280 INVERTEBRATE PHYSIOLOGY 



not appear to have a specific influence and thus does not prove that extrin- 

 sic regulation exists. As far as pharmacological evidence is concerned, we 

 are again confronted with the contradictions already mentioned in the 

 discussion of the neurogenic or myogenic nature of the pacemakers. We 

 therefore feel that the data available are not sufficient to postulate the 

 presence of cholinergic and/or adrenergic extrinsic nerves. 



A question which deserves our attention is the cause of reversal. As we 

 know, the periodic reversal of the direction of pulsation is a normal phe- 

 nomenon in the tunicate heart. The possible cause and purpose of this re- 

 versal have long been a matter of discussion. A number of workers have 

 advocated the so-called "back-pressure theory" (see Krijgsman, 1956). 

 According to them the capacity of the capillary beds is so small that 

 a gradual congestion builds up when the heart is pumping blood in 

 a given direction. This should cause a reversal in order to obviate the 

 back-pressure. Arrest of the leading center by a possible back-pressure 

 is a tenable hypothesis, but one cannot understand why such a back- 

 pressure could stimulate the resting center and thus cause a reversal of 

 beat. Haywood and Moon ( 1950), who recently revived the back-pressure 

 theory, clearly understood this and wanted to restrict the influence of the 

 possible back-pressure to the arrest of the leading center. Haywood and 

 Moon treated the subject in a mathematical way. Unfortunately, they in- 

 troduced many simplifications in order to make such a treatment possible. 

 Moreover, they adjusted their arbitrary constants to fit the observations, 

 which makes the resulting agreement between theory and experiment 

 rather less convincing. 



Other workers maintain that the cause of reversal is an inherent prop- 

 erty of the pacemakers. The leading center apparently cannot maintain 

 its optimal frequency because of a kind of fatigue. There are several points 

 in favor of this hypothesis : 



(1) It has been shown by Quincke and Stein (1932) that the thresh- 

 old for electrical stimulation of a pacemaker increases near the end of the 

 pulsation period. This indicates a kind of fatigue, not inhibition by in- 

 creasing back-pressure. 



(2) If there is no back-pressure (isolated heart), reversal still occurs 

 fairly regularly. 



(3) An isolated center or halved heart shows, in spite of the absence 

 of back-pressure, a pattern of alternating high and low frequency or 

 temporary rest. 



(4) The fundamental assumption of the "back-pressure theory" is a 

 lower capacity of the capillary bed than that of the large vessels. This has 

 never been proved. 



