458 DISCOVERY REPORTS 



to suppose that any tension on the pericardial floor, such as must occur on contraction 

 of the pericardial dilator, would also cause these valves to close. 



It thus appears that, when the pericardial dilator contracts, the cardiac valves must 

 close, and hence that the heart cannot be in systole. This leads to the second possibility 

 that the heart and pericardium contract and dilate together. 



It is quite possible for the heart and pericardium to contract together, but they 

 cannot dilate together. The expansion of the heart must be passive. There are no 

 muscles attached to its walls by which it could be actively dilated, and the structure 

 of the parenchymatous cells covering the outer surface of the heart is such that they 

 could not exert any tension on the heart walls. This being so, the pressure around the 

 heart as it expands must be the same as, or slightly higher than, the pressure in the heart. 

 Only in these circumstances could the ostia open and allow blood to pass in, and the two 

 ostia are the only entrances to the heart, the aortic and hepatic valves being closed by 

 the contracting pericardial dilator. Now enlargement of the pericardium would tend 

 to make this a region of low pressure. Blood would tend to be sucked in from all 

 possible sources. That is, blood would tend to be sucked out of the passively expanding 

 heart, and this would immediately close the ostia. 



The conclusion of the above reasoning is that there can be no diastole and systole 

 of the pericardivmi synchronous with that of the heart. There is still another possibility, 

 namely, that the volume of the pericardium remains practically constant, and this 

 I believe actually to be the case. The pericardial muscles, by their activity, control 

 the volume and internal pressure of the pericardium, so that the heart is free to 

 pulsate and, at the same time, blood is admitted to replace that forced out by 

 the heart. 



I suggest that the pericardial dilator and the compressors contract together during 

 diastole of the heart. 



At the sides of the attachment of the median sub-pericardial muscle are the attach- 

 ments of the pericardial compressors which run forwards and outwards to their anterior 

 attachments in the lateral walls of the pericardium. Contraction of the latter muscles 

 will thus pull inwards both the lateral and the posterior walls of the pericardium, and 

 so tend to reduce the pericardial space. 



Also the upper attachment of the median sub-pericardial muscle is in the middle 

 point of the lower edge of the soft flexible hinder wall of the pericardium. Hence, 

 contraction of the pericardial dilator, through this muscle, will pull downwards and 

 slightly forwards the hinder wall and this will tend to counteract, but only slightly, 

 the enlarging effect of the dilator muscle. 



Thus I deduce that contraction of the pericardial dilator closes the aortic valve and, 

 therefore, that during this contraction the heart must be dilating. At the same time, 

 it must tend to increase the pericardial space and so diminish the intra-pericardial 

 pressure. But, if this were to happen, the heart could not dilate. Hence, to counteract 

 this, the pericardial compressors contract and so, during diastole, both the pericardial 

 dilator and the pericardial compressors contract. 



