128 



320 J. A. macwilliam 



verse relation of heart rate and arterial pressure only occurs in certain 

 conditions, such as are not usually present. It does not occur in the 

 great majority of normal elevations of blood pressure, e.g., in muscular 

 exercise with its raised pressure and quickened heart, nor in the similar 

 conjunction seen in emotional excitement, nor in sleep where both 

 pressure and heart rate are -lowered, nor in some forms of circulatory 

 depression accompanied by a slowed heart and a reduced blood 

 pressure. 



A more warrantable statement, much more limited in scope than the 

 so-called law of inverse relation, is that when the blood pressure in the 

 head is raised by an increase of the peripheral resistance in the circula- 

 tion or by local causes acting on the head (hydrostatic factor, etc.), 

 such pressure tends to increase the controlling power of the vagus 

 centre, provided no other influence plays upon that centre in the direc- 

 tion of reducing its activity — as occurs during motor effort, emotional 

 stress, etc. Conversely a lowered pressure in the head involves di- 

 minished activity of the vagus centre unless this is opposed, as may 

 happen, by some concomitant influence tending to stimulate the 

 centre. 



It is evident that if persistent high blood pressure is due, as is com- 

 monly assumed, to excessive peripheral resistance there must be some 

 agency in action which counteracts the working of Marey's law — 

 since, as is well known, the heart is not slowed even in presence of 

 exceedingly high arterial pressures. Thus in Mannaberg's (93) ob- 

 servations on 241 cases of high pressure, 55 per cent had normal pulse 

 rates, while 43 per cent showed tachycardia and 3 per cent bradycardia; 

 the tachycardias were chiefly in women and probably related to endo- 

 crine disturbances (thyroid, etc.). The mechanism of this is unknown. 

 There is no evidence to show why the usual slowing influence of high 

 pressure is not exercised — through direct influence on the vagus centre; 

 and also reflexly through high pressure in the heart and distention of 

 the aortic walls, if such a mechanism exists — as affirmed by Eyster and 

 Hooker (41) for the normal animal, though this view is not supported 

 by the recent work of Anrep and Starling (5) with cross-circulation 

 experiments. 



While it is known that high venous pressure acting on the right 

 heart reduces vagus control and accelerates the heart, as Bainbridge 

 found by increasing the volume of the blood, there is no ground for 

 regarding this as a means of abrogating the slowing effect of an ex- 

 cessively high arterial pressure due to abnormally great peripheral 



