Biomedical Engineering Reference
In-Depth Information
4.3 Differences Between Neural and Humoural Effects
It has been observed in dogs that bilateral vagal stimulation results in a lower heart
rate in combination with stellate ganglion stimulation than in combination with
norepinephrine infusion [57]. Although an intricate prejunctional interaction may
explain this observation, functional inhomogeneity may provide a more simple
explanation for this remarkable difference. High vagal tone will shift the pacemaker
to the area with lowest innervation. Such an area may still accelerate in response to
circulating catecholamines, but not or much less to sympathetic stimulation, simply
because the nerves do not impinge on that particular area.
5 The Transplanted Heart
The transplanted heart is a rich source of information for the relation between the
autonomic nervous system and the heart [9]. Blood pressure results from the product
between cardiac output and peripheral resistance. Cardiac output is—in its turn—
composed of the product between heart rate and stroke volume. The basic
physiological concept that only cardiac output is directly, i.e. on a 'per cycle' basis is
affected by vagal influences, whereas peripheral resistance is only affected by
sympathetic influences with its concomitant 0.1 Hz dominant frequency seems
untenable, given the fact that recipients of a donor heart are able to stand up at all.
However, this reasoning applies in fact also to a normal heart.
The pivotal loss of information after heart transplantation is not the loss of information
from the receptors in the sinus caroticus and in the arch of the aorta (baroreflex), but from
the intracardiac receptors. Indeed, the main problems of these patients are blunted
responses to volume expansion and to natriuremia. Thus these patients function in a
permanent state of a large circulating volume and hypertension [9].
It has been reported that—at least—sympathetic reinnervation may occur after
cardiac transplantation [65]. The evidence is based on the fact that the donor heart is
able to produce noradrenaline after an injection with tyramine in the left anterior
descending or circumflex coronary arteries. Although very interesting and probably
functionally relevant, such experiments prove that the nerves in the donor heart still
have or have regained metabolic activity. In my opinion it does not unequivocally
prove that the central nervous system of the recipient has sympathetic neural control
over the donor heart. In dogs with autotransplantation it has been reported that the
maximal heart rate during exercise increases much more slowly and to a substantially
lower maximum heart rate [17]. Never theless, in patients with a transplanted heart
the maximum exercise tolerance can be large [9].
By and large, the most severe problems in patients with a transplanted heart,
besides the problems with rejection, reside in the relation between heart and kidneys
and focus on regulation of the total blood volume and blood pressure and to a lesser
extent on exercise tolerance and postural changes. Probably this results from the fact
that the intrinsic response to preload changes of donor hearts (Starling law) remains—
at least partially—effective. I think, therefore, that innervation of a
biological
pacemaker
is less important than the capacity to respond to circulating
catecholamines (see below).
