Severe peripheral ischemia after vasospasm may be prevented by spinal cord stimulation. A preliminary report of a study in a free-flap animal model.
Electric spinal cord stimulation (SCS) is at present used in many centers to treat ischemic pain and ischemia in peripheral vascular disease. The most promising results have been obtained in cases where a vasospastic component is dominating. The knowledge concerning the mechanisms behind these effects has been scanty, but recent experimental studies indicate that suppression of sympathetic activity and the release of vasoactive substances may be important. A problem with many of the animals studies aimed at exploring these mechanisms is that they have almost exclusively been performed on normal animals without ischemia. However, in studies of the responsiveness of local ischemia to various pharmacological substances and to electrical transcutaneous nerve stimulation, animal models with ischemic skin flaps have been used. We applied SCS via chronically implanted electrodes in a model of local vasospasm in the rat, induced by mechanical stimulation of the vessel supplying an island flap in the groin. Male Sprague-Dawley rats were used. First, a monopolar system for spinal cord stimulation, with the intraspinal cathode at vertebral level T11, was implanted in halothane anaesthesia. After about three days of recovery the rats were anaesthetized with chloral hydrate ip and a groin neurovascular flap based on the epigastric vessels was raised. Microcirculation in the flap as well as in a control area in the contralateral groin was monitored by laser Doppler technique. Vasospasm was induced by gently pinching the superficial epigastric artery with microforceps. Two groups of animals were submitted to two spasm periods, one with SCS applied for 20 min. by 50 Hz; 0.2 msec and with 2/3 of the intensity required for a motor response before the first period. The second group, receiving sham SCS, served as a control. Both degree of ischemia after spasm provocation and the time to recovery were evaluated. In general SCS affected basal flow very little. In the control group the rats demonstrated increasing vasospastic reactions with subsequent flap ischemia to the two mechanical provocations. In the experimental group a response pattern emerged indicating that pre-spasm SCS could both reduce the spasm amplitude and significantly shorten the time for restoration of a satisfactory microcirculation in the flap. Some few trials with pharmacologically induced spasm by topical application of noradrenaline onto the feeding vessel also followed the same pattern. In conclusion, SCS seems to be able to reduce vasospasm, especially if the treatment is given before the ischemic period. This approach may supply an animal model for further studies of possible mechanisms behind the microcirculatory effects of SCS.
Linderoth
B
B
Department of Neurosurgery, Karolinska Hospital, Stockholm, Sweden.
Gherardini
G
G
Ren
B
B
Lundeberg
T
T
D000818:Animals; D004599:Electric Stimulation Therapy / Q000295:instrumentation*; D007511:Ischemia / Q000503:physiopathology / Q000628:therapy*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D012867:Skin / Q000098:blood supply*; D013116:Spinal Cord / Q000503:physiopathology*; D013524:Surgical Flaps / Q000502:physiology; D014655:Vascular Resistance / Q000502:physiology*; D014666:Vasomotor System / Q000503:physiopathology*