G. Gherardini et al., Spinal cord stimulation improves survival in ischemic skin flaps: An experimental study of the possible mediation by calcitonin gene-related peptide, PLAS R SURG, 103(4), 1999, pp. 1221-1228
Currently, spinal cord stimulation is used to treat ischemia and ischemic p
ain, with the best results observed in vasospastic cases. It was earlier de
monstrated that spinal cord stimulation may attenuate experimentally induce
d vasospasm in an island flap in the rat. The present study was designed to
investigate whether preemptive spinal cord stimulation could increase long
-term flap survival and to explore the neurohumoral mediation of the effect
.
A total of 56 rats were implanted with chronic spinal cord stimulation syst
ems. Three days later, a groin flap based on the superficial epigastric ves
sels was harvested, and the single feeding artery was occluded by a detacha
ble microvascular clip. After 12 hours, the clip was removed. Flap survival
was evaluated after 7 days. Immediately before flap surgery, two groups of
animals received 30 minutes of stimulation using current clinical paramete
rs and with stimulation amplitudes of 70 (n = 10) or 90 percent (n = 8) of
that evoking muscular contractions. The outcomes in these groups were compa
red with those in two control groups (n = 20; n = 10). In one group, an add
itional calcitonin gene-receptor peptide (CGRP) antagonist was intravenousl
y injected before stimulation (n = 8).
In the control groups without stimulation, virtually all flaps necrotized.
In treated groups, flap survival was 60 percent at the lower intensity and
almost 90 percent at the higher one. The administration of a CGRP antagonis
t before treatment reduced its efficacy to below 40 percent survival. The d
ifferences between the untreated and treated groups were significant. The d
ecrease in survival after CGRP-receptor black was significant in one of two
tests.
Preemptive spinal cord stimulation increases survival of skin flaps with cr
itical ischemia. The effects are dependent on the stimulation intensity and
are possibly mediated by the release of CGRP in the periphery.