Centralised system of humidification for respiratory treatment.
A centralised system of hot water humidifiers for an intensive therapy unit has been described and its performance examined.
Biomedical subjects
Publications and source records attributed to J E Pedersen.
A centralised system of hot water humidifiers for an intensive therapy unit has been described and its performance examined.
The admixture of air in inspired gas with a paediatric insufflation system based on a gas jet has been investigated. During anaesthesia with spontaneous ventilation 1% of air per kg body weight was found in tracheal gas samples. A venturi effect was virtually absent even at high jet flows, which suggests that artificial ventilation prevents air admixture.
This clinical investigation confirms the results of previous reports on the possibility of safely replacing blood lost during operations with physiological saline. The percentage saving of blood transfusions has been 50.1%. We are convinced that even greater saving will be made when surgeons become accustomed to the method.
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Azomycin riboside (2-nitro-1-beta-D-ribofuranosylimidazole) (AR), a nucleoside analogue with the base component replaced by a 2-nitroimidazole was studied to determine its potential as a radiosensitizer. In vitro evidence showed that AR is as good as or slightly better than misonidazole (MISO) as a hypoxic cell radiosensitizer. AR was also found to kill hypoxic cells directly and this cytotoxicity was at least as great as MISO cytotoxicity. However, when tumor regrowth delay was used to assess in vivo radiosensitization, AR was found to be inferior to MISO while the LD50 host toxicity assay indicated that AR might be nearly as toxic as MISO. Unless AR proves to be less toxic than MISO or can be selectively distributed with nucleoside transport inhibitors, these preliminary observations have not shown any advantage of AR over MISO as a potential clinically useful radiosensitizer.
Cyclophosphamide and the radiosensitizer misonidazole were combined to determine if any therapeutic benefit could be demonstrated with this combination in treating the murine Lewis lung tumor. The results of our in vivo studies indicated that when various dosage schedules of misonidazole were combined with cyclophosphamide, the tumor effect was greater than when cyclophosphamide was administered alone. However, the increased effect of the two drug combination was determined to be no greater than an additive effect of cyclophosphamide tumor cell toxicity plus misonidazole cytotoxicity. Furthermore, host toxicity was enhanced when the two drugs were combined as indicated by the LD50 assay. We conclude that combining cyclophosphamide with misonidazole offers little if any therapeutic advantage since the increase in host toxicity appears to be as greater as the increase in tumor cell killing.