Soman depots

The oxime HI-6 with atropine is reasonably effective against soman regardless of the choice of experimental animals while currently used oximes (pralidoxime and obidoxime) seem to be practically uneffective to protect mammals poisoned with supralethal dose of soman (Table 4). Presented data confirm that soman appears to be one of the most resistant nerve agent to the antidotal treatment because of the rapid aging of soman-phosphonylated AChE and the existence of a soman depot in the poisoned organisms (31, 54, 55). The soman-AChE complexes age very quickly and this fact prevents the oxime-induced reac-... 

There is a difference in distribution of nerve agents for different organs of the body as well as different locations within the heart. Roth et al. (1993) detail effects on the heart. Also, soman is deposited in depots where time-release effects cause unsuspected difficulties in treatment. 

Volume of distribution is slightly different for each of the nerve agents. Sarin is distributed to the brain, liver, kidney, and plasma of mice (Little et al, 1986). Soman is distributed throughout the mouse brain, with the highest levels found in the hypothalamus (Wolthuis et al, 1986). Tabun is also found in high concentrations in the hypothalamus after IV administration in mice (Hoskins et al, 1986). Soman is unique in that it has apparent storage in body depots and is released over time. This release can result in eventual death in animals who survive the initial dose of soman (Wolthuis et al, 1986). 

The data in Table 2.6 show that the apparent elimination half-life of the C(-)P(-)-stereoisomer after respiratory exposnre to 0.8 LCtjo in 8 min is somewhat longer than for the eqnitoxic i.v. dose. Moreover, the maximnm concentration in blood of C(+)P(-)-soman in case of the 4-min exposnre is reached not earlier than 2 min after cessation of the exposnre. This snggests that, despite rapid absorption, some depot formation occnrs at the absorption site, from which absorption continnes after termination of the exposnre. A fnrther argnment for some depot formation in the respiratory tract can be gleaned from Fignre 2.15, where the concentration-time profiles for C(-)P(-)-soman are compared for the 8-min respiratory exposure and for an 8-min i.v. infusion of an eqnitoxic dose (0.8 LDjq) of C( )P( )-soman. Evidently, the absorption phase of respiratory absorption is closely mimicked by the i.v. infusion, but blood levels subsequent to the respiratory exposure are distinctly higher than those after the i.v. infusion. 

No attempt was made to describe the time-concentration course in the 120 min post-exposure period. The blood levels decrease clearly in the first 90 min postexposure but remain remarkably constant over the next 90 min period. One intriguing explanation, although needing validation, is the formation of a depot of intact soman, for example in the epithelial tissue of the respiratory tract, from which the C(-l-)P(-)- and C(-)P(-)-stereoisomers diffuse into the bloodstream. 

Suppressing NATO s nuclear capabilities which are widely dispersed over Western Europe in air bases and supply depots is another major Soviet priority. Should nuclear weapons be withheld, persistent chemical agents, such as thickened soman, delivered by SCUD missiles, could be extremely effective. After a few repeated strikes, these bases could be rendered inoperative for an extended period of time or reduced in readiness as time was consumed in elaborate decontamination. Chemical weapons could also be employed in fulfilling another basic principle of Soviet operations, namely attacks upon the enemy throughout the entire depth of this deployment . Die targets would include air bases, command, control and communication facilities, harbours, airports and other transportation centres. 

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