Reorganization of spinal circuitry and removal of supraspinal influences after spinal cord injury (SCI) result in pathophysiologic conditions, such as motor and autonomic hyperflexia (AH) in response to noxious stimuli. Individuals with SCI are thus at increased risk during surgical procedures and require special anesthetic management, but few studies that have addressed this problem. An animal model to assess changes in anesthetic effects on spinal reflexes following SCI would aid in developing effective anesthetic management of the SCI population. Changes in anesthetic (isoflurane) effects on motor and sympathetic reflex pathways after acute and chronic spinalization, and the effects of NMDA antagonists on these changes, will be investigated in rats. These will be studied using quantitative measurement of responses evoked by noxious stimuli (pinch, heat), including limb movement, blood pressure, and electrophysiological recording of single dorsal horn neurons, along with simultaneous recording of sympathetic and motor nerve activity. Changes in isoflurane dose-response functions for these parameters., and correlations among them, will be determined before and after acute (complete and partial) and chronic spinalization. Thus, these studies aim to determine how and where changes in spinal reflex pathways occur after SCI, and how they relate to anesthetic requirements. This knowledge will lead to safer anesthesia in SCI patients, and to a better understanding of nociceptive/spinal reflex pathways occur after SCI, and how they relate to anesthetic requirements. This knowledge will lead to safer anesthesia in SCI patients, and to a better understanding of nociceptive/spinal reflex pathways, their supraspinal control, and changes in spinal circuitry following SCI.

Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Postdoctoral Individual National Research Service Award (F32)
Project #
5F32NS043935-02
Application #
6626204
Study Section
Special Emphasis Panel (ZRG1-F01 (21))
Program Officer
Kleitman, Naomi
Project Start
2002-09-30
Project End
Budget Start
2003-05-01
Budget End
2004-04-30
Support Year
2
Fiscal Year
2003
Total Cost
$46,420
Indirect Cost
Name
University of California Davis
Department
Anesthesiology
Type
Schools of Medicine
DUNS #
047120084
City
Davis
State
CA
Country
United States
Zip Code
95618
Jinks, Steven L; Atherley, Richard J; Dominguez, Carmen L et al. (2005) Isoflurane disrupts central pattern generator activity and coordination in the lamprey isolated spinal cord. Anesthesiology 103:567-75
Jinks, Steven L; Dominguez, Carmen L; Antognini, Joseph F (2005) Drastic decrease in isoflurane minimum alveolar concentration and limb movement forces after thoracic spinal cooling and chronic spinal transection in rats. Anesthesiology 102:624-32
Jinks, Steven L; Carstens, Earl; Antognini, Joseph F (2004) Isoflurane differentially modulates medullary on and off neurons while suppressing hind-limb motor withdrawals. Anesthesiology 100:1224-34
Antognini, Joseph F; Jinks, Steven L; Carstens, Earl E et al. (2004) Preserved reticular neuronal activity during selective delivery of supra-clinical isoflurane concentrations to brain in goats and its association with spontaneous movement. Neurosci Lett 361:94-7
Jinks, Steven L; Martin, John T; Carstens, Earl et al. (2003) Peri-MAC depression of a nociceptive withdrawal reflex is accompanied by reduced dorsal horn activity with halothane but not isoflurane. Anesthesiology 98:1128-38
Antognini, J F; Jinks, S L; Atherley, R et al. (2003) Spinal anaesthesia indirectly depresses cortical activity associated with electrical stimulation of the reticular formation. Br J Anaesth 91:233-8
Jinks, Steven L; Antognini, Joseph F; Carstens, Earl (2003) Isoflurane depresses diffuse noxious inhibitory controls in rats between 0.8 and 1.2 minimum alveolar anesthetic concentration. Anesth Analg 97:111-6, table of contents