Amelioration of post-ischemic brain damage with barbiturates.
Author(s) -
Peter Šafář
Publication year - 1980
Publication title -
stroke
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.397
H-Index - 319
eISSN - 1524-4628
pISSN - 0039-2499
DOI - 10.1161/01.str.11.5.565
Subject(s) - medicine , resuscitation , anesthesia , cardiopulmonary resuscitation
PERHAPS THERE IS NO major pathological state so profound in its damaging effects on the sufferer, on his family, and on society as the brain injury produced by cardiac arrest, ischemic stroke, or other anoxic states. Thus, there is great interest among physicians and the lay public in experimental results which suggest a protective effect against brain damage after either focal or global brain ischemia by the use of barbiturate administration," measures to increase blood flow' n or subject immobilization with controlled ventilation.' 12 These experimental results have also increased interest in what might be called "therapeutic anesthesia" programs expanding cardiopulmonary resuscitation (CPR) and cardiopulmonary-cerebral resuscitation (CPCR) procedures and the possibility of improved brain survival in a variety of injurious processes. The potential importance of these experimental results is obvious, but confusion and controversy have arisen because of incautious conclusions drawn from comparisons of experimental results with different animal models, treatment regimens, and post-insult management. In this brief overview the present status of barbiturate therapy in anoxic-ischemic brain injury will be described. When interpreting experiments or analyzing clinical situations, one must keep in mind the sometimes subtle but nonetheless distinct differences between the kinds of injury that may be produced in the brain by ischemia, anoxia, hypoglycemia, anemia, trauma, hemorrhage, metabolic or toxic abnormalities, inflammation, or by different combinations of these processes. Furthermore, with ischemic insults there are important distinctions between global ischemia as in shock states or cardiac arrest and the focal ischemia of transient or permanent embolic occlusion with cerebral infarction. There are also important differences between reduced flow states such as in shock and the total cessation of flow with cardiac arrest. In considering therapeutic measures, there is an obvious but sometimes overlooked distinction
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