Feline Cortical SEPs during Fentanyl or Halothane Anesthesia followed by Spinal Cord Injury and Naloxone.
10.4097/kjae.1992.25.6.1085
- Author:
Il Ok LEE
1
;
Young Suk CHOI
Author Information
1. Department of Anesthesiology, College of Medicine, Korea University, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Somatosensory evoked potentials;
Fentanyl;
Halothane;
Naloxone
- MeSH:
Analgesics, Opioid;
Anesthesia*;
Anesthesia, General;
Anesthetics;
Animals;
Arterial Pressure;
Catheters;
Cats;
Congenital Abnormalities;
Epidural Space;
Evoked Potentials, Somatosensory;
Fentanyl*;
Halothane*;
Inflation, Economic;
Naloxone*;
Receptors, Opioid;
Spinal Cord Injuries*;
Spinal Cord*
- From:Korean Journal of Anesthesiology
1992;25(6):1085-1092
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Spinal cord injury may occur during surgical correction of spinal deformity. In this situations, administrations of opiate receptor antagonists have known to improve spinal cord damage. Although those therapeutic modalities for the management of acute trauma of the spinal cord, impsoved the mean systemic arterial pressure controversy continues regarding their effectiveness Because opioids or inhalational anesthetics are used clinically, the effect of an opiate antagonist was evaluated by cortical somatosensory evoked potentials(cortical SEPs) which occur in 24 cats undergoing compressive injury on the posterior spinal cord during fentanyl or halothane anesthesia. Anesthesia was induced with pentobarbiturate(50 mg/kg, im). A balloon tipped catheter was inserted in the epidural space with tip located at thoracolumbar Junction. Spinal cord compressive injury was produced by balloon inflation for 20 minutes during intravenous saline infusion (control group), fentanyl(group l) or halothane(group 2) anesthesia Naloxone(5mg/kg) was administered intravenously following injury to all animals. Cortical SRPs were determined before and after induction of anesthesia, during the spinal cord compressive injury for 5 minutes, 10 minutes, l5 minutes, 20 minutes, after naloxone administration, and after removal of compressive injury. General anesthesia resulted in increases of latency and reductions of amplitude in the cortical SEPs. The reductions of amplitude were more marked than increases of latency in group 1, 2. During the cord injury, group 1 resulted in more reductions of amylitude than the other groups. But there were no significant differences among the groups. The administration of naloxone far improved latencies and amplitudes in the cortical SEPs of group 1 more than in other two groups. But there were no significant differences among the groups. Less recovery of the cortical SRPs response to naloxone in control group than the other groups. These results do nat support the supposition that opioid anesthesia produces an adverse effect upon cortical SEPs following spinal cord compressive injury and treatment with naloxone in the dose used in this study improves neurologic recovery of cortical SEPs less significantly.
