Dramatic Increase in Cerebral Blood Flow following Soman Intoxication If Signs of Symptoms Can Be Seen

Abstract

Organophosphate poisoning is associated with adverse effects on the central nervous system such as seizure/convulsive activity and long term changes in neuronal networks. This study report an investigation designed to assess the consequences of Soman, a highly toxic organophosphorus compound, exposure on regional blood flow in the rat brain and peripheral organs. We performed repeated blood flow measurements in the same animal, using the microspheres technique, to characterize changes in regional blood flow at different times after Soman intoxication. In addition, the cardiopulmonary effects of Soman were followed during the intoxication. Administration of Soman (1 LD 50 ; 90 g/kg, s.c.) to anaesthetized rats produced a decrease in blood acetylcholinesterase activity in all animals tested. Although, only six out of ten rats showed signs of poisoning like a decrease in respiratory rate, the results show that only animals with significant signs of poisoning demonstrated an increase in cerebral blood flow. We conclude that it is of great importance to treat all data individually. An overall mean can easily be misinterpreted and conceal important effects. We also conclude that the increase in cerebral blood flow has an important role in the effect on respiration and that this effect is independent of the blood acetylcholinesterase activity.

Mechanism and Clinical Importance of Respiratory Failure Induced by Anticholinesterases

“…Best examples of such molecules are nerve agents tabun, sarin, soman and VX, insecticides dichlorvos (DDVP) and paraoxon (metabolite of parathion) and the oldest known anticholinesterase carbamate, physostigmine, which had become a model-substance in pharmacological research (15,18). Soman is so highly lipophilic, that it reaches the brain circulation just 1 min after IV injection and completely distributes throughout the brain tissue in only 3 min (19).…”