228 K. G. HOSKHSTS 



but soon subsides as the animal drowns in its own exudate. The possibility 

 of such an 'outcome should be kept in mind in the therapeutic use of 

 epinephrin in any condition in which failure of the right heart threatens. 



Effect of Epinephrin upon Venous Pressure 



Venous pressure may be increased in a number of different ways. The 

 three chief possibilities are by interference with the flow into the thoracic 

 cavity, by a decrease in the peripheral resistance, allowing relatively more 

 blood to pass from the arterial to the venous side, and by a decrease in the 

 caliber of the veins themselves. The flow into the thorax may be impeded 

 either by factors which interfere with respiration or by factors which de- 

 p'ress cardiac efficiency. Epinephrin conceivably may affect venous pres- 

 sure by modifying any of these factors. 



That epinephrin may directly stimulate the veins to contraction has 

 been shown by a number of observers. Gunn and Chavasse (1913) ap- 

 plied epinephrin (1:100,000 solution) directly to isolated ring prepara- 

 tions from various veins of the sheep. These included the external jugular 

 and mesenteric veins, and the superior and inferior venae cavae. They 

 noted constriction similar to that which occurs in artery rings under like 

 conditions. The external jugular contracted more extensively than did 

 the cavaB. It was concluded that the veins probably receive venoconstrictor 

 fibers from the sympathetic nervous system. Crawford and Twombly, in 

 the same year, publiished observations corroborating the findings of Gunn 

 and Chavasse. They worked with ring preparations from the femoral, 

 iliac, and saphenous veins of the dog, noting contraction in each. In case 

 of veins from fowls, however, some veins were found to contract and 

 others to fail to do so. 



Other observers had previously investigated the problem by making 

 intravenous injections of suprarenal extract or epinephrin and measuring 

 the pressure reactions in the large veins. Hill (1900) found that the 

 administration of sufficient suprarenal extract to a vagotonized dog to 

 cause a rise in arterial pressure of 1170 mm. of magnesium sulphate 

 solution left the pressure in the vena cava unchanged. Plumier(b) (1909) 

 administered epinephrin to the intact dog and noted a rise in the pressure 

 in the superior and inferior venae cavse. This he attributed to the slowing 

 of the heart which ensues under the conditions of his experiments. The 

 fact that the rise in caval pressure was not so great as might be expected 

 from the slowing of the heart that was produced, he interpreted as due 

 to increased force of the heart beat. After cutting the vagi, unless very 

 large doses were administered, there was little or no change in venous 

 pressure. This was true in spite of the fact that the marked vasoconstric^ 

 tion resulting from the epinephrin administered materially decreased the 



