Inflammatory Reaction after Brain Damage and Prospective Therapy Against Damage Impending Cerebral Infarction

• Published in: Keio journal of medicine Vol. 45; no. 3; pp. 270 - 274
• Main Authors: Kogure, Kyuya, Yamasaki, Yasundo, Matsuo, Yoshiyuki
• Format: Journal Article
• Language: English
• Published: Japan The Keio Journal of Medicine 1996
• Subjects: adhesion molecule; Animals; Brain Ischemia - complications; Brain Ischemia - drug therapy; Cerebral Infarction - prevention & control; cerebral ischemia; Humans; Neuritis - etiology; Neuroprotective Agents - therapeutic use; phospholipase A2; platelet activating factor; thromboxane
• ISSN: 0022-9717; 1880-1293
• DOI: 10.2302/kjm.45.270

Cytokines which promote emigration of leukocytes from the vascular lumen into the injured brain tissue are produced at the site of incipient cerebral infarction. The blood-borne invaders then accelerate the decomposition of brain cells by their toxic by-products, phagocytic action, and by the immune reaction. Recently accumulated data in our laboratories and other research facilities show that depleting the amount of circulating leukocytes or administering anti-inflammatory chemicals such as cytokine blocking agents, anti-adhesion molecule antibodies, and immunosuppressants effectively minimize the size of ischemia induced cerebral infarction. Based on the fact that leukocyte invasion of the affected brain tissue occurs 6 to 24 hours after onset of ischemia, administration of an anti-inflammatory therapy may widen the therapeutic window against stroke.