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BAINBRIDGE (1915)3) found that increased venous filling of the heart in dogs following intravenous injection of saline and defibrinated blood led to cardiac acceleration. This acceleration was thought to have been brought about chiefly by diminution of vagal tone and partly by increased accelerator tone. SASSA & MIYAZAKI (1920)18) confirmed in cats and dogs the findings of BAINBRIDGE. However, many authors have subsequently observed varied effects, tachycardia and bradycardia, in response to intravenous infusion (for further references see AVIADO & SCHMIDT 19552)). Some investigators (PATHAK 195917), TIITSO 193720), 193921)) showed that cardiac acceleration produced by raised venous pressure or auricular distension could be elicited even after section of the vagi. They concluded therefore that the acceleration was due to a local action directly on the sino-auricular node. On the other hand, AVIADO, LI, KALOW, SCHMIDT, TURNBULL, PESKIN, HESS & WEISS (1951)1) isolated and perfused the right side of the heart in dogs. They observed a fall of blood pressure and heart rate when the pressure was raised in the right heart. Such effects were abolished by cutting the vagi.

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