[The effect of alphamethyltyrosine on cerebral vascular occlusive disease (author's transl)].
A double blind prospective study of the modification by alphamethyltyrosine (AMT) of experimental occulusion of the middle celebral artery (MCA) was performed on squirrel monkeys.  The transorbital microsurgical technique was employed to expose the origin of the left MCA.  A miniture Levis-Scoville clip was placed on the left MCA for 3 hours.  Thirteen monkeys were given 10 ml/kg of 2% AMT solution approximately on hour prior to occlusion and just after revascularization.  Thirteen control monkeys were given an equal volume of normal saline.  After the removal of hte clip, detailed evaluation of neurological condition was recored every hour for 6 hours and at frequent intervals thereafter until the monkey expired or was sacrificed.  The brain was perfused with biological carbon/saline solution and fixed glutaraldehyde using catheters placed in both common carotoid arteries.  Brain samples were cut to 100 microns and examined with a light microscope.  Immediately after the clip was placed on the MCA, all the animals demonstrated severe hemiparesis or hemiplegis of the contralateral side.  When the clip was removed gradual recovery of function of the right side occured over a period of several hours.  How,ever recovery was less complete in the control group, and even with seeming fair recovery of function in some animals, sudden death occured within 24 hours.  Ten of the thirteen controls expired within 24 hours but only 2 AMT treated animals expired within 6 hours.  Changes in blood pressure and gases due to AMT were negligible.  In gross and microscopic examination, considerable brain edema with midline shift to the the contralateral side was observed in all untreated animals 6 hours after revascularization.  Leakage of carbon, indicating microvasculature damage, occured in the infarcted areas and in the surrounding tissues.  The sam degree of brain edema and infarction was observed in the AMT treated animals which were died within 6 hours after revascularization.  Better  perfusion with carbon black and less edema were, however, seen in other AMT treated animals 6 afters after revacularization...
D000818:Animals; D001921:Brain / Q000187:drug effects / Q000473:pathology; D001923:Brain Chemistry; D001929:Brain Edema / Q000473:pathology; D002561:Cerebrovascular Disorders / Q000188:drug therapy* / Q000473:pathology; D003404:Creatinine / Q000097:blood; D004298:Dopamine / Q000032:analysis; D000882:Haplorhini; D006651:Histocytochemistry; D008781:Methyltyrosines / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D009638:Norepinephrine / Q000032:analysis
D008781:Methyltyrosines; D003404:Creatinine; D004298:Dopamine; D009638:Norepinephrine