The protective effect of acetamide in poisoning by sodium monofluoroacetate (MF) and by eight Brazilian sudden death causing plants (BSDCP) (Palicourea marcgravii, P. juruana, Pseudocalymma elegans, Arrabidaea bilabiata, Amorimia (Mascagnia) rigida, M. pubiflora, Amorimia (Mascagnia) exotropica and M. aff. rigida) was studied using rats. Additionally the clinical and pathological picture of the poisoning was described. In these experiments 33 Wistar rats (Rattus norvegicus albinus) were used. Nine rats ate spontaneously the fresh leaves of P. marcgravii at amounts of 2.0 and 4.0g/kg. Two of the rats received orally single doses of acetamide (2.0 and 4.0g/kg) one minute before the plant was supplied. A third rat received 4.0g/kg of acetamide after consumption of 4.0g/kg of the plant and showed severe symptoms of poisoning. In the experiments with MF, doses of 4.0 and 8.0mg/kg were administered to four rats. The interval between the administration of either acetamide and concentrated plant extracts or MF ranged from 2 to 4 hours; the dose of acetamide ranged from 2.0 to 8.0g/ kg. In the experiments with concentrated extracts of eight BSDCP, 20 rats were orally poisoned with single or repeated doses. Acetamide, when previously administered, prevented the appearance of clinical signs and death in all of the rats poisoned by MF, as well as of the ones poisoned by fresh P. marcgravii leaves and by the concentrated extracts of each of the other BSDCP. These rats were re-subjected to the same experimental protocol, yet without the administration of acetamide. In these experiments, all of the rats evidenced clinical signs and death (except M. aff. rigida). All of the rats showed mild to markedly engorged atria, and sometimes also of the cranial and caudal vena cava. In three of the rats, there was a moderate right and left cardiac dilatation. The liver of all rats was slightly or markedly congested, with lobular pattern in some. There was frothy liquid on the cut surface of the lungs in three of the rats. The histopathology of the kidneys in six rats showed slight cytoplasmic swelling of the distal convoluted tubules and sometimes also of the collecting tubules. But only in four rats a vacuolar-hydropic degeneration with nuclear pyknosis was seen. Twenty-six rats showed liver congestion, three of them with compressive narrowing of the hepatic cords, and in eight rats shock corpuscles were observed; another three rats showed slight to moderate focal liver necrosis. A slight to moderate vacuolation of hepatocytes was observed in 16 rats. It can be concluded that acetamide had a protective effect, capable to prevent clinical signs and death of the rats poisoned by MF, and by fresh P. marcgravii leaves and concentrated extracts of seven other BSDCP. The clinical and pathological picture observed in the rats poisoned by MF and BSDCP, associated with the protective effect of acetamide, indicate that MF is the toxic principle responsible for death of the rats, and by extension, for the death of cattle that ate BSDCP.
Acetamide; sodium monofluoroacetate poisoning; sudden death; rat
