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Messrs. J. C. Bramwell and A. V. Hill. 



very slowly, allowing the tissue a long time to reach its final equilibrium. 

 From the point of view of the static effect of the diastolic pressure on the 

 arteries, he succeeded ; from that, however, of the dynamic effects occurring 

 in the rapid cycle of events associated with the pulse, his precautions aggra- 

 vated the error, and must have caused the increase of volume per milli- 

 metre of Hg to be much larger than that occurring in a rapid change of 

 pressure. It is quite conceivable that a pressure, lasting (say) for - l second, 

 causes an expansion not greater than half of that resulting from an equal 

 pressure maintained for 10 minutes ; in this case a calculated velocity based 

 on the latter would be only about two-thirds of an observed velocity depend- 

 ing on the former. This elastic " after-action " therefore probably causes all 

 the velocities in Table I to be too low ; the effect is similar in character to 

 that caused by adopting the formulas for the isothermal expansion of a gas in 

 calculating the velocity of sound. The safest thing to do is to measure the 

 velocity directly, and so to deduce the constants of the true adiabatic 

 expansion. Finally, we see (in I) that in a vein the calculated velocity 

 at low pressures is very low, a conclusion which agrees with an observation of 

 Morrow (6), and must be borne in mind in comparing the time relations of the 

 jugular pulse with those of other events in the heart or circulation. 



The most important point brought out by Table I is the dependence of the 

 velocity upon the pressure. In the case of man, the pressure involved is the 

 diastolic pressure, that on which the wave is superimposed. This implies a 

 decrease in extensibility with increase in length, an effect analogous to that 

 occurring in muscle. This is important in various ways, but particularly in 

 experimental work, where it shows the necessity of recording the diastolic 

 pressure at the same time as the velocity of the pulse wave. Its magnitude 

 is emphasised in the experiment described below. 



It is often suggested that in the living animal the velocity of the pulse 

 wave may be affected by contraction of the involuntary muscle around the 

 arteries. In so far as the contraction of involuntary muscle may affect the 

 extensibility of the artery this will be the case, but in no other way. The 

 part of the wave whose velocity is measured is the very rapid rise at the 

 opening of the aortic valves, a rise which is detectible in a few thousandths 

 of a second. It is inconceivable that a contraction of slow involuntary muscle, 

 as we ordinarily know it, could affect the rate at which such a sudden rise is 

 transmitted. The transmission of the pulse wave, therefore, is a purely 

 mechanical phenomenon, its velocity being an indicator of the elasticity of 

 the vessels, as modified by any conditions (muscular or otherwise), obtaining 

 at the moment. 



The chief difficulty in the observation of the velocity of the pulse wave in 



