[Thrombolytics and neuroprotective agents in the treatment of the patient with an acute cerebrovascular ischemic accident].
BACKGROUND
Cerebrovascular disease occupies second place amongst the causes of mortality in the world. Rapidly after onset of an acute ischemic cerebrovascular accident (CVA) there is irreversible formation of an area affected by the ischemic process (necrotic centre) surrounded by a zone in which reduction of blood flow is less marked. Although the neurons of this region, known as the 'ischemic penumbra', are in a state of 'electrical silence', they may recover if effective treatment is started in time.


METHODS
Treatment of the patient with an acute ischemic CVA should be concentrated in two areas: restoration of blood flow and neuroprotection. In spite of better understanding of the biochemical, genetic and molecular processes which occur during the process of cerebral ischemia, the development of neuroprotector strategies has been largely fruitless. However, restoration of cerebral blood flow is currently possible in a certain group of patients. The fibrinolytic system is formed by an inactive proenzyme, plasminogen, which may be converted to the active form, plasmin, in the presence of specific activators such as tissue plasminogen activator (t-PA) and urokinase-type plasminogen activator (u-PA).


CONCLUSIONS
The effect of thrombolytic treatment is due to dissolution of the fibrin present in the occluding thrombus, with subsequent restoration of the blood flow to the ischemic area. Nevertheless the use of thrombolytic agents has dramatically changed the clinical management of patients with acute ischemic cerebrovascular incidents. Their use involves a significant risk of intracerebral bleeding, which together with the narrow therapeutic window, has made this one of the most controversial fields of current neurology.
Yepes
M S
MS
Departamento de Neurología, Unidad de Enfermedad Cerebrovascular, Georgetown University Medical Center, Washington, DC, USA. yepesm@aol.com
D000208:Acute Disease; D002545:Brain Ischemia / Q000188:drug therapy*; D002118:Calcium / Q000502:physiology; D016923:Cell Death; D002543:Cerebral Hemorrhage / Q000139:chemically induced / Q000453:epidemiology; D002560:Cerebrovascular Circulation; D002986:Clinical Trials as Topic; D000075202:Contraindications; D005341:Fibrinolysin / Q000096:biosynthesis; D005342:Fibrinolysis / Q000187:drug effects; D005343:Fibrinolytic Agents / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use*; D005609:Free Radicals; D006801:Humans; D007269:Injections, Intra-Arterial; D009474:Neurons / Q000502:physiology; D018696:Neuroprotective Agents / Q000627:therapeutic use*; D009498:Neurotoxins / Q000378:metabolism; D009566:Nitrates / Q000502:physiology; D009569:Nitric Oxide / Q000502:physiology; D010958:Plasminogen / Q000378:metabolism; D017410:Practice Guidelines as Topic; D016032:Randomized Controlled Trials as Topic; D011994:Recombinant Proteins / Q000627:therapeutic use; D012306:Risk; D013300:Streptokinase / Q000627:therapeutic use; D015912:Thrombolytic Therapy / Q000009:adverse effects; D010959:Tissue Plasminogen Activator / Q000037:antagonists & inhibitors / Q000502:physiology / Q000627:therapeutic use; D014568:Urokinase-Type Plasminogen Activator / Q000037:antagonists & inhibitors / Q000502:physiology / Q000627:therapeutic use; D014715:Vertebrobasilar Insufficiency / Q000188:drug therapy
D005343:Fibrinolytic Agents; D005609:Free Radicals; D018696:Neuroprotective Agents; D009498:Neurotoxins; D009566:Nitrates; D011994:Recombinant Proteins; C039642:peroxynitric acid; D009569:Nitric Oxide; C081981:lanoteplase; D010958:Plasminogen; C087896:reteplase; D013300:Streptokinase; D010959:Tissue Plasminogen Activator; D005341:Fibrinolysin; D014568:Urokinase-Type Plasminogen Activator; D002118:Calcium