Paraquat poisoning: an experimental model of dose-dependent acute lung injury due to surfactant dysfunction.

M.F.R Silva,P.H.N Saldiva

doi:10.1590/s0100-879x1998000300018

M.F.R Silva, P.H.N Saldiva

Open Access

https://doi.org/10.1590/s0100-879x1998000300018

Copy DOI

Abstract

Since the most characteristic feature of paraquat poisoning is lung damage, a prospective controlled study was performed on excised rat lungs in order to estimate the intensity of lesion after different doses. Twenty-five male, 2-3-month-old non-SPF Wistar rats, divided into 5 groups, received paraquat dichloride in a single intraperitoneal injection (0, 1, 5, 25, or 50 mg/kg body weight) 24 h before the experiment. Static pressure-volume (PV) curves were performed in air- and saline-filled lungs; an estimator of surface tension and tissue works was computed by integrating the area of both curves and reported as work/ml of volume displacement. Paraquat induced a dose-dependent increase of inspiratory surface tension work that reached a significant two-fold order of magnitude for 25 and 50 mg/kg body weight (P < 0.05, ANOVA), sparing lung tissue. This kind of lesion was probably due to functional abnormalities of the surfactant system, as was shown by the increase in the hysteresis of the paraquat groups at the highest doses. Hence, paraquat poisoning provides a suitable model of acute lung injury with alveolar instability that can be easily used in experimental protocols of mechanical ventilation.

Highlights

Paraquat, a herbicide widely used in agriculture, has caused many deaths due to suicidal or accidental ingestion
There was a shift to the right of the inspiratory limb as well as an increase in the area of hysteresis in the paraquat-intoxicated animal
The degree of paraquat poisoning depends on the amount used; the most characteristic feature is lung damage, which is usually the cause of death

Summary

Introduction

A herbicide widely used in agriculture, has caused many deaths due to suicidal or accidental ingestion. The primary damage in mammals occurs in the lung. The pathogenesis of paraquat-induced damage to alveolar structure is related to its accumulation in type II pneumocytes [1]. The concentration of paraquat in the lung after exposure rises progressively to several times that in plasma or in any other organ. Central nervous derangements and hepatic and renal tubular lesions may be present, but such toxicity is observed only after intoxication with high doses. The degree of lung damage seems to be dose-dependent [2], is enhanced by high oxygen concentrations [3] and persists in spite of lowering paraquat levels by hemoperfusion [1]

Methods

Results

Conclusion