Blood and milk concentrations of captopril, a new antihypertensive agent, were studied in 12 lactating normotensive subjects after the administration of 100 mg captopril tablets on a three times daily regimen for a total of seven doses. Peak blood concentrations (± S.E.M.) of captopril after the administration of the seventh 100‐mg tablet averaged 713.1 ± 140.6 ng/ml, as compared to average peak milk concentrations of 4.7 ± 0.7 ng/ml. Time to peak blood concentrations averaged 1.1 ± 0.2 hour, while time to peak milk concentrations averaged 3.8 ± 0.6 hours. The data suggest that the human breast selectively restricts the passage of captopril from blood into milk.

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The etiology of immune polioencephalomyelitis (IPE) and the mechanisms of resistance to IPE induction were investigated in C58 mice. IPE was found to be induced by a lipid-solvent-sensitive, filterable replicating agent present in line Ib leukemic cell suspensions. IPE was serially transmitted in immunosuppressed mice with filtered extracts of spleens from diseased animals. The IPE-inducing activity of Ib cell extracts was abolished by chloroform or deoxycholate. Gel filtration of Ib cell extracts showed that the IPE agent has a molecular weight of at least 107. Electron microscopy of the active fractions from columns and of spinal cord extracts from mice with IPE revealed a virus-like particle, 40 nm in diameter, which is probably the IPE agent. Administration of cyclophosphamide at various times after challenge increased the incidence of IPE in mice, suggesting that IPE is not autoimmune mediated. Immunosuppression resulted in maintenance of high levels of IPE agent in the central nervous system tissue, while immunization resulted in low levels. Moreover, immunized mice produced neutralizing antibodies. These data suggest that antibodies help restrict the amount of IPE agent in the nervous tissue, and that this restriction is required for resistance to IPE induction in C58 mice.

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