JOHN BUCK 75 



unclear whether or not the more prolonged oscillations which occur at the end 

 of the burst can be considered to be basically the reverse of the spiracular open- 

 ing, the response as a whole seemingly differs also from reversible or self- 

 restoring events like the muscle twitch and nerve impulse. Because of the 

 necessarily arduous type of recording, Scheiderman and his co-workers quite 

 naturally chose for their observations pupae with high frequencies of burst 

 production (tig. 3). Judging from our manometric records on another species, 

 such pupae tend to have a more prolonged and 'smeary' type of burst than 

 long-period pupae. It is, therefore, possible that both start and end of a normal 

 burst may often involve sharper transitions between closed and open valve 

 positions. 'Sharper' bursts are in fact seen when the ambient O2 concentration 

 is increased (lig. 4). Furthermore, though the spiracular flutter prior to full 

 opening is a reasonable explanation of similar perturbations in continuous 

 respirometer records (fig. 2), the possibility of such flutter being abnormally 

 exaggerated should not be excluded in view of the fact that the valves have 

 to be exposed surgically before direct observation is possible. 



The mean respiratory quotient for an entire pupal CO2 release cycle is a 

 conventional 0.78, but during the interburst period it is 0.3 or less (15, 4). 

 This indicates that although metabolic CO2 is being produced steadily it is 

 mainly impounded during the interburst periods and released in the inter- 

 vening bursts. This suggests that tracheal and tissue COo concentration must 

 rise during the interburst period and that the eventual occurrence of a burst 

 may mark the attainment of a critical value or threshold. For present purposes 

 it does not matter w^hether the ultimate trigger is molecular CO2, bicarbonate 

 ion or hydrogen ion. 



There is, however, no indication that such a critical concentration could in- 

 volve any sort of biochemical discontinuity. On the contrary, all available evi- 

 dence suggests that if attainment of a particular CO2 concentration is the 

 stimulus for spiracular opening, the actual trigger is simply one additional 

 regular increment — the 'final straw,' so to speak. Thus it has been found (5) 

 by equilibration of normal Agapema pupae with various CO2-N2 mixtures of 

 constant O2 concentration that the average internal CO2 concentration is of the 

 order of 6 per cent, and that the change during the interburst period does not 

 exceed 20 per cent of that value (i.e., a range from 5.5 to 6.5%). This fits well 

 with the observed steady 20 per cent rise in CO2 release rate over the inter- 

 burst period. ISIoreover, equilibration of drawn blood with similar gas mixtures 

 has confirmed both the absolute values of the internal CO2 concentration range 

 and the expectation that the gas is taken up linearly with ambient CO2 con- 

 centration over a wide range (2, 3). Hence there is every reason to believe that, 

 whatever the absolute value of the tracheal or tissue CO2 concentration at the 

 time of the burst, the increase which ultimately sets off the burst is small. 

 Actually, considering the fact that the concentration rises only i per cent over 



