Polymorphonuclear leukocyte accumulation in brain regions with low blood flow during the early postischemic period.

Abstract

In an anesthetized canine model in which ischemia was induced by incremental air embo-lism, 16 animals were exposed to 1 hr of ischemia and monitored for 10 min (n = 4), 60 min (n = 6), or 240 min (n = 6). Fourteen animals were observed for corresponding periods without being subjected to ischemia 70 min (n = 4), 120 min (n = 4), or 300 min (n = 6). Autologous granulocytes were labeled with '"in and reinfused just before ischemia. At the conclusion of each experiment, a M C-iodoantipyrine autoradiographic blood flow study was performed. Granulocyte accumulation measured by gamma scintig-raphy (cpm/gm) occurred in the injured hemisphere of ischemic animals at 60 min in anterior brain segments and at 240 min in anterior, middle, and posterior segments. By means of a double-label autoradiography technique, clustering of punctate granulocyte images was detected in regions of low flow or heterogeneous flow in half of the animals at both 60 min and 240 min post ischemia. Granulocyte clustering did not occur in the autoradiograms of nonischemic animals. The results implicate granulocyte participation hi the acute phase of ischemic brain injury and signal a convergence of hemostatk and inflammatory processes during the immediate postischemic period.

Pathophysiology of Cerebral Ischemia and Brain Trauma: Similarities and Differences

“…Leukocytes may contribute to stroke damage by re-occluding vessels after reperfusion or by entering infarcted tissue and exacerbating cell death through cytotoxic interactions (del Zoppo, 1997). Evidence that leukocytes may contribute to infarction has been obtained by many investigators (Barone et al, 1991;Hallenbeck et al, 1986;Zhang et al, 1994).…”

“…However, with longer ischemic periods, other cellular responses can be observed, ultimately producing ischemic infarction (Petito et al, 1982). With reperfusion injury, damage to cerebral blood vessels and the activation of inflammatory processes can produce hemorrhagic transformation of infarcted tissue and severe brain swelling (del Zoppo and Mabuchi, 2003;Hallenbeck et al, 1986).…”

Attenuation of Ischemic Inflammatory Response in Mouse Brain Using an Adenoviral Vector to Induce Overexpression of Interleukin-1 Receptor Antagonist

“…Key Words: lmmunohistochemis try-Ischemia-Mice-Middle cerebral artery occlusion Myeloperoxidase-Neutrophil. after experimental stroke was demonstrated in 1974 (Garcia and Kamijyo, 1974). Using indium-Ill-labeled autologous PMNL in a model of air embolism-induced cerebral ischemia in dogs, Hallenbeck et al (1986) con firmed that PMNL accumulate progressively during the first 4 hours of reperfusion. Much of the research litera ture has demonstrated that brain injury caused by isch emia and reperfusion can be attenuated by PMNL deple tion (del Zoppo et aI., 1991;Dutka et aI., 1989;Shiga et aI., 1991), Schurer et al (1990) showed that antineutro phil serum blocks brain injury after reversible bilateral carotid artery occlusion in rats.…”

Antibody to intercellular adhesion molecule 1 protects the kidney against ischemic injury.

“…Neutrophils accumulate in various organs (16,17) including the kidney (3) after ischemia/reperfusion. Neutropenia decreases renal ischemia/reperfusion injury in some studies (3, 7) but not in others (18,19).…”