Herpes simplex virus detection by macroscopic reading after overnight incubation and immunoperoxidase staining.

Human diploid foreskin fibroblast cells grown in 24-well plates were inoculated with clinical specimens by centrifugation at 1,000 X g for 45 min. Cultures were incubated at 37 degrees C overnight, fixed, and stained with peroxidase-labeled monoclonal antibodies against herpes simplex virus types 1 and 2. Stained plaques of infected cells were large enough to be detected with the naked eye, and microscopic examination did not reveal any further positive specimens. The method was compared with standard isolation in human fibroblasts grown in shell vials and inoculated by centrifugation at 4,000 X g, observed microscopically for the occurrence of typical cytopathogenic effect three times a week for 10 days, and then typed by enzyme immunoassay. Of the 289 specimens tested, 105 were positive and 174 were negative by both methods. Six specimens were positive by standard isolation only, two of them containing varicella-zoster virus, and two specimens were stored frozen before being tested by immunoperoxidase staining. Two specimens found negative by standard isolation were positive by immunoperoxidase staining. For two specimens negative by immunoperoxidase staining, the standard isolation cultures were lost due to microbial contamination. Forty-two specimens found positive by standard isolation were clearly positive when stained only 8 h after inoculation. By standard isolation, positive results were reported on the average 3 to 4 days after inoculation, whereas by immunoperoxidase staining the result was available within less than 24 h. Immunoperoxidase staining of infected cells is a sensitive method for rapid laboratory diagnosis of herpes simplex virus infections, and 24-well plates are convenient for the handling of a large number of specimens.     

Human Pharmacokinetics of Sotalol

Abstract The pharmacokinetics of sotalol were studied in healthy volunteers after a single dose and in hypertensive patients after chronic administration. A single 160 mg and two 80 mg socator® tablets were compared and found to be bioequivalent in terms of relative total bioavailability. Sotalol was well absorbed, about 73 % of the dose being excreted in the urine within 72 hours. The absolute bioavailability on oral administration was 100% indicating that both first–pass hepatic metabolism and metabolic destruction are negligible. There was no protein binding and the distribution volume was 171 1 after oral administration. The graphical fit of the plasma levels after a single oral dose was compatible with a two–compartment open model. The curve consisted of a distribution phase with a t_1/2 of 6 hrs followed by a disposition phase with a t_1/2 of 9.5 hrs. After chronic administration the t_1/2 during the disposition phase was 10 hrs. Computer fitting of the data gave a terminal body half–life of 17.2 hrs which corresponded well with the terminal body half–life of 15 hrs calculated manually from urinary excretion rate data. In the computer analysis the steady–state plasma levels to be expected after long–term oral dosing were simulated and found to be in good agreement with experimental data, indicating that there is no induction of sotalol metabolism or increase in efficiency of excretion during long–term sotalol administration.