A wealth of evidence has revealed that the heart can be "conditioned" and rendered less vulnerable to ischemia-reperfusion injury via the upregulation of endogenous protective signaling pathways.
Because the catecholamine levels remain steady after a brief decrease in levels after initiating the ECMO, sustained hemodynamic support from catecholamine is expected in patients initiated on ECMO. A lack of sustained support as expected from catecholamine infusion is unlikely the result of drug adsorption to the ECMO circuit.
