creased frequency of heart bc;it when the heart is stretched, while
Kriebel (1970) reports on increiines in coriduction velocity.
Whilc t h r eviclencv~ is ,still incomplete it does seem likely that the
dominance exerted on the heart by the two terminal pacemakers is
linked to differences in excitability and activity thresholds between
cells of the pacemaker area and those of the rest of the heart. It is also
itpparent that i~ stretch stimulus rnay alter the frequency of a pacemaker and the speed of conduct ion from it.
P . Heart b e d r ~ v t r s a l
In the rLbseiicv! of nervous innervation of the end pacemaker the
control of Itcart bectt rcvcrsal must, be intrinsic to the heart itself.
A number ofthcories huvc been put forward to explain this phenomenon,
the most important of which arc btwtl on the following :
(a) Changing partid 1)rcssin-e of curbon dioxide in the heart (Brocaa
et al., 1966).
(I)) Thr clevcdopiiient of extrasyntjolen or interpolated contractions
(Mislin, l!N4, 1 !)fi5 ; Mislin and Krauae, 1!)64).
((1)
Back prwsure in the arterial tystem (Lahille, 1890; Haywood
and Moon, 1050 ; Kriebel, 1968tt).
(d) Paremctker fatigue (Krijgsman, 1 !G6 ; Krijgsman and Krijgsman, 1057).
(e) Changes in the frequency level of pacemakers (Anderson, 1968).
Brocas et al. (1 966) coilsidered that thc hypobranchial pacemaker is
dominant to the visceral iind that, the frequency of contraction in the
visceral pacemaker varies with the part ial pressure of carbon dioxide.
In high levels of carbon dioxide the visccral pacemaker increases in
frequency and at the same time thc hypobranchial pacemaker is
simultaneously depressed by an undefined relay mechanism and not by
the influence of carbon dioxide. Whtw the carbon dioxide level drops
the visceral pacemaker declines in frequency. While such an effect
could be due to changing pH and not dircctly to carbon dioxide there
is no clear evidcuce to show how such metabolic change8 might he
taking place in the heart so as to var,y their influence on the pacemaker.
Nevertheless, in the light of Anderson’s (1968) finding8 that there i H a
rhythmic variation in the frecpenay of the visceral pacemaker (see
below), thk work of Brocas et nl. mcrits careful consideration.*
Aiiderson (1968) appears to have Inixinturprotod the conclusions of Brocw et al.
She ntates (p. 383): ‘‘ Their reaultn indicated that tho activity of the hypobranchial end
of the heart is Rlowctd by increasing the p CO, while tho visceral end is not greatly affected.”
Broom et u6. (1966, p. 02) stab: “ C‘est tlonc le ilivetlu d’activite du centre viscbral qm
determine le sens de la ciroulation, ce niveau d’activit6 &ant fonction de la pression
partielle du gaz oarbonique. ”
Kriebel (1970) reports on increiines in coriduction velocity.
Whilc t h r eviclencv~ is ,still incomplete it does seem likely that the
dominance exerted on the heart by the two terminal pacemakers is
linked to differences in excitability and activity thresholds between
cells of the pacemaker area and those of the rest of the heart. It is also
itpparent that i~ stretch stimulus rnay alter the frequency of a pacemaker and the speed of conduct ion from it.
P . Heart b e d r ~ v t r s a l
In the rLbseiicv! of nervous innervation of the end pacemaker the
control of Itcart bectt rcvcrsal must, be intrinsic to the heart itself.
A number ofthcories huvc been put forward to explain this phenomenon,
the most important of which arc btwtl on the following :
(a) Changing partid 1)rcssin-e of curbon dioxide in the heart (Brocaa
et al., 1966).
(I)) Thr clevcdopiiient of extrasyntjolen or interpolated contractions
(Mislin, l!N4, 1 !)fi5 ; Mislin and Krauae, 1!)64).
((1)
Back prwsure in the arterial tystem (Lahille, 1890; Haywood
and Moon, 1050 ; Kriebel, 1968tt).
(d) Paremctker fatigue (Krijgsman, 1 !G6 ; Krijgsman and Krijgsman, 1057).
(e) Changes in the frequency level of pacemakers (Anderson, 1968).
Brocas et al. (1 966) coilsidered that thc hypobranchial pacemaker is
dominant to the visceral iind that, the frequency of contraction in the
visceral pacemaker varies with the part ial pressure of carbon dioxide.
In high levels of carbon dioxide the visccral pacemaker increases in
frequency and at the same time thc hypobranchial pacemaker is
simultaneously depressed by an undefined relay mechanism and not by
the influence of carbon dioxide. Whtw the carbon dioxide level drops
the visceral pacemaker declines in frequency. While such an effect
could be due to changing pH and not dircctly to carbon dioxide there
is no clear evidcuce to show how such metabolic change8 might he
taking place in the heart so as to var,y their influence on the pacemaker.
Nevertheless, in the light of Anderson’s (1968) finding8 that there i H a
rhythmic variation in the frecpenay of the visceral pacemaker (see
below), thk work of Brocas et nl. mcrits careful consideration.*
Aiiderson (1968) appears to have Inixinturprotod the conclusions of Brocw et al.
She ntates (p. 383): ‘‘ Their reaultn indicated that tho activity of the hypobranchial end
of the heart is Rlowctd by increasing the p CO, while tho visceral end is not greatly affected.”
Broom et u6. (1966, p. 02) stab: “ C‘est tlonc le ilivetlu d’activite du centre viscbral qm
determine le sens de la ciroulation, ce niveau d’activit6 &ant fonction de la pression
partielle du gaz oarbonique. ”