title: The role of microthrombi and microcirculatory factors in localization and evolution of focal cerebral ischemia.
abstract: Ischemic cerebral infarction is caused primarily by occlusion of a large arterial vessel. Local circulatory disturbances in the center of ischemic tissue and in ischemic penumbra and the degree of sensitivity to ischemia in different brain regions influence subsequent ischemic progression. Postischemic recirculation is impaired by hemodynamic disturbances and formation of microthrombi, hemorrheologic changes and degeneratively altered vessels of microcirculation. Increased postischemic coagulation can be demonstrated in laboratory tests of few minutes extending up to two weeks after the onset of ischemia. Morphological observations on microthrombi after experimental focal ischemia as well as in patients with cerebral infarction show that formation of microthrombi is dependent on the duration of ischemia and the extent of infarcted tissue. Microthrombi are most prevalent in early stages of tissue damage. This suggests that microthrombi have an effect on the progression of ischemic necrosis. On the basis of our results, we can state that 1) microcirculatory disturbances are triggered by focal cerebral ischemia, 2) formation of microthrombi is a contributing factor to the evolution of postischemic microcirculatory disturbances, and 3) microthrombi promote the progression of ischemic necrosis.
authors.affiliation: Institute of Neuropathology, Free University of Berlin, Fed. Rep. of Germany.
authors.forename: N
authors.initials: N
authors.lastname: Heye
authors.forename: C
authors.initials: C
authors.lastname: Paetzold
authors.forename: J
authors.initials: J
authors.lastname: Cervós-Navarro
mesh_terms: D000818:Animals; D004730:Endothelium, Vascular / Q000648:ultrastructure; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D002542:Intracranial Embolism and Thrombosis / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D002546:Ischemic Attack, Transient / Q000097:blood / Q000473:pathology / Q000503:physiopathology*