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POINT-COUNTERPOINT
1Department of Nephrology,
Herlev University Hospital;2Neurobiological Research Centre,
Rigshospitalet,
Copenhagen, Denmark
e-mail: svst{at}heh.regionb.dk
It is intuitively clear that the cerebral circulation cannot take part in general cardiovascular regulation. During states of shock, where the sympathetic nervous system is activated, leading to a decrease in the perfusion of kidneys and mesenteric vascular bed, the cerebral circulation is kept functioning as long as possible and experiences only a modulating effect on autoregulation by sympathetic perivascular nerves.
The cerebral arteries are innervated like other vascular beds by neurons arising in the peripheral nervous system and also by intrinsic neurons (4, 9). Sympathetic nerves in contact with the cerebral arteries originate from the superior cervical ganglion, but peculiarly under normal conditions seem to have little influence on cerebral blood flow (CBF). Already Fog (3) in his early studies of pial arteries in cats found no effect of acute sympathetic, vagal, or baroreceptor denervation on the autoregulatory responses. Chronic sympathetic denervation in animals does not influence CBF autoregulation (2, 15). Electric stimulation or acute sympathetic denervation in animals likewise has little effect on CBF if blood pressure is kept stable. In humans, bladder distension caused a powerful sympathetic activation with a 35% rise in blood pressure with a rise in heart rate and papillary dilatation, but did not influence CBF (11).
A weak modulatory effect of the sympathetic perivascular nerves on CBF autoregulation can only be detected at extremes of blood pressure. During hemorrhagic hypotension, the otherwise inactive nerves constrict the larger cerebral resistance vessels, the "inflow tract" of the brain, thereby counteracting the autoregulatory response of the smaller arteries and arterioles (1, 5). This response is a weak analog of the intense vasoconstriction seen in the peripheral and visceral vascular beds. Likewise, during acutely induced hypertension, sympathetic activation, either endogenously or by electric stimulation, can constrict the inflow tract and hence contribute to autoregulation and exert a protective effect on the cerebral resistance vessels (8, 12). The net effect is a shift of the autoregulation curve toward higher blood pressure. Interestingly, during acutely induced hypertension in the anesthetized rat an interaction between the sympathetic nervous system and the renin-angiotensin system can be demonstrated. Blockade of the renin-angiotensin system with captopril causes a shift of the upper limit of autoregulation toward lower blood pressure, and this shift is abolished by concomitant electric stimulation of the cervical sympathetic trunk (14).
In a study in normal humans, lower body negative pressure was used to create a baroreflex-induced activation of the sympathetic nervous system. Such activation did not alter cerebrovascular reactivity to hypercapnia or hypocapnia, as studied by medial cerebral artery velocity (7). Likewise, the same group found no effect of ganglionic blockade on cerebrovascular CO2 reactivity (10). By contrast, in a related study, where sympathetic activation was achieved by head-up tilt and sympathetic tone was removed by ganglionic blockade, a slight effect of sympathetic activation was found on CO2 reactivity (6). These finding may have been influenced by methodological errors, as discussed in detail by LeMarbre et al. (7). Interestingly, ganglionic blockade with trimetaphan did not appear to influence cerebrovascular CO2 reactivity in normotensive and hypertensive humans (13). Lower body negative pressure induces a decrease in cerebral blood flow velocity even if blood pressure is maintained by infusion of a pressor drug. This cerebral vasoconstrictor response was preserved in healthy individuals under ganglionic blockade with trimetaphan, excluding participation of the sympathetic nervous system (16).
Thus it may be concluded that the sympathetic perivascular nerves have little or no effects on CBF and its regulation under normal conditions, but may be activated to constrict the inflow tract cerebral vessels at very high or very low blood pressure. It is gratifying that this point of view was also expressed in a recent review on perivascular nerves and the regulation of cerebrovascular tone (4).
REFERENCES
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