Physiopathological approach to the management of cerebral ischaemia.
Pharmacological therapy in ischemic and in microcirculatory and cerebral metabolic damage is considered. In the first case osmotic drugs and membrane stabilisers are useful, i.e., cortisone and non-steroid anti-inflammatory drugs, as well as anti-aminics and spasmolytics. Platelet anti-aggregants and increase in perfusion pressure are also useful in order to prevent the 'no-reflow' phenomenon. In the second case the theoretical possibilities of pharmacological action concern activation of glycogen synthetase and adenylcyclase or inhibition of phosphodiesterase. It will be necessary to remove the lactate increase and to raise the glucose supply, while for the oedema, osmotic and oncotic drugs will need to be used.
D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D001921:Brain / Q000378:metabolism; D002545:Brain Ischemia / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D002560:Cerebrovascular Circulation; D006490:Hemostatics / Q000627:therapeutic use*; D006801:Humans; D008833:Microcirculation; D010276:Parasympatholytics / Q000627:therapeutic use*; D010974:Platelet Aggregation / Q000187:drug effects; D014662:Vasoconstrictor Agents / Q000627:therapeutic use*; D014665:Vasodilator Agents / Q000627:therapeutic use*
D000893:Anti-Inflammatory Agents; D006490:Hemostatics; D010276:Parasympatholytics; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents