carollyncheeyen
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Kinda confusing but acc to experimental date thy seemed to be dependent of time-of-exposure.
All values were compared wth a control model.
APD in Purkinje fibers(PF) & ventricular muscles(VM) seemed to 1st incr slightly(due to prolonged phase2,most obvious 15min aft exposure);
&then decr quite significantly wth time(due to abbriev of phase2+incr of it's slope).
Changes in ERP was even more confusing,wth a triphasic change--slight incr at 30min;
slight decr at 90min;
then slight incr again at 120min.
http://www.pubmedcentral.nih.gov/picrender.fcgi?a...
In this study conc. of digoxin was a const.
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| carollyncheeyen
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Katzung,too described it,BUT it's for DIGITALIS generally,not for DIGOXIN only:
At therapeutic doses(absence of overt toxicity),
a brief prolongation of APD,followod by protracted period of shortening(esp in plateau--ie phase2).
Decr in APD is probably the result of incr'd K+conductance caused by incr'd intracellular Ca++.
While at higher doses,resting mb potential is reduced(made less -ve) due to inhibition of Na+ pump& reduced intracellular K+,APD is markedly reduced.
ERP of atria incr'd(due to PsympANS,but i dun understand how,shdn't it decrease then..?);
ERP of AV node decr'd(due to PsympANS);
&ERP of Purkinje systems&ventricles decr'd(direct effect).
For effect on ERP Katzung mentioned the link btw dosage&effects of the drugs on ANS--Lower dose range cardioselective psymp-mimetic effect predominates;toxic doses increases Symp outflow.
I'm sorry that's all i found out,can anyone plz explain the mechanism.
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