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低溫法때 Quinidine의 抗細動作用에 關한 實驗的 硏究

Antifibrillary Action of Quinidine upon Ventricalar Fibrillation in the Hypothermic Dog

경북의대잡지 1967년 8권 2호 p.169 ~ 187
신도관 (  ) - 경북대학교 의과대학 외과학교실

Abstract


An experimental study was carried out to determine the effect of quinidine upon ventricular ~ibriIIation occurring during total circulatoryocclusion. in the hypothermia. Hypothermia was induced in 58 dogs by body surface cooling with ice water and rewarming with hot water (45-48℃).
Following induction of hypothermia, quinidine was given intravenously in dose of 3440mg/kg of body weight at 30C and again at 2~C of esophageal temperature. The experiments were divided in 2 groups; group I was the one in which thoracotomy was not performed and coo-ling was continued until death, group II seas the other in which it was performed thoracotomy. `´Vhen the esophageal temperature fell to 20 C, cooling was stopped and cardiac inflow and out flow tracts were occluded for 10 (20 dogs) and for 20(10 dogs) minutes at the esophageal temperature of 19_1C, during which time atrioto ny suns performed.
Results were summerized as follows;
1) In control groups ventricular fibrillation Bras occurred in about 50 ~ in group I and 100 in group II. In contrast to these, there suns no ventricular fibrillation in quinidine group of group II ar_d in 40mg. quinidine group of group I, and ventricular fibrillation developed in 16.7% of 30mg. quinidine group of group I.
2) The mortality of contral group in group II was 100%, but in 10 and 20 minutes occludedquinidine group of group II resulted in ?0% and 10% respectively.
3) Right ventricular systolic pressure was lewered during cooling and recovered by rewarming. There was no notable changes to right vE~ntricular end diastolic pressure during both cooling and rewarming in all groups. The venous pressure was elevated during cooling and returned to normal by rewarming.
4) Heart rate and cardiac output were markedly decreased during cooling and these ss~:re not recovered to precooling state despite resvarming. Stroke volume was not changed during entire experimental course in all groups.
5) arterial 0, content and C0~ content were slightly increased during cooling in all groups. pFI was decreased during cooling and recovered to precooling state in group II, in contrast to these, there ss-as increased during cooling in group I.
6) PR interval, QRS compex and QT correcte~3 of E. C. G. were gradually or markedly elongated during cooling and returned to precooling findings by rewarmng.

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