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The surface of neonatal rat cells in culture, neonatal rat hearts, and adult rabbit hearts have qualitatively similar responses to lanthanum, ruthenium red, and colloidal iron stains. All demonstrate a surface coat and external lamina with abundant negatively charged sites. Cells with intact surface structure do not permit entry of lanthanum (La) intracellularly. The surface of all the myocardial cells studied contained abundant sialic acid distributed in two distinct layers, one in the surface coat next to the lipid bilayer, the other in the external lamina at the interstitial interface. The removal of sialic acid from the cellular surface increases calcium (Ca) exchangeability 5to 6-fold. Its removal also permits La to enter the cell and displace more than 80% of cellular Ca. Despite these marked alterations in Ca and La permeability, sialic acid removal has no effect on potassium <K) permeability. This indicates that the integrity of surface coat is critical in the regulation of Ca (and La) exchange but that K* permeability is controlled at the bilayer region. Exposure of the cells to [Ca]0 = 5 /»M produces a change in the surface. A peeling of the external lamina from the surface coat occurs with separation of the two sialic acid layers and the formation of a fluid-filled bleb between them. We propose that Ca removal ruptures Ca carbohydrate couplings (e.g., fucose-Ca-fucose bridges) which may anchor the external lamina to the surface coat. The effect of Ca removal on ionic permeability is not specific. The cell demonstrates increased permeability to both La and K. This indicates that Ca depletion affects both the surface structure and the bilayer region.

The myocardial cell surface, its histochemistry, and the effect of sialic acid and calcium removal on its stucture and cellular ionic exchange.