Disturbances of biogenic amines and other putative neurotransmitters due to disorders of energy-depending synthesis, degradation and transport mechanism have been demonstrated in both experimental cerebral ischemia and human brain infarction. Their changes depend on the type, severity and duration of ischemia. Since neurotransmitters have variable effects on cerebral vasculature, blood-brain barrier, (BBB), cerebral blood flow and metabolism, their disorders may contribute to the development of postischemic brain damage and the complicating cerebral edema. During short-term experimental cerebral ischemia there are only minimal changes in cerebral biogenic amines, but despite improved cerebral energy metabolism significant alterations in catecholamine and indoleamine turnover and in the activity of degradating enzymes (MAO, COMT, etc.) occur in the postishemic reperfusion period, suggesting a ,,maturation phenomenon". Long-term cerebral ischemia and cerebral infarction are associated with severe depletion of dopamine, serotonin, with increased levels of their metabolites homovanillic acid and 5-hydroxy-indole acetic acid as well as of GABA and cyclic AMP in both the necrotic area and the surrounding tissue. These changes are related to increased release, decreased synthesis, degradation and washout, and disorders of vascular amine transport due to reduced activity of related enzymes. Simultaneous increase of the 5-HT precursor tryptophan and its main metabolite kynurenine suggest decreased synthesis and turnover of 5-HT. Reduced activity of tyrosine hydroxylase and other degradating enzymes indicate reduced activities of catecholamine and serotonergic neuronal systems in postischemia. There is reduced synaptosomal uptake of DA, 5-HT and GABA with reduction in the number of aminergic receptor binding sites due to irreversible ischemic damage to synaptosomal membranes. Transient opening of the blood-brain barrier and increased amine transport from blood into brain tissue may promote postishemic disorders of microcirculation and edema. Bilateral changes in energy metabolism and decrease in monoamines seen after unilateral focal ischemia (in experimental models and human brain) are caused by remote effects of ischemia (,,diaschisis") due to reduced cerebral blood flow and edema. However, no bilateral effect of ischemia on the number of specific neuronal DA- and 5-HT binding sites and on DA uptake are evident which indicate a certain resistance of synaptosomal membranes towards ischemia. These data and rather normal activity of cerebral tyrosine hydroxylase in metabolic encephalopathies (hepatic and diabetic coma) indicate a preferential oxygen supply to neuronal transmitter systems. Severe and long-lasting ischemia, cerebral infarction with destruction of neurons and metabolic catastrophes (hepatic coma), however, induce a breakdown of energy-depending systems and are associated with disorders of the BBB. The perifocal edema zone surrounding recent infarction shows increased concentrations of 5-HT, 5-HIAA, TRP and GABA due to both increased release and turnover and reduced washout which may cause local disorders of microcirculation, dysfunctions of the BBB and may contribute to postischemic edema. In old cerebral infarctions monoamines are reduced in the necrotic area, while almost normal levels of indoleamines and their metabolites in the surrounding scar and intact brain tissue indicate ,,normalization" of amine 5-HT metabolism in the previously ischemic brain. The time course and the interrelations between disorders of brain amine metabolism and of specific amine uptake and synaptosomal receptor kinetics in cerebral ischemia need further elucidation. The relevance of brain monoamine changes to the progression of cerebral ischemia and its complications remain to be further established, but experimental data may provide the basis for further elucidation of pathophysiological mechanisms involved. Pharmacologic influence on neurotransmitter metabolism and other metabolic changes operative in the pathophysiology of ischemic brain injury may provide also a basis for hope that it will be possible to achieve improvements in the treatment of cerebral ischemia and stroke. Zerebrale Ischämie und Hirninfarkt führen infolge Störungen energieabhängiger Synthese-, Abbau- und Transportvorgänge zu Veränderungen im zentralen Stoffwechsel biogener Amine und anderer mutmaßlicher Neurotransmitter, die von der Art, Schwere und Dauer der Ischämie abhängen und bei experimenteller Ischämie wie beim menschlichen Hirninfarkt auftreten. Da Neurotransmitter unterschiedliche Wirkungen auf Hirngefäße, Blut-Hirnschranke (BHS), Hirndurchblutung und -Stoffwechsel besitzen, dürften ihre Veränderungen an der Entwicklung postischämischer Hirngewebsschäden sowie des komplizierenden Hirnödems beteiligt sein. Während kurzdauernder experimenteller zerebraler Ischämie treten nur geringe Veränderungen biogener Amine auf, doch kommt es trotz voller Erholung des zerebralen Energiestoffwechsels in der Postischämiephase zu protrahierten Störungen des Katecholamin- und Indolaminstoffwechsels sowie seiner wichtigen abbauenden Enzyme (MAO, COMT u.a.), die mit Ödementwicklung und neuronaler Erholung korrelieren dürften. Nach anhaltender zerebraler Ischämie sowie beim Hirninfarkt bestehen massiver Abfall von Dopamin (DA), Serotonin (5-HT) und Anstieg ihrer Hauptmetaboliten Homovanillinsäure (HVS) und 5-Hydroxyindolessigsäure (5-HIES) sowie von GABA und zyklischem AMP in der Infarktzone und ihrer Umgebung infolge gesteigerter Freisetzung, vermindertem Abbau und BHS-Störungen für Amine durch reduzierte Aktivität zugehöriger 02-abhängiger Enzyme. Simultaner Anstieg des 5-HT-Vorläufers Tryptophan (TRP) und seines Hauptmetaboliten Kynurenin (KYN) weisen auf eine...