324 



E. LUNDSGAARD 



VOL. 4 (1950) 



S 5 



i 





From these simple observations it seems safe to conclude that the observed drop 

 in oxygen uptake in an isolated liver is due to changes in the blood and not to changes 

 in the liver tissue as such. 



Though as mentioned the most probable assumption is that the decline in oxygen 

 uptake is due to the disappearance of some substance from the blood the possibility 

 remains that it is due to accumulation of some inhibitory substance. Also in that case 

 addition of fresh blood might be expected to cause an increase by dilution of the inhi- 

 bitory agent. Though the course of the fall in oxygen uptake appears incompatible with 

 such an assumption an attempt has been made to elucidate this possibility experimentally. 

 Some livers were perfused with washed red, blood corpuscles suspended in an arti- 

 ficial plasma. Dextran, a polysaccharide preparation, was added to the artificial plasma 

 to secure a normal colloid osmotic pressure. Though the result of these experiments was 

 not quite clearcut due to technical difficulties which need not be mentioned here it can 

 safely be stated that only a very slight initial fall in oxygen uptake was observed in 



these experiments. 



The observations so far 

 mentioned support the assump- 

 tion that the liver normally is 

 supplied by the blood with a 

 substance which affects its me- 

 tabolic rate. 



That this hypothetic sub- 

 stance probably is not a specific 

 hormone formed in one of the 

 endocrine glands is indicated by 

 experiments carried out in the 

 following way. 



A perfusion apparatus with 

 a double pump and two circuits 

 but with a common oxygenator and blood reservoir was used. A liver was isolated and 

 attached to one of the circuits, the other being short circuited. The oxygen uptake of the 

 liver was followed in the usual way and when the oxygen uptake had dropped a hind 

 limb preparation was attached to the previously short circuited circuit. The venous blood 

 returning from the liver and the hind limb preparation in this way is mixed in the oxy- 

 genator and the blood reservoir and the liver is supplied with a mixture of blood retur- 

 ning from the liver and the hind limb preparation. As seen from Fig. 3 the oxygen 

 uptake of the liver starts to increase as soon as the hind limb preparation is shunted 

 in. In about 15 minutes it reaches a fairly constant level which is maintained until the 

 hind limb preparation is shunted out. The shunting out of the hind limb preparation 

 is followed by a gradual decline in the oxygen uptake following a course similar to that 

 of the initial fall. The increase is marked though the initial high oxygen uptake is not 

 restored. In the experiment presented in Fig. 3 the hind limb preparation after having 

 been left without circulation for 35 minutes again was shunted in for 20 minutes. The 

 response was practically identical with the first response. The correspondence between 

 the two response must be emphasized inasmuch as it speaks strongly against the possi- 

 bility that lactic acid may be responsible for the increase in oxygen uptake. This point 

 will be discussed later ; it may be only mentioned that the lactic acid concentration in 



References p. 32g. 



30 



60 



90 



120 



150 180 



time in min. 



Fig. 3. Oxygen consumption of isolated cat liver. Hind 

 limb preparation shunted in at f and out at | . 



