Drastic decrease in isoflurane minimum alveolar concentration and limb movement forces after thoracic spinal cooling and chronic spinal transection in rats.
BACKGROUND
Individuals with spinal cord injury may undergo multiple surgical procedures; however, it is not clear how spinal cord injury affects anesthetic requirements and movement force under anesthesia during both acute and chronic stages of the injury.


METHODS
The authors determined the isoflurane minimum alveolar concentration (MAC) necessary to block movement in response to supramaximal noxious stimulation, as well as tail-flick and hind paw withdrawal latencies, before and up to 28 days after thoracic spinal transection. Tail-flick and hind paw withdrawal latencies were measured in the awake state to test for the presence of spinal shock or hyperreflexia. The authors measured limb forces elicited by noxious mechanical stimulation of a paw or the tail at 28 days after transection. Limb force experiments were also conducted in other animals that received a reversible spinal conduction block by cooling the spinal cord at the level of the eighth thoracic vertebra.


RESULTS
A large decrease in MAC (to </= 40% of pretransection values) occurred after spinal transection, with partial recovery (to approximately 60% of control) at 14-28 days after transection. Awake tail-flick and hind paw withdrawal latencies were facilitated or unchanged, whereas reflex latencies under isoflurane were depressed or absent. However, at 80-90% of MAC, noxious stimulation of the hind paw elicited ipsilateral limb withdrawals in all animals. Hind limb forces were reduced (by >/= 90%) in both chronic and acute cold-block spinal animals.


CONCLUSIONS
The immobilizing potency of isoflurane increases substantially after spinal transection, despite the absence of a baseline motor depression, or "spinal shock." Therefore, isoflurane MAC is determined by a spinal depressant action, possibly counteracted by a supraspinal facilitatory action. The partial recovery in MAC at later time points suggests that neuronal plasticity after spinal cord injury influences anesthetic requirements.
Jinks
Steven L
SL
Department of Anesthesiology and Pain Medicine, University of California School of Medicine, Davis 95616, USA. sljinks@ucdavis.edu
Dominguez
Carmen L
CL
Antognini
Joseph F
JF
D018685:Anesthetics, Inhalation / Q000493:pharmacokinetics*; D000818:Animals; D005121:Extremities / Q000502:physiology; D005260:Female; D007530:Isoflurane / Q000493:pharmacokinetics* / Q000494:pharmacology; D009068:Movement; D009128:Muscle Spasticity / Q000209:etiology; D009473:Neuronal Plasticity; D011650:Pulmonary Alveoli / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D011930:Reaction Time / Q000187:drug effects; D013119:Spinal Cord Injuries / Q000378:metabolism*
D018685:Anesthetics, Inhalation; D007530:Isoflurane