INFARTO DE MIOCARDIO EXPERIMENTAL EN PERROS: VALORACIONES BIOPATOLÓCICAS, ELECTROCARDlOGRÁFICAS E HISTOPATOLÓGlCAS

Resumen

In this work, we have studied the experimental myocardium heart-attack in dogs, for which we began by performing a surgical acclusion of the coronary arteries. We divided the animals into three separate groups. In the first group, a ligature of the left coronary arterywas performed was the branch, interventricularis paraconalis, in the second group a ligature in the branch of the left coronary artery and the in the third group a ligature in the branch circunflexus of the right coronary artery. Previously, the catheterization of the crotid artery had been carried out on all the animals with the objetive of easily obtanining blood samples. Blood samples and electiocardiograms are taken before the occlusion and 4, 8, 12, 24 hours and 2, 3, 4, 5, 6, 7, 8 days after the ligature. From the studies ans evaluations carriedout, we can deduce that a leukocitosis originates 4 hours after the ischemia and which reaches its maximum at 12 and 24 hours, with 29050 +- 3410,82 leukocytes per cubic millimetre. Other observations which we have been able to verify, were the changes which occred in the leukocyte formula, underlining the neutrophilia as one of the most important with a clear swing to the left. This neutrophilia appears few hours after the heart-attack, a recovery towards normal figures ocurring after 6 days. In groups 1 and 2, the partial presure of carbon anhidride (pCO₂) increases in a significant way with respect to figures taken before the animals were operated on. The alkaline reserve suffers a drop a few hours after the coronary occlusion, then increases gradually during the following days. The partial oxigen pressure suffers a slight decrease in every group. The most notable variations are in enzymatic activity. The CK-MB which initially give us a value of 52,8 +- 6,48 and 66,7 +- 4.65 Ul/L., rises rapidly after 4 hours reaching maximum activity after between 12 and 24 hours with figuures of 2312,9 +- 508,37 Ul/L. The same thing happens with the LDH and the GOT-ASAT, an increase ocurring after a few hours reaching its maximum after between 12 and 48 hours, leter recovering after around 6 days. With regard to the serie ferogram, we must underline the obvious increase, statiscallly checked, which occurred in the albumins, obtaining a slow but progressive decrease in them, reaching its minimun in between 4 and 5 days, from which time its graual increase begins. The globulines alpha₂ also suffer variations since after 24 hours a increase begins which reaches its maximum limitin between 3 and 4 days after the attack, then slowly decreasing again. In relation to the zinc and copper determined, a slight hipercupremia and hipozincemia was obteined respectively although thid was not a dominant feature in all the groups. As for the most obvious changes in the electrocardiographic study, we would like to point out the rapid appearance (after 4 hours) of alterations in rhythm and cardiac conduction with a tachycardia wich reached the order of 200-210 p.p.m. reaching its maximum 8-12 hours after ligature, then going down from 2 days onwards. Ventricular extrasystoles with VPC complexes appeared at this time just as sinusal-type blockages diding the course of 12 and 24 hours. The voltages of QRS and T waves were high. The typical heart-attack sings like uneven S-T segment T negative and Q deep were the obvious norms in all the recordings taken after ligature. In the histology study the canges in the cardiac tissue 4-8 hours after the ligature appearing were checked perivascular edema and congestion. Between 24 hours and 2 days , fibrolisis areas of hemorrhaging and inflamatory reaction in intrafibral areas appeared. After 2 and 3 days fibral breakdown, miocitolisis and necrobiosis, there are few collagen fibres with reticulina.