Microcirculatory Stasis in the Brain: Proceedings of the Symposium Held in Tokyo, Japan, 20-21 May 1993(v. 1031 International Congress S.)

Microcirculatory stasis is one of the most unclarified fields. This book aims to define this subject, giving a better understanding of ischemic tissue damage. It includes contributions from distinguished experts in the field of brain research as well as the basic sciences covering nonbrain fields, and consists of four major themes: blood events., vessel changes, feedback from ischemically damaged tissue, and clinical relevance. It will be of great value to all those involved in brain research, and will help to establish improved means of treating stroke patients.

Table of Contents:
Limitation of space allows only a selection of papers to be mentioned Preface. List of active participants. List of abbreviations. Presidential Address. Microcirculatory stasis in the brain (M. Tomita). Blood Rheological Disturbance. Microvascular stasis caused by deranged blood flow structure in microvessels (G. Mchedlishvili). Hemorheological changes during low shear flow: causes or consequences of stasis? (P. Gaehtgens). Brain capillary perfusion at reduced perfusion pressure (W. Kuschinsky, H. Theilen). Cerebral blood flow heterogeneity does not involve vascular recruitment (S.C. Jones et al.). Chronic changes of the rat pial microcirculation caused by reduction of the arterio-venous pressure gradient: effects on hemodynamics, morphology and reactivity of the microvessels (K. Irikura et al.). Endothelium-blood Corpuscle Interactions. Leukocytes and endothelial cells: adhesion and cytotoxicity (G.W. Schmid-Schonbein et al). White cell involvement in cerebral ischemia and reperfusion injury (R.E Tuma et al.). Factors contributing to progressive hypoperfusion following middle cerebral artery occlusion in the rat (J.H. Garcia et al). Current evidence on leukocyte/endothelial interactions in cerebral ischemia (L. Schurer et al). Mechanism of endothelial cell injury by activated leukocytes: involvement of cell adhesion molecules LFA- i and ICAM- I (S. Murota et al). Involvement of the Microvascular Wall. Endothelial injury and transient ischemic attack: a new theory based on new evidence (W.I. Rosenblum). Ultrastructural features of altered cerebrovascular permeability: structural/functional relationships (J.T. Povlishock, M. Kapasia). Experimental model of endothelial injury of common carotid artery and subsequent thrombosis in mongolian gerbils (H. Nishimura et al). Cerebral microcirculatory changes after microsphere embolization with relation to microsphere flow measurement (T. Yamakawa et al.). Microcirculatory consequences of collateral circulation during arterial occlusion: implications for a penumbra (M.G. Muhonen et al). Ischemic Tissue Damage and Chemical Mediators. Can the glutamate cascade contribute to microcirculatory stasis? (D.W. Choi). Mediators inducing stasis in cerebral microvessels during ischemia (M. Wahl, L. Schilling). Swelling and damage of glial cells by arachidonic acid (F. Staub et al.). Flow thresholds for amino acid transmitter and purine catabolite elevation in experimental ischemia (R. Graf et al). Modulation of transmitter release in cerebral ischemia (H. Ooboshi et al). Physical Factors and Other Topics. Excitotoxicity and ischemia in the rat brain studied in vivo with high resolution magnetic resonance imaging (H. Benveniste, G.A. Johnson). Perfusion-sensitive MRI of hyponatremic encephalopathy (T.P.L. Roberts et al.). Loss of facilitation of hydrogen gas diffusion in asphyxiated cultured glial cell suspensions (M. Tomita et al.).