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 LD50; 90 µg/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.
Highlights
Organophosphorus compounds (OP) irreversibly inhibit the enzyme acetylcholinesterase (AChE), which is responsible for terminating the neurotransmitter action of acetylcholine (ACh) at the various cholinergic nerve endings
Three subsequent injections of differently labelled (141Ce, 103Ru, and 98Sn) microspheres were given to each animal, which has the advantage that the animal can serve as its own control
In the group with significant decrease in respiration rate, total cerebral blood flow was increased by about 290%, while no change in cerebral blood flow could be seen in the rats showing no signs of poisoning
Summary
Organophosphorus compounds (OP) irreversibly inhibit the enzyme acetylcholinesterase (AChE), which is responsible for terminating the neurotransmitter action of acetylcholine (ACh) at the various cholinergic nerve endings. This results in the accumulation of cholinergic receptor sites producing continuous stimulation of cholinergic fibers throughout the central and peripheral nervous systems [1, 2]. Antidotal treatment of OPinduced poisoning usually consists of two steps: anticholinergic drug to block the overstimulation of the cholinergic receptors by ACh and oximes to reactivate OP-inhibited AChE. Reactivation of OP-inhibited AChE by oximes can generate enough active AChE to restore normal cholinergic neurotransmission after exposure to OP [2, 4]
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