402 



Mr. D. T. Harris. 



2°. Diminution of the plasma chlorides and increase of the alkali reserve 

 (L. J. Henderson, 1909) 



H a C0 3 + NaCl ^ NaHCOs + HCl. 



from 1° of plasma alkali reserve. 



3°. Some free lactic acid is formed from part of the sodium lactate in (1) 

 and part of the HC1 in 2° 



Sod. lactate + HC1 — Lactic acid + NaCl. 



This lactic acid penetrates the corpuscles just as the HC1 from 2° does 

 (Hamburger, 1904) and the H 2 C0 3 from 1° (Buckmaster, 1918). 



4°. The oxidative removal of lactic acid continues for some minutes 

 (Fletcher and Hopkins) and coincides with the recovery heat production (Hill) 

 and the increased oxygen intake (Verzar) following muscular activity. 



It is believed by many, though on insufficient data, that lactic acid and CO2 

 act by increasing the H-ion concentration. Calculation of the Ph of the blood 

 from measurements of the alveolar CO2 may show a difference of 002 during 

 muscular exercise (Campbell, Douglas, Hobson, 1914) ; a rise of acidity has 

 been inferred from estimations of the affinity of the blood for oxygen 

 (Mathison); more recently Barcroft and Parsons (1920) have found that 

 muscular work causes a fall in Ph of - 08 in the blood when defibrinated "and 

 completely reduced. 



The erythema arising in electro-therapeutics in the area of the kathode 

 suggests the possibility of a direct action by the H-ions (or Na-ions ?). In 

 normal activity, such a direct action of lactic acid is impossible in the- 

 presence of the bicarbonate of the tissue fluids ; the increase of alkali reserve 

 seen to occur above must also tend to keep down the H-ion concentration 

 of the plasma, hence the ultimate depressant of the blood-vessel wall must be 

 the CO2. Patterson and Starling (1914), working on the isolated heart-lung 

 preparation, have shown that the heart relaxes more and more as CO2 is 

 added to the air ventilating the lungs. Evidence is accumulating that C0 2 

 possesses specific properties in its action upon the tissues which are not 

 possessed by other acids (Schwarz and Lemberger, 1914, C. Lovatt-Evans) ;. 

 fig. 17 is interesting in this connection. 



Finally, we have shown in § 5 that C0 2 and lactic acid, when injected into 

 the blood stream, act as powerful vaso-dilator substances, and again in § 6 

 that these acid metabolites are formed in increased amount during muscular 

 activity. In so far as functional hypersemia is adequately explained by the 

 vaso-dilator action of metabolites, we are in full agreement with Barcroft 

 (1914); but in § 4 we have shown the separate existence of vaso-dilator 

 nerves which were not, at least in the above experiments, called into play 



