TIKE PtlYYIOIAOQY OF ASCIDIAHS
51
heart, and by application of suit,tiblc. stiriiuli it is possible to drive the
Iieart and artificially tdtm the Iwrtt (Kriclwl. l!M7 ; Anderson, 1968).
((1) Mcchtmic:nl stiniiilatiori ot' tL quicncwit, cwd will acktivate ~ p o n -
tmeoiis r*ontrt~ctioiis arid stret c+ing of iiti rwtive cnd itic*rctkscH t h c h
frequency of bvat (Andcrson, 1 !#OH).
Although loculized priceriialwrn can be identified in this way at
either end of t h c heart it is clear that spontaneous contractions ban take
place a t any point in the heart and in isolated strips of muscle (Schultze,
1901 ; Hunter, I903 ; Krijgsman tind Krijgsman, 1957 ; Mislin and
Krause, 1964 ; Anderson, 1968 ; Kriebel, 1968~). Kriebel and Anderson
have both shown that small pieces of myoendothelium lacking any
portion of the niphe or undifferentiated line will beat spontaneously and
synchronously, and in some cases will exhibit reversal of beat. It seems
clear therefore that rather than having defined pacemaking centres at
either end, the heart is composed of u series of multiple pacemakers and
that any portion of it, may have potential for driving the system. Under
normal circumstances the threshold of the two end regions must be
different from that in the rest of the heart so that they remain in control
snd the critical question is to dotermine what causes them to maintain
this situation and how do they exercise control over the whole system.
Such control could hc exerainrd through nervous pathways, by
ueurohumoral transrnission or by ronduotion through the myoendothelium itself. All evidenw points to thc fact that the heart itself is
lacking in tiny nervous itinervation. Hunter ( 1903) claimed to have
found nerve cells at, either end of thr heart but, subsequent workers,
using more refined techniques, htive been unable to confirm this and
Millar (1 9 5 3 ~ ) suggested that Hunter really saw connertive tissue
c4ements a t the junction of the hwrt and blood sinuses. Alexandrowicz
( 1913) and Jones (197 L) both reported fine nerve fibres extending onto
the heart, wall, but the very careful work of Bone and Whitear (1958),
liriebel (1!M7), Anderson (1968) and Kalk ( 1970) amongst others has
failed to confirm these findings. Furthermore the illustration in Jones
(1971) suggests that, the fibres in question were in the pericardium and
not in the heart.
Hunter (1903) destroycd thr ganglion of Molgub manhattensis by
rauterization and reported that this caused irregularity of beat. Ebara
( 11)71) stitnulated the ganglion of Yerophoru orientdis Arnback and
found that frequency of beat first declined but latcr increased again, and
that this effect was transmitted to the heart of a secorid zooid attached
by a stolon. Hc claimed that the cffec-t icl potei~tiatcd by enerine and
concluded that the heart is undcr ncurcd and rieurohumoral c-ontrol.
51
heart, and by application of suit,tiblc. stiriiuli it is possible to drive the
Iieart and artificially tdtm the Iwrtt (Kriclwl. l!M7 ; Anderson, 1968).
((1) Mcchtmic:nl stiniiilatiori ot' tL quicncwit, cwd will acktivate ~ p o n -
tmeoiis r*ontrt~ctioiis arid stret c+ing of iiti rwtive cnd itic*rctkscH t h c h
frequency of bvat (Andcrson, 1 !#OH).
Although loculized priceriialwrn can be identified in this way at
either end of t h c heart it is clear that spontaneous contractions ban take
place a t any point in the heart and in isolated strips of muscle (Schultze,
1901 ; Hunter, I903 ; Krijgsman tind Krijgsman, 1957 ; Mislin and
Krause, 1964 ; Anderson, 1968 ; Kriebel, 1968~). Kriebel and Anderson
have both shown that small pieces of myoendothelium lacking any
portion of the niphe or undifferentiated line will beat spontaneously and
synchronously, and in some cases will exhibit reversal of beat. It seems
clear therefore that rather than having defined pacemaking centres at
either end, the heart is composed of u series of multiple pacemakers and
that any portion of it, may have potential for driving the system. Under
normal circumstances the threshold of the two end regions must be
different from that in the rest of the heart so that they remain in control
snd the critical question is to dotermine what causes them to maintain
this situation and how do they exercise control over the whole system.
Such control could hc exerainrd through nervous pathways, by
ueurohumoral transrnission or by ronduotion through the myoendothelium itself. All evidenw points to thc fact that the heart itself is
lacking in tiny nervous itinervation. Hunter ( 1903) claimed to have
found nerve cells at, either end of thr heart but, subsequent workers,
using more refined techniques, htive been unable to confirm this and
Millar (1 9 5 3 ~ ) suggested that Hunter really saw connertive tissue
c4ements a t the junction of the hwrt and blood sinuses. Alexandrowicz
( 1913) and Jones (197 L) both reported fine nerve fibres extending onto
the heart, wall, but the very careful work of Bone and Whitear (1958),
liriebel (1!M7), Anderson (1968) and Kalk ( 1970) amongst others has
failed to confirm these findings. Furthermore the illustration in Jones
(1971) suggests that, the fibres in question were in the pericardium and
not in the heart.
Hunter (1903) destroycd thr ganglion of Molgub manhattensis by
rauterization and reported that this caused irregularity of beat. Ebara
( 11)71) stitnulated the ganglion of Yerophoru orientdis Arnback and
found that frequency of beat first declined but latcr increased again, and
that this effect was transmitted to the heart of a secorid zooid attached
by a stolon. Hc claimed that the cffec-t icl potei~tiatcd by enerine and
concluded that the heart is undcr ncurcd and rieurohumoral c-ontrol.