-C--O-CH-CH2-C-O-CH-CH2 HKH> =(C2Hs)2

Medical opinion regarding intravenous admininstration of procaine has changed markedly in the past few years. Formerly the intravenous injection of this as well as other local anesthetic agents was avoided as an accident of serious consequence. Today the judicious venoclysis of procaine is accepted in many quarters as safe and as a quite useful procedure. Within the past five to ten years numerous publications have appeared to document the utility of intra-venous procaine as an analgesic, antianaphylactic, antipruritic or peripheral anesthetic agent, or as an inhibitor of cardiac irregularities. Usually, the local anesthetic agent has been administered slowly and in large volume after the method of Lundy (1942). For the heroic management of cardiac fibrillation or asystole, high concentrations of procaine contained in a small volume have been administered (Lampson et al., 1948; Roualle, 1950). The usually short duration of action that attends the intravascular administra-tion of procaine has been accounted for by Brodie, Lief and Poet (1948) as being due to the cleavage of its ester linkage by plasma esterases (Glick, 1942; Soehring, 1948), in the general manner described by Kisch, Koster and Strauss (1943). To avoid rapid inactivation by hydrolysis, the ester linkage has been replaced by an amide group in an agent that has been proposed recently for the control or prevention of ventricular arrhythmias (Irvin, 1951; Kinsman et al.