THE PHYSTt )LO(> l7 OP ASCIDTANS
55
froni cell to cell. I n u ht,w piper Kriebel (1 968b) has shown that the
cell membrtmes in the heart hsve t i resistivity of 210 ohms/cma but the
nexuses (see p. 46) have a cell resistivity of only 0.2 ohm/cm2. This
suggests that the nexuses, us well as forming a transepithelial ionic
barrier, rire also low resistance pathwtiys for electrical conduction. In
order to show that such condriction is possible Kriebel replaced the
intercelliilur fluid by u sucrose 1)arric.r and demonstrated that an electrical impiilsc wuld still pass along the heart. The only pathway left
to it nndw these c.ir(.rinlst,illlcew is tlirough the nexuses.
On tlic basis of d l this evitlmcc it is reasonable to conclude that
propagutlion of the w u v ~ of (*ontrwtion in the ascidian heart is by
clectricul condiwtion from cell t o c c h l l .
Under normd conditiona t h r hewt is (.ontrolled by the pacemakers
located ttt either end of the heart, but in C i o m intestinalis during
longitudinal c~~itraction a third pacemaker may become active and
drive the blood towards either cntl. This is the C centre of Skramlik
(1938). The ( ” ceiitre w i i tw w t ivutchd experimentally by applying
pressure to this region of the hcurt. ‘l’hp cells of the remainder of the
hewt ctll hrbve pacemaker c.aptihilitic.s but do not at any time take
coiitrol of thc hcwt. The question arises then as to how the two end
pticemalwrs rntrintain their domiimwe over the rest of the heart and
thereby control heart beat. Most of our understanding of this is due to
the work of Kriebel (lO(i8c, 1970) itnd Anderson (1968).
In order to generate ;L wuve of contraction in a passive heart it is
necessary to apply several stimuli to thc end of the heart and in order to
mcinipulatc~ hewt beat reversid it is necessary to apply a train of
impulses of t~ higher frequency at the other end. The heart cells have a
‘‘ low safety margin for condurtion ” (Kriebel) and a low degree of
(witability whivh perrnits them to engage in independent activity.
I’or co-ordinated activity c~nd t lie generation of u contraction wave a
number of relln must dcpolurize simultaneously ; the input of a train of
impulses must in fact syncihronize the beat of a large number of cells
and thereby produce a contraction. According to Kriebel conduction
velocity is faster in the middle of the heart than at either end (Fig. 16)
and he attribatcs this to cliffercnces in thc. level of excitability of cells ;
those near the eiids being lees excitable than those in the centre. Whilo
this does make it more difficwlt for an irnpulsc to spread from the cnch
it also means that only well co-ordinatccl contraction8 involving a
number of cells can mukc their way out from these terminal pacemakers.
Sugi et rtl. ( I 965) maintain that tlic threshold for provoking contraction
is highest in thc centre of the heart in Ciona. This would imply that the
cells in the centre are less excitable than at the ends. Occasionally
55
froni cell to cell. I n u ht,w piper Kriebel (1 968b) has shown that the
cell membrtmes in the heart hsve t i resistivity of 210 ohms/cma but the
nexuses (see p. 46) have a cell resistivity of only 0.2 ohm/cm2. This
suggests that the nexuses, us well as forming a transepithelial ionic
barrier, rire also low resistance pathwtiys for electrical conduction. In
order to show that such condriction is possible Kriebel replaced the
intercelliilur fluid by u sucrose 1)arric.r and demonstrated that an electrical impiilsc wuld still pass along the heart. The only pathway left
to it nndw these c.ir(.rinlst,illlcew is tlirough the nexuses.
On tlic basis of d l this evitlmcc it is reasonable to conclude that
propagutlion of the w u v ~ of (*ontrwtion in the ascidian heart is by
clectricul condiwtion from cell t o c c h l l .
Under normd conditiona t h r hewt is (.ontrolled by the pacemakers
located ttt either end of the heart, but in C i o m intestinalis during
longitudinal c~~itraction a third pacemaker may become active and
drive the blood towards either cntl. This is the C centre of Skramlik
(1938). The ( ” ceiitre w i i tw w t ivutchd experimentally by applying
pressure to this region of the hcurt. ‘l’hp cells of the remainder of the
hewt ctll hrbve pacemaker c.aptihilitic.s but do not at any time take
coiitrol of thc hcwt. The question arises then as to how the two end
pticemalwrs rntrintain their domiimwe over the rest of the heart and
thereby control heart beat. Most of our understanding of this is due to
the work of Kriebel (lO(i8c, 1970) itnd Anderson (1968).
In order to generate ;L wuve of contraction in a passive heart it is
necessary to apply several stimuli to thc end of the heart and in order to
mcinipulatc~ hewt beat reversid it is necessary to apply a train of
impulses of t~ higher frequency at the other end. The heart cells have a
‘‘ low safety margin for condurtion ” (Kriebel) and a low degree of
(witability whivh perrnits them to engage in independent activity.
I’or co-ordinated activity c~nd t lie generation of u contraction wave a
number of relln must dcpolurize simultaneously ; the input of a train of
impulses must in fact syncihronize the beat of a large number of cells
and thereby produce a contraction. According to Kriebel conduction
velocity is faster in the middle of the heart than at either end (Fig. 16)
and he attribatcs this to cliffercnces in thc. level of excitability of cells ;
those near the eiids being lees excitable than those in the centre. Whilo
this does make it more difficwlt for an irnpulsc to spread from the cnch
it also means that only well co-ordinatccl contraction8 involving a
number of cells can mukc their way out from these terminal pacemakers.
Sugi et rtl. ( I 965) maintain that tlic threshold for provoking contraction
is highest in thc centre of the heart in Ciona. This would imply that the
cells in the centre are less excitable than at the ends. Occasionally