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[Hemodynamics and microcirculation in a rat poisoned by scorpion venom]]
1Laboratoire d'histo-embryologie, faculté de médecine de Sfax, 3029 Sfax, Tunisie.
Abstract:
The clinic table of serious scorpionic envenimation is dominated by cardiovascular and pulmonary perturbations. The physiopathology of cardiac failure in man as well as at animal is again badly elucidated. The aim of our study has consisted in evaluating the hemodynamic variations of the Rat poisoned by the venom of the Buthus occitanus scorpion and to contribute through the analyse of plasmatic concentrations of catecholamines and by an histomorphometric study of muscular microcirculation to explain the mechanism of the hemodynamic perturbations and cardiac failure. 51 rats corresponding to 9 groups (witness and poisoned) have been used. The venom of the scorpion Buthus occitanus has been administrated at 850 micrograms/kg. Two groups have been served for hemodynamic study, three groups for the dosage of catecholamines and four groups for histomorphometric study. It has been observed a biphasic variation of arterial pressure and cardiac frequency after venom injection. Four minutes after envenimation, the plasmatic level of catecholamines was strongly higher in the poisoned according to the witness one. Histomorphometric study of muscular skeletal microcirculation has shown a decrease of relative vascular volume contemporary with the increase of plasmatic catecholamines concentration and the peak of arteriel pressure appeared just after envenimation. 10 and 20 minutes after envenimation, the relative vascular volume has significantly increased as well as that interstitium according to witness lot. These hemodynamic perturbations can be attributed to the important dump in catecholamines. This hyperadrenergy was contemporary with decrease of relative muscular vascular volume. This decrease would be explained by a constriction of vessels. On the other hand, the second increase of the vascular relative volume suggests the possibility of development of venous stasis at the muscular microcirculation. It would be induced by a cardiac failure and/or the effect of vasoplegic mediators being able to entail an interstitial oedema in the muscular skeletal that would led to increase the relative interstitial volume observed in this study.