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

We investigated the cardiovascular consequences of acute intoxication by the organophosphate poison, mevinphos (Mev), and delineated the underlying mechanism. Based on on-line power spectral analysis of systemic arterial pressure (SAP) signals in rats anesthetized and maintained by propofol, we iden...

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Bibliographic Details
Published in:Shock (Augusta, Ga.) Ga.), 2001-01, Vol.15 (1), p.35-41
Main Authors: Yen, D H, Yen, J C, Len, W B, Wang, L M, Lee, C H, Chan, S H
Format: Article
Language:English
Subjects:
Animals
Arteries
Blood Pressure - drug effects
Blood Pressure Determination - methods
Heart Rate - drug effects
Injections, Intravenous
Insecticides - poisoning
Male
Mevinphos - administration & dosage
Mevinphos - poisoning
Microinjections
Muscle, Smooth, Vascular - drug effects
Neurons - drug effects
Neurons - physiology
Poisoning - physiopathology
Rats
Reticular Formation - drug effects
Reticular Formation - physiology
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Summary:We investigated the cardiovascular consequences of acute intoxication by the organophosphate poison, mevinphos (Mev), and delineated the underlying mechanism. Based on on-line power spectral analysis of systemic arterial pressure (SAP) signals in rats anesthetized and maintained by propofol, we identified two distinct phases after intravenous administration of Mev (160 or 320 microg/kg). Phase I was characterized by transient hypertension and mild tachycardia, 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 low-frequency (BVLF; 0-0.25 Hz) components of SAP signals. Phase II exhibited significant hypotension, a reversal of the BVHF and BVLF power to control levels, and further reduction in the power density of both BHF and BLF components to below baseline. Microinjection of Mev (2 microg) into the bilateral nucleus reticularis ventrolateralis (NRVL), the medullary origin of sympathetic neurogenic vasomotor tone, essentially duplicated those phasic cardiovascular changes. Similarly, sympathoexcitatory NRVL neurons exhibited respectively an elevation and a decline in their spontaneous activities during Phase I and Phase II Mev intoxication. We conclude that the progressive accumulation of acetylcholine over time induced by a direct inhibition of Mev on cholinesterase in the NRVL may be responsible for the phasic changes 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 inhibitory action.
ISSN:1073-2322
1540-0514
DOI:10.1097/00024382-200115010-00006