Intravenous terbutaline was well tolerated in asthmatic children for < or =305 continuous hours and at varying doses up to a maximum of 10 microg/kg/min. There was no relationship between the magnitude of CPK-MB concentrations and the terbutaline or epinephrine doses used. Arrhythmias were rare and not related to either terbutaline or epinephrine doses. However, ST-segment depression did occur in two patients requiring high-dose epinephrine. Terbutaline significantly lowered DBP when used between 0.4 and 1.0 microg/kg/min, which required epinephrine to be initiated. Epinephrine was not required at terbutaline doses of >2 microg/kg/min. There was no mortality.

SUMMARYUsing a guinea-pig model of genital herpes simplex virus (HSV) infection we explored the protection afforded by preinfection immunization with HSV glycoproteins. Glycoprotein immunogens prepared by recombinant DNA technology were found to be as effective as immunogens purified from HSV-infected cell cultures. Immunized animals developed less severe primary disease and also experienced less frequent recurrent infections. Protection was influenced by both adjuvant and route of administration. These studies suggest that recombinant HSV glycoproteins may be effective immunogens for human clinical trials, but that the development of an effective vaccine will require identification of new potent adjuvants that are safe for human use.

SUMMARY5-Azacytidine (5-AZC) reduces cytosine methylation in DNA and has been reported to activate quiescent virus genes. Treatment of explant cultures of latently herpes simplex virus type 2 (HSV-2)-infected guinea-pig dorsal root ganglia and spinal cords in vitro with 5-AZC significantly enhanced the rate of HSV recovery. Both the number of isolates from ganglia (P < 0.001) and the rate of recovery (P < 0.001) were significantly increased with the addition of 50 ~tM-5-AZC to explant cultures. Increased virus recovery appeared to be due to the induction of reactivation of latent virus, rather than an increase in replication, since 5-AZC inhibited HSV replication. These data support a role for methylation in HSV latency and reactivation.

Recovery from arsenic poisoning was attributable to the restoration and maintenance of adequate cardiac output and renal perfusion in early shock, which allowed depot intramuscular British anti-Lewisite to circulate and eliminate the poison. Although an intravenous antiarsenical chelating agent would be advantageous in treating shock from arsenic poisoning, none is currently available. We urge the immediate use of British anti-Lewisite therapy on patient presentation with suspected toxic arsenic ingestion.