Spectral changes in systemic arterial pressure signals during acute mevinphos intoxication in the rat

We investigated the cardiovascular consequences of acute intoxication by th e organophosphate poison, mevinphos (Mev), and delineated the underlying me chanism. Based on on-line power spectral analysis of systemic arterial pres sure (SAP) signals in rats anesthetized and maintained by propofol, we iden tified two distinct phases after intravenous administration of Mev (160 or 320 mug/kg). Phase I was characterized by transient hypertension and mild t achycardia, concurrent with an increase in the very high-frequency (BVHF; 5 -9 Hz), high-frequency (BHF; 0.8-2.4 Hz), low-frequency (BLF; 0.25-0.8 Hz), and very few-frequency (BVLF; 0-0.25 Hz) components of SAP signals. Phase I i exhibited significant hypotension, a reversal of the BVHF and BVLF power to control levels, and further reduction in the power density of both BHF a nd ELF components to below baseline, Microinjection of Mev (2 mug) into the bilateral nucleus reticularis ventrolateralis (NRVL), the medullary origin of sympathetic neurogenic vasomotor tone, essentially duplicated those pha sic cardiovascular changes. Similarly, sympathoexcitatory NRVL neurons exhi bited respectively an elevation and a decline in their spontaneous activiti es during Phase I and Phase II Mev intoxication. We conclude that the progr essive accumulation of acety[choline over time induced by a direct inhibiti on of Mev on cholinesterase in the NRVL may be responsible for the phasic c hanges in cardiovascular events over the course of acute Mev intoxication. Whereas the initial amount of acetylcholine is excitatory to NRVL neurons, overstimulation by the amassed acetylcholine results instead of an inhibito ry action.