-1+ macrophage infltration in patients with fatal myocardial infarction (MI) type 1.
Materials And Methods:
Te study included 31 patients with fatal MI type I. Te control group comprised 10 patients of 18-40 age group who died from injuries incompatible with life. Patients with MI were divided into two groups. Group 1 comprised patients who died during the frst 72 hours of MI, group 2 comprised patients who died on days 4‒28. Macrophage infltration in the brain was assessed by immunohistochemical analysis. We used CD68 as a marker for the cells of the macrophage lineage and stabilin-1 as an M2-like macrophage biomarker.
Results:
In group 1 the number of brain CD68+ macrophages was signifcantly higher than in the control group. In group 2 the intensity of brain CD68+ cells infltration was lower than in group 1 and higher than in the control group. Tere was a small amount of stabilin-1+ macrophages in the brain of healthy people, as well as of patients who died from MI. Tere were no signifcant differences in the number of stabilin-1+ cells between group 1 and group 2. Correlation analysis revealed the presence of positive correlation between the number of CD68 + macrophages in the infarct, peri-infarct, and non-infarct areas of the myocardium and the number of CD68+ macrophages in the brain in patients with MI. Tere were not correlations between the number of CD68 + and stabilin-1+ cells and the presence of diabetes mellitus, history of stroke, history of MI, and pre-infarction angina.
Conclusion:
Te number of brain CD68+ macrophages signifcantly increased during the frst three days of MI. Te number of brain stabilin-1+ macrophages did not increase and did not differ from the control values. We observed a positive correlation between the number of CD68+ macrophages in the brain and myocardium.
Related Concept Videos
02:20Dynamic Equilibrium
02:15SN1 Reaction: Stereochemistry
In the first step of an SN1 reaction, the bond between the electrophilic carbon and the leaving group ionizes to generate the carbocation intermediate. The second step of the mechanism is the nucleophilic attack.
In the formed carbocation, the positively charged carbon is sp2 hybridized with a trigonal planar geometry. As all the three substituents lie on the same plane, a plane of symmetry for the...
02:05SN1 Reaction: Kinetics
However, Sir Christopher Ingold and Edward D. Hughes, who studied the kinetics of various nucleophilic substitution reactions, noticed that a tertiary alkyl halide does undergo a nucleophilic substitution reaction in the presence of a weak nucleophile. While studying the substitution...
02:25SN1 Reaction: Mechanism
Firstly, the haloalkane ionizes to generate a carbocation intermediate and a halide ion. This heterolytic cleavage is highly endothermic with large activation energy. The ionization of the substrate, facilitated by a...
02:42Acidity of 1-Alkynes
The acidic strength of hydrocarbons follows the order: Alkynes > Alkenes > Alkanes. The strength of an acid is commonly expressed in units of pKa — the lower the pKa, the stronger the acid. Among the hydrocarbons, terminal alkynes have lower pKa values and are, therefore, more acidic. For example, the pKa values for ethane, ethene, and acetylene are 51, 44, and 25, respectively, as shown here.
02:27Predicting Products: SN1 vs. SN2
With increased substitution on the alkyl halide,...