麻醉下的家犬及白兔用OCPC法分別測定實驗前及因腎上腺素所引起的動物心律不整時，主動脈及冠狀竇血液的鈣離子含量。用足以消除此種心律不整的Taurine劑量處理後再注入腎上腺素，同樣測定其動脈及靜脈血鈣含量。腎上腺素注入後6分鐘家犬及白兔的動脈及靜脈鈣含量分別為5.9 ± 0.25 mEq/l與7.5 ± 0.39 mEq/l，及5.6 ± 0.30 mEq/l與6.6 ± 0.34 mEq/l。經Taurine處理後再以腎上腺素注入則家犬靜脈血鈣含量為5.6 ± 0.28 mEq/l，白兔為5.3 ± 0.37 mEq/l；但家犬動脈血鈣含量則為5.8 ± 0.29 mEq/l，白兔則為5.5 ± 0.34 mEq/l。腎上腺素注入後6分鐘動物靜脈血鈣含量經Taurine處理者較未經Taurine處理者呈顯著悵減少（5.6 ± 0.28對7.5 ± 0.39 mEq/l；5.3 ± 0.37對6.6 ± 0.34 mEq/l），而靜脈血鈣含量則僅略為下降。此結果可獲一結論，就是腎上腺素確實可加速家犬及白兔的心肌鈣離子釋放，而Taurine均顯示具有結合心肌內鈣離子傾向，以致產生抗腎上腺素性心律不整的效果。 The effect of taurine on calcium flux of the heart in vivo during epinenhrine-induced arrhythmia was studied in anesthetized dogs and rabbits. The blood sample was drawn from aorta and coronary sinus before and after adruinist.rat ion of a minimal dose of epinephrine which caused ventricular premature contraction (VPC). The same procedure was repeated after taurine infusion. The plasma calcium content was measured by orthocresolphthalein complexon method. Six min after epinephrine administration, the calcium content of arterial and venous plasma was 5.9 ± 0.25 mEq/l and was 7.5 ± 0.39 mEq/l in dogs respectively. It was 5.6 ± 0.30 mEq/l and 6.6 ± 0.34 mEq/l respectively in rabbits. In response to epinephrine with taurine treatment, venous calcium content was 5.6 ± 0.28 mEq/l in dogs and 5.3 ± 0.37 mEq/l in rabbits; while arterial calcium cotent was 5.8 ± 0.29 mEq/l in dogs and 5.5 ± 0.34 mEq/l in rabbits respectively. Six min after 2nd dose of epinephrine, venous calcium content was shown significantly lower after taurine than before (5.6 ± 0.28 vs. 7.5 ± 0.39 mEq/l; 5.3 ± 0.37 vs. 6.6 ± 0:34 mEq/l), whereas arterial calcium content was shown slightly decrease. The results suggest that epinephrine facilitates calcium release from myocardium both in dogs and rabbits, while taurine tends to bind calcium in heart and thereby abolishes the irregular rhythm induced by epinephrine.
