This study addresses the mechanism of transport of the H2-receptor antagonist, cimetidine, by the human placenta. A 4-h recycling perfusion of a single placental cotyledon of normal, term, human placenta was used. At a maternal concentration of 1 ug/ml, cimetidine clearance from the maternal circulation was 0.58±0.16 ml/min per g placenta, a rate about one third that of antipyrine. There was no evidence of cimetidine metabolism by the placenta. Transfer of cimetidine from maternal to fetal compartments showed no saturation kinetics and was not inhibited by putative carrier competitors. Cimetidine did not accumulate against a drug concentration gradient. Fetal clearance of cimetidine was similar to maternal clearance. Studies with placental apical vesicles confirmed lack of saturability of cimetidine transport and of its concentration within vesicles. Thus, (a) cimetidine is transported across the human placenta bidirectionally at a rate about one third that of antipyrine, (b) the drug is not metabolized by the placenta, and (c) the transport is a passive one.
Removal of bilirubin by hemoperfusion with ion exchange resin particles is suggested to replace exchange transfusion of blood of jaundiced infants in some cases of unconjugated hyperbilirubinemia. The hemoperfusion system developed here consists of a packed bed of a macroreticular resin which is made biocompatible by a coating of a monomolecular layer of albumin. The choice of the appropriate ionic form of the resin and the proper albumin coating and crosslinking procedure assures a high bilirubin adsorption capacity and excellent blood compatibility of the resin. The albumin coated resin removes in vitro 80-90% of the bilirubin initially present in the plasma. The results encourage in vivo clinical studies.
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