TY - JOUR
T1 - Endogenous cytokine antagonists during myocardial ischemia and thrombolytic therapy
AU - Airaghi, Lorena
AU - Lettino, Maddalena
AU - Manfredi, Maria Grazia
AU - Lipton, James Matthew
AU - Catania, Anna
PY - 1995
Y1 - 1995
N2 - 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 α-melanocyte-stimulating hormone (α-MSH), interleukin-1 receptor antagonist (IL-1 ra), 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 α-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-1 ra 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.
AB - 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 α-melanocyte-stimulating hormone (α-MSH), interleukin-1 receptor antagonist (IL-1 ra), 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 α-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-1 ra 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.
UR - http://www.scopus.com/inward/record.url?scp=0029146204&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0029146204&partnerID=8YFLogxK
U2 - 10.1016/0002-8703(95)90430-1
DO - 10.1016/0002-8703(95)90430-1
M3 - Article
C2 - 7631597
AN - SCOPUS:0029146204
VL - 130
SP - 204
EP - 211
JO - American Heart Journal
JF - American Heart Journal
SN - 0002-8703
IS - 2
ER -