Survival of the ischemic brain: a progress report.
The number of patients with cerebral infarctions increases as the population ages, despite campaigns against hypertension, the greatest risk factor. Cerebral ischemia initiates events that are presumed to defer the stage of irreversible injury. These events cause an increase of perfusion around the central ischemic zone and trigger the Bohr effect, both of which preserve tissue viability. Almost simultaneously, mitochondrial function fails, resulting in insufficient energy for the enzyme systems to control Na and K ion equilibrium. At the same time, protein synthesis slows and cellular respiratory enzymes decrease their activity, initiating an irreversible state of tissue change. Tissue fatty acids increase as a result of dissolution of cell membrane lipoprotein structure. Barbiturates reduce the extent of experimental infarction. Resperine and aminophylline are also effective, but there are no corroborative clinical trials. That ischemic brain damage may be the result of toxic substances in the ischemic tissue represents a new concept.
D000255:Adenosine Triphosphate / Q000378:metabolism; D001786:Blood Glucose; D001921:Brain / Q000098:blood supply; D002545:Brain Ischemia / Q000401:mortality* / Q000473:pathology; D002561:Cerebrovascular Disorders / Q000378:metabolism; D000242:Cyclic AMP / Q000096:biosynthesis; D006706:Homeostasis; D006801:Humans; D009638:Norepinephrine / Q000378:metabolism; D010100:Oxygen / Q000097:blood
D001786:Blood Glucose; D000255:Adenosine Triphosphate; D000242:Cyclic AMP; D010100:Oxygen; D009638:Norepinephrine