Removal of sarcolemmal sialic acid residues results in a loss of sarcolemmal functioning and integrity.

Treatment of neonatal rat heart cells with neuraminidase results in a large increase of cellular-associated Ca2+. The study described below was designed to test the hypothesis that neuraminidase produces its effects by increasing the transient Ca2+ channel current, as proposed by Yee et al. (24). This ICa,T can be inactivated by dodecylsulfate (DDS) (17). The experimental data show that 1) the increase in cellular Ca2+ during neuraminidase treatment cannot be explained by an increased ICa,T; 2) neuraminidase treatment has a much more profound effect on sarcolemmal permeability than has been recognized previously; and 3) the effect of neuraminidase treatment can be prevented by 50 microM DDS. The study indicates that glycocalyx-lipid bilayer interactions are important in maintenance of selective permeability of the sarcolemma. The protective effect of 50 microM DDS is probably mediated by insertion of the negatively charged amphiphilic molecule in the sarcolemma, although the exact mechanism remains to be elucidated.