[Possibilities of pharmacologic correction of Na, K-ATPase activity in the spinal cord in botulism].
The experiments on white rats have shown that gutimin is capable of reactivating Na, K-ATPase of the synaptosomes of the jugular spinal cord in type C botulinic intoxication. Serotonin prevented Na, K-ATPase activity inhibition only in preclinical period of intoxication. Parmidin injection did not prevent suppression of Na, K-ATPase activity either in preclinical period or in skeletal muscle paresis.
D000818:Animals; D001906:Botulism / Q000188:drug therapy* / Q000201:enzymology; D017301:Ca(2+) Mg(2+)-ATPase / Q000378:metabolism; D002219:Carbamates / Q000627:therapeutic use*; D006164:Guanylthiourea / Q000627:therapeutic use*; D011727:Pyridinolcarbamate / Q000627:therapeutic use*; D051381:Rats; D012701:Serotonin / Q000627:therapeutic use*; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*; D013116:Spinal Cord / Q000201:enzymology*; D013890:Thiourea / Q000031:analogs & derivatives*
D002219:Carbamates; D012701:Serotonin; D011727:Pyridinolcarbamate; D017301:Ca(2+) Mg(2+)-ATPase; D000254:Sodium-Potassium-Exchanging ATPase; D013890:Thiourea; D006164:Guanylthiourea
O vozmozhnostiakh farmakologicheskoĭ korrektsii aktivnosti Na, K-ATF-azy spinnogo mozga v dinamike botulinicheskoĭ intoksikatsii.