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Endogenous cytokine antagonists during myocardial ischemia and thrombolytic therapy
L Airaghi1, M Lettino, M G Manfredi
1Third Division of Internal Medicine, Ospedale Maggiore di Milano, Italy.
Abstract:
We tested the idea that cytokine antagonists are released during acute myocardial ischemia to counteract proinflammatory effects of cytokines. We investigated changes in plasma concentrations of the anticytokine molecules alpha-melanocyte-stimulating hormone (alpha-MSH), interleukin-1 receptor antagonist (IL-1ra), and soluble tumor necrosis factor receptor (sTNFr) in patients with acute myocardial infarction (AMI) or unstable angina (UA). Blood samples were collected at presentation in the coronary care unit, at 3-hour intervals for 24 hours, and daily for 4 days thereafter. There were no significant differences in the concentrations of cytokine antagonists in patients with AMI or UA. However, whereas concentrations of alpha-MSH were increased in early samples of patients with AMI or UA who were treated with a thrombolytic agent, they were consistently low in untreated patients. IL-1ra concentrations likewise were greater 3 and 6 hours after treatment in patients who underwent thrombolysis, whereas there was no significant difference in plasma sTNFr between the two groups. We suggest that during myocardial ischemia and thrombolysis anticytokine molecules released from the injured myocardium become available to reduce inflammation caused by cytokines and other mediators of inflammation.
Insights
During acute myocardial infarction (AMI) and unstable angina (UA), specific anticytokine molecules like alpha-melanocyte-stimulating hormone (alpha-MSH) and interleukin-1 receptor antagonist (IL-1ra) increase after thrombolytic treatment, suggesting a role in reducing inflammation.
Area of Science:
- Cardiology
- Immunology
- Biochemistry
Background:
- Acute myocardial infarction (AMI) and unstable angina (UA) involve inflammatory processes mediated by cytokines.
- Cytokine antagonists may be released during ischemia to mitigate these proinflammatory effects.
Purpose of the Study:
- To investigate plasma concentrations of anticytokine molecules in patients with AMI or UA.
- To determine if these antagonists change in response to thrombolytic therapy.
Main Methods:
- Plasma levels of alpha-melanocyte-stimulating hormone (alpha-MSH), interleukin-1 receptor antagonist (IL-1ra), and soluble tumor necrosis factor receptor (sTNFr) were measured.
- Blood samples were collected serially over 4 days in patients with AMI or UA, with and without thrombolytic treatment.
Main Results:
- No significant differences in overall cytokine antagonist concentrations were observed between AMI and UA patients.
- Alpha-MSH and IL-1ra levels increased significantly 3-6 hours post-thrombolysis in treated patients.
- Plasma sTNFr levels showed no significant difference between treated and untreated groups.
Conclusions:
- Myocardial ischemia and subsequent thrombolysis may lead to the release of anticytokine molecules from injured myocardium.
- These released molecules, including alpha-MSH and IL-1ra, may help reduce inflammation associated with myocardial infarction and its treatment.