低溫下 心室顫動에 미치는 adrenergic β-receptor 封鎖藥物의 效果

Abstract

[한글]

[영문]

Although there are many studies concerning the prevention or treatment of vontricular fibrillation during hypothormia, the need for a better understanding of the basic mechanism of cardiac fibrillation has become increasingly apparont.

The sympathetic nervous system has long been known to be a factor in the production of ventricular fibrillation. Intravenous injection of opinophirno or isoproteronol induces cardiac arrhythmia, which may pregress to a fatal ventricular fibrillation, ospecially when cardiac muscle has been proviously sonsitized by chlaroform, hypothormis, otc. (Danes, 1952; Moore & Swain, 1960). Moro recently it has boon roported that the protreatment with bretylium, which is known to blook the reloase of catochalominos, signifcantly decreased the incidonce of ventricular fibrilation in cats undor hypothormia (Lee, 1963). Mendoz et al. (1961) and Shumackor et al. (1956) showed that sympathectomy, with or

Summary and Conclusion

1. In normal cats, during the course of hypotheraia the heart rate gradually slowed as the temporature fell. The average temperature of seven animals, after heart rate reduction to one-third of normal, was 24.1℃. when the espohageal temperature reached an average 20.5℃(17-22℃), vontricular fibrillation occurred in all animals. the electrocardiogram revealed a marked prolongation of the P-R interval and !-T interval, and a widening of the QRS complox. A significant elevation of the ST segment, inversion of T-wave and arrhythmia were observed at nean temperatures of 25.6℃, 25.4℃ and 21.9℃.

2. Nothalide (0.1-0.2 mg/kg/min) or MJ-1999 (0.01-0.02 mg/kg/min) was administered by continuous infusion during the induction of hypothermia. Changes in the heart rate, ST segment and T-wave in these animals were the same as those observed in the control group. However, the administretion of these drugs

completely prevented ventricular fibrillation. The acction of MJ-1999 was more potent than that of Nethalido. However, the administration of dichloroisoproterenol (DCI) failed to protect the cats from ventricular fibrillation induced by hypothormia.

From the above results, it may be concluded that ventricular fibrillation during hypothermia is related to the adronergic beta-recoptor in the heart.

Wihtout adrenalectomy, caused a decroase in the incidence of ventricular fibrillation under the same conditions.

Recently dichloroisopratorenol (DCI), Nethalide or MJ-1999, has boon introduced as a potont blaocking agent for t:: beta-adronorgic receptor (Powell & slater, 1958; Black & Stophenson, 1962; Dungan & Lish, 1964). these drugs have made it possible to investigate the importance of caridac sympathetic activity in the

production of arrhythmias.

Present studies investigate whether or not these adrenergic bota-receptor blockig agents possess a protective action against ventricular fibrillation during hypothermia, and to study the relationship between sympethetic activity and hypothermic ventricular fibrillation.

Cats weighing 3-4 kg wore anesthetized with pentobarbital sodium, 25-35 mg/kg intraperitoneally and artificially ventilatod by a respirator. The apparatus and method of hypothermic were described proviously (Lee, 1963). The electrocardiogram was recorded with a Sanborn Model 52, electrocardiograph,and asophageal temperature was checked with a telethermemetor. DCI(15-20 mg/kg), Nathalido (0.1-0.2 mg/kg/min) and MJ-1999 (0.01-0.02 mg/kg/min) were injected intravenoualy.