Spinal sympathetic neurons are distributed in cord segments from Th1 to L3.
High spinal cord injury demonstrates severe orthostatic hypotension, but n
ot lower cord injury. It remains to be clarified as to where is the critica
l spinal level disturbing neural cardiovascular regulations in response to
orthostatic stress. To address this issue, beat-to-beat blood pressure (BP)
(measured using a Finapres device) and RR interval (measured electrocardio
graphically) were recorded at rest and in a 60 degrees head-up position in
26 patients with varying levels of spinal cord injury (C4 to Th12) and in 1
5 healthy (control) subjects. Sympathetic vascular tone was examined by the
Mayer wave power spectrum of systolic blood pressure (SBP) variability. Ba
roreflex sensitivity was examined by transfer function analysis of SEP and
RR interval variabilities. The Mayer wave power spectrum increased in respo
nse to postural shift in most patients injured at Th4 or below, whereas thi
s parameter either remained unchanged or decreased in patients with higher-
level injury. Baroreflex sensitivity tended to decrease with postural shift
in patients injured at Th3 or below, whereas this parameter increased in a
ll patients with higher-level injury. We divided spinal pa tients into high
-level injury (Th3 or above, n = 14) and low-level injury (Th3 or below, n
= 12) groups. Systolic blood pressure significantly fell (-10 +/- 4 mm Hg,
P <.05) with postural shift in high-level injury group but did not change i
n low-level injury group or in control subjects. The low-level injury group
and the control group demonstrated essentially similar autonomic nervous r
esponses to postural shift, ie, a significant increase in Mayer wave power
and an insignificant decrease in baroreflex sensitivity. On the contrary, t
he high-level injury group showed opposite responses, ie, an insignificant
decrease in Mayer wave power and a significant increase in baroreflex sensi
tivity in response to postural shift. We conclude that spinal cord injury a
t Th3 or above eliminates normal neural cardiovascular responses to mild or
thostatic stress in humans. Am J Hypertens 2001;14:141-148 (C) 2001 America
n Journal of Hypertension, Ltd.