بررسی ارتباط بین سموم خرزهره در سرم و آریتمی های قلبی در مسمومیت تجربی گوساله

Poisoning with poisonous plants, because of it’s high rate of mortality, has it’s own significance in veterinary medicine. Oleander (Nerium oleander) is one of the highly toxic plants, originally is a Mediterranean and Asian plant, and now is widely distributed in the world, it grows rapidly and consequently needs frequent pruning. Because of Iran’s optimum environmental condition, oleander has a wide distribution and it is grown as a shrub or a medium-size tree in most parts of Iran. All parts of oleander are toxic to animals and human beings, although it is said that the seeds are more toxic than the other parts. The green leaves and young branches cut off after trimming are the most
frequent causes of poisoning. Dry leaves, whether mixed with forage or left under the tree, can also be the cause of poisoning. Although animals are not fully attracted to this plant, they consume dry leaves especially when no other food is available. The most common manifestation of oleander poisoning is cardiac rhythm disturbances, arrhythmias or dysrhythmias. Cardiac glycosides, like poison of oleander, are responsible for these signs and acts pharmacodynamically similar to digitalis. Possible mechanisms for arrhythmogenic effects of digitalis include delayed after potential, enhanced diastolic depolarization and reentry that appear to be due to intracellular calcium overload which is due to inhibition of the sarcolemmal Na+-K+ stimulated Atpase by glycosides that produce alteration in the electrical properties of both the contractile cells and the specialized automatic cells. The glycosides also prolong the functional refractory period of the trioventricular node directly as well as through enhanced vagal effect. This study of oleander poisoning in animals has ascertained that oleander has a selective pharmacodynamic effect on the : 1) Autonomic and central nervous system, 2) On the myocardium and 3) On the gastrointestinal tract; and alomst all of known arrhythmias were observed in the animals. In this study the correlation between cardiac dysrhythmias and the concentration of oleander toxina with its mode of action were evaluated. Six calves of both sexes, aged between 5 to 9 months were selected. Powderd dry leaves in single Lethal dose were administered orally. The vital signs of the animals at the time experiments were examined carefully and electrocardiograms of animals were monitored. Blood samples and electrocardiograms were taken simultaneously. The serum of blood samples was then submitted to the laboratory for extraction of oleander toxins. Studying on toxins and assaying them were made by UV spectrometer model PU 8750-Philips. This study showed that absorption of oleander toxins in early hours of our experiment produces Brady arrhythmia that is probably due to its direct effects on the heart and vagal effects of cardiac glycosides. With the progress of poisoning more absorption of toxins occurred, and concentration of the new chemical complexes in the blood become adequate to produce tachyarrhythmias. Almost in all cases that ventricular tachycardia occurred, ventricular fibrillation was consequently formed which caused by death in few minutes. The spectrome of alterations of oleander toxins, absorption in UV range (200-350nm) showed that absorption of toxins alone cannot cause lethal arrhythmias, and the production of new chemical complexes in 240-260nm is needed for the occurance of death.