00
IVAN (IOODBODY
metabolite, bvhttving i t s sensory rwcptors. It is then postulated that in
an active pacemtkkcr t8he tlirt~shold of rcsponse to this " metabolite "
slowly incrcttses iintil the piwcmakrr no longer rcsponds to it and
bccorncs inwtive. At this p i n t thr t h ~ s h o l d of response in the other
pacemttkcr hw fallen i b t l ( l it, (xi ti now rcspo~id to the. stimulus. Pt~cwniiltrr
fatigric tnity their bc t~xpliLiricd, tiot i t 1 tmns of inunctlr fibt igiir, hut in
terms of incw?asing rc-sistanw to scmory stimulation.
If we awept thc postulate that d l heart cells have pacemaker
properties (see p. 51) we can only iwcept thc hypothesis of pacemaker
fatigue if it can be shown that the terminal pacemakers respond differently to other cells. That this is probably the case is shown by the
differences in electrical aictivity already demonstrated.
Positive identificaat ion of t~ " metitbolite " which might control
pacemaker activity awaits confirmation but it is significant that in
Aecidia Kalk ( 1970) has demonstritted the existence of multivacuolar
vesicles in cytoplasmic lobes projecting into the heart lumen (see p. 48)
and Kalk believed that thesc vesicles itre discharged into the blood
it passes through the heart. She ralculsted that there are about 100 of
these vesicles per cell and suggested that during contraction the active
end of the hcwt will be slowly depleted of the substance secreted by the
vacuoles while the other end ofthe hcart will be subjected to a continued
flow of the rriitterial secreted by the cells prewding it in the heart. She
further siiggchfited thiLt concentration gradient will develop along the
length of the heart with thc highest concentrution at the opposite end
to thc active prcernakcr. ' Chis eiisurw that this end is the first part of
the heart to bc subjected to ii high enough internal concentration of the
substtlnce to start " firing " before the rest of the heart. Kalk states
that " In this way pacemaking will be taken over by alternate ends of
the heart after a period of quiescence. " She suggeRted that acetylcholine may be the substance iiivolved but in view of evidence presented
earlier on the effect of acetylcholine on the ascidian heart (p. 52) this
is unlikely.
Anderson (1968) hiis suggested that fatigue as such need not be
involved to account for heart best reversal but that it is due to changes
in the levels of frequency at either end of the heart. As long as one
portion of the heart, has a higher frequency than the rest it will remain
dominant and she has shown (Fig. 18) that while frequency remains
fairly cwnstant at the hypobranchial end it fluctuates at the visceral
end between periods of high and low frequency. She has also shown that
the electrical characteristics of the visceral end are different and that
the threshold voltage for onc-to-one driving of the heart at different
frequencies shows a liricitr response in the case of the hypobranchial
IVAN (IOODBODY
metabolite, bvhttving i t s sensory rwcptors. It is then postulated that in
an active pacemtkkcr t8he tlirt~shold of rcsponse to this " metabolite "
slowly incrcttses iintil the piwcmakrr no longer rcsponds to it and
bccorncs inwtive. At this p i n t thr t h ~ s h o l d of response in the other
pacemttkcr hw fallen i b t l ( l it, (xi ti now rcspo~id to the. stimulus. Pt~cwniiltrr
fatigric tnity their bc t~xpliLiricd, tiot i t 1 tmns of inunctlr fibt igiir, hut in
terms of incw?asing rc-sistanw to scmory stimulation.
If we awept thc postulate that d l heart cells have pacemaker
properties (see p. 51) we can only iwcept thc hypothesis of pacemaker
fatigue if it can be shown that the terminal pacemakers respond differently to other cells. That this is probably the case is shown by the
differences in electrical aictivity already demonstrated.
Positive identificaat ion of t~ " metitbolite " which might control
pacemaker activity awaits confirmation but it is significant that in
Aecidia Kalk ( 1970) has demonstritted the existence of multivacuolar
vesicles in cytoplasmic lobes projecting into the heart lumen (see p. 48)
and Kalk believed that thesc vesicles itre discharged into the blood
it passes through the heart. She ralculsted that there are about 100 of
these vesicles per cell and suggested that during contraction the active
end of the hcwt will be slowly depleted of the substance secreted by the
vacuoles while the other end ofthe hcart will be subjected to a continued
flow of the rriitterial secreted by the cells prewding it in the heart. She
further siiggchfited thiLt concentration gradient will develop along the
length of the heart with thc highest concentrution at the opposite end
to thc active prcernakcr. ' Chis eiisurw that this end is the first part of
the heart to bc subjected to ii high enough internal concentration of the
substtlnce to start " firing " before the rest of the heart. Kalk states
that " In this way pacemaking will be taken over by alternate ends of
the heart after a period of quiescence. " She suggeRted that acetylcholine may be the substance iiivolved but in view of evidence presented
earlier on the effect of acetylcholine on the ascidian heart (p. 52) this
is unlikely.
Anderson (1968) hiis suggested that fatigue as such need not be
involved to account for heart best reversal but that it is due to changes
in the levels of frequency at either end of the heart. As long as one
portion of the heart, has a higher frequency than the rest it will remain
dominant and she has shown (Fig. 18) that while frequency remains
fairly cwnstant at the hypobranchial end it fluctuates at the visceral
end between periods of high and low frequency. She has also shown that
the electrical characteristics of the visceral end are different and that
the threshold voltage for onc-to-one driving of the heart at different
frequencies shows a liricitr response in the case of the hypobranchial