THE HEART BEAT. 561 



manometer, which registered the lowest pressure reached during 

 the period of observation. By this method they and others have 

 shown that in an animal (dog) with an opened thorax the pressure 

 in the interior of the ventricles may be negative to an extent equal 

 to 20, 30, or even 50 mms. of mercury. Moreover, by the use of 

 some form of elastic manometer, such as the Hiirthle instrument 

 (p. 495), it has been shown that this negative pressure occurs at the 

 end of the period of relaxation', at the time, therefore, at which it 

 might be supposed to exert a marked influence upon the inflow of 

 venous blood. It should be added, however, that a negative 

 pressure can not be shown for every heart beat. It may be absent 

 altogether or slight in amount, varying, no doubt, with the force of 

 contraction and the condition of the heart. Physiologists have 

 attempted to determine the cause of this negative pressure and the 

 extent of its influence on the blood-flow. With regard to the first 

 question, so many answers have been proposed that it is difficult 

 to arrive at a satisfactory opinion. According to some, the heart 

 tends to dilate at the end of its systole by virtue of its own elasticity, 

 that is, the elasticity of its own musculature or of the connective 

 tissue contained in its substance, for example, beneath the en- 

 docardium, in the walls of the arteries, etc. This view, however, 

 finds little or no support from direct experiments made upon the 

 fresh, living heart. If such a heart in a bloodless condition is 

 squeezed by hand there is no evidence of an elastic recoil as in the 

 case of a syringe bulb. Others have traced the expansion of the 

 ventricle and the resulting negative pressure to the sudden in- 

 jection of the coronary system from the aorta at the beginning of 

 diastole. The heart in contracting exerts a force greater than that 

 of the blood in the coronary vessels, and probably, therefore, these 

 vessels are emptied and their cavities obliterated in part. At the 

 beginning of diastole they are rein jec ted with blood under a pressure 

 of perhaps 100 mms. of mercury, and this fact seems to offer a 

 probable explanation for a partial dilatation of the ventricular cavity 

 and a production of negative pressure in the brief interval before the 

 opening of the auriculo-ventricular valves. No view, however, has 

 met with general acceptance, and the cause or causes that produce the 

 negative intraventricular pressure are still a subject for investiga- 

 tion. Regarding the second question proposed above, namely, 

 the extent of the influence of this negative pressure on the flow 

 of venous blood to the ventricles, much diversity of opinion also 

 exists. Direct experiments made by Martin and Donaldson* 



* Martin and Donaldson, "Studies from the Biological Laboratory, Johns 

 Hopkins University," 4, 37, 1887; also Martin's "Physiological Papers," 

 Baltimore, 1895. See also, for confirmatory results, von den Velden, "Zeit- 

 schrift f. exp. Pathol. u. Therapie," 1906, iii., 432. 

 36 



