HOSPEX in the antipodes.

The Australian Army recently adopted the British concept of hospital exercise (HOSPEX) as a means of evaluating the capabilities of its deployable NATO Role 2E hospital, the 2nd General Health Battalion. The Australian approach to HOSPEX differs from the original UK model. This article describes the reasons why the Australian Army needed to adopt the HOSPEX concept, how it was adapted to suit local circumstances and how the concept may evolve to meet the needs of the wider Australian Defence Force and our allies.

Gold(I) heteroatom-substituted imido complexes. Amino nitrene loss from.

The heteroatom-substituted imido complexes [(LAu)3(mu-NX)]+ (X = NR2, R = Ph, Me, Bz; X = OH, Cl; L = a phosphine) have been prepared from the reactions of NH2X with [(LAu)3(mu-O)]+. Thermally unstable [(LAu)3(mu-NNMe2)]+ (L = P(p-XC6H4)3, X = H, F, Me, Cl, MeO) decompose to the gold cluster [LAu]6(2+) and tetramethyltetrazene Me2NN=NNMe2. The decomposition is first-order overall with a rate constant that increases with increasing pKa of the phosphine ligand. Activation parameters for the decomposition are deltaH(not equal to) = 99(4) kJ/mol and deltaS(not equal to) = 18.5(5) J/K.mol for L = PPh3 and deltaH(not equal to) = 78(3) kJ/mol and deltaS(not equal to) = -47(2) J/K.mol for L = P(p-MeOC6H4)3. The decomposition of analogous [(LAu)3(mu-NNBz2)]+ produces bibenzyl, indicative of the release of free amino nitrene Bz2NN.

Continuous administration of barbital by pellet implantation.

Mice were continuously administered with barbital by the sc implantation of 16 mg barbital pellet (acid form). Serum and brain barbital levels were assessed at different times after pellet implantation. After 3 days of implantation the barbital pellet was removed and the mice were observed for a 96 hr period. A 30% decrease in sleeping time was observed 72 hr after pellet removal when mice were challenged with 400 mg/kg of barbital ip. Brain and serum barbital levels upon awakening were also assessed with a dose of sodium barbital, 400 mg/kg ip, administered 72 hr after removal of either a barbital or placebo pellet. It was observed that serum and brain barbital concentrations were significantly higher in barbital treated animals than in controls. The effect of barbital pellet implantation on pentobarbital (75 mg/kg, ip) sleeping times was also assessed. Cross tolerance to pentobarbital was observed 24, 48, and 72 hr after barbital pellet implantation. The results demonstrated that barbital pellet implantation enhanced hepatic drug metabolism as evidenced by significant increases in hepatic microsomal N-demethylase and hydroxylase activities. CNS hyperexcitability, an indication of dependence, was assessed by the method of pentylenetetrazol (PTZ) induced convulsions (60 mg/kg, sc). At 48 and 72 hr after pellet removal, PTZ induced convulsions increased by 41% and 35%, respectively, over control values. Index of dependence was also substantiated by a decrease in threshold for electroshock. These studies substantiate the validity of this experimental model for the assessment of the development of tolerance to and physical dependence on barbiturates.

Enhancement of pharmacologic responses of pentobarbital by dopram.

The effect of Dopram (doxapram hydrochloride, A. H. Robins Co.) on the pharmacologic responses to pentobarbital was evaluated. In naive and pentobarbital-tolerant mice, Dopram was shown to enhance significantly sodium pentobarbital-induced narcosis in a dose-related manner. The effect of the duration of action of Dopram on pentobarbital narcosis also was assessed. It was observed that Dopram (40 mg/kg, i.p.) significantly increased pentobarbital-induced narcosis even when administered 2 hr prior to challenge with sodium pentobarbital (60 mg/kg, i.p.) A significantly increased hypothermic response to sodium pentobarbital was seen in Dopram-treated animals. The half-life of pentobarbital in brain and serum was shown to be increased significantly in animals receiving Dopram, 40 mg/kg, i.p. The waking brain and serum pentobarbital concentrations were not significantly different in either group. These studies show that Dopram potentiates pentobarbital's effects. Further study is necessary to determine the sites of operation and mechanism of this potentiation.

Evaluation of Dopram(R) and its effects on hexobarbital narcosis.

The effect of Dopram(R) on hexobarbital induced narcosis and hypothermia was determined. Sodium hexobarbital (70mg/kg, i.p.) sleeping times were assessed in saline, Dopram(R), 20 and 40 mg/kg, i.p., administered mice. A dose-response increase in sodium hexobarbital induced narcosis was produced by Dopram(R). The duration of Dopram(R) effect on hexobarbital narcosis was also assessed. Dopram(R) potentiated significantly hexobarbital sleeping times when administered two hours prior to sodium hexobarbital challenge. Dopram(R) also was observed to significantly increase the hypothermic response to hexobarbital. The effect of the individual components of Dopram(R) (doxapram hydrochloride and chlorobutanol) on hexobarbital narcosis and hypothermia was evaluated. It was found that doxapram hydrochloride (20 and 40 mg/kg, i.p.) and chlorobutanol (5 and 10 mg/kg, i.p.) potentiated sodium hexobarbital narcosis and hypothermia. It seems that doxapram hydrochloride and chlorobutanol are both responsible for the potentiation of hexobarbital narcosis and hypothermia by Dopram(R).