scholarly journals Modification of noxious stimulus in the spinal cord.

1997 ◽  
Vol 17 (6) ◽  
pp. 357-365
Author(s):  
YUTAKA TAIRA
Keyword(s):  
1992 ◽  
Vol 580 (1-2) ◽  
pp. 172-179 ◽  
Author(s):  
Elizabeth Bullitt ◽  
Chong Lam Lee ◽  
Alan R. Light ◽  
Helen Willcockson

1999 ◽  
Vol 90 (1) ◽  
pp. 208-214 ◽  
Author(s):  
Joseph F. Antognini ◽  
Earl Carstens

Background The spinal cord appears to be the site at which isoflurane suppresses movement that occurs in response to a noxious stimulus. In an attempt to localize its site of suppressant action, the authors determined the effect of isoflurane on dorsal horn neuronal responses to supramaximal noxious stimulation at end-tidal concentrations that just permitted and just prevented movement. Methods Rats (n = 14) were anesthetized with isoflurane, and after lumbar laminectomy, the minimum alveolar concentration (MAC) for each rat was determined using a supramaximal mechanical stimulus. In these same rats, after extracellular microelectrode placement in the lumbar spinal cord, dorsal horn neuronal responses to the supramaximal stimulus were determined at the concentrations of isoflurane that bracketed each rat's MAC (0.1% higher and lower than MAC). The MAC of isoflurane was then re-determined. Results Dorsal horn neuronal response was 1,757+/-892 impulses/min at 0.9 MAC and 1,508+/-988 impulses/min at 1.1 MAC, a 14% decrease (P < 0.05). Cell responses varied, with some cells increasing their response at the higher concentration of isoflurane. The MAC of isoflurane was 1.38+/-0.2% before and 1.34+/-0.2% after determination of dorsal horn neuronal responses. Conclusions Isoflurane, at concentrations that bracket MAC, has a variable and minimal depressant effect on dorsal horn cell responses to noxious mechanical stimulation. These data suggest that the major action of isoflurane to suppress movement evoked by a noxious stimulus might occur primarily at a site other than the dorsal horn.


Neuroscience ◽  
1996 ◽  
Vol 70 (3) ◽  
pp. 791-798 ◽  
Author(s):  
K. Tsou ◽  
K.A. Lowitz ◽  
A.G. Hohmann ◽  
W.J. Martin ◽  
C.B. Hathaway ◽  
...  

2000 ◽  
Vol 92 (2) ◽  
pp. 559-559 ◽  
Author(s):  
Joseph F. Antognini ◽  
Xiao Wei Wang ◽  
E. Carstens

Background Isoflurane depresses the electroencephalographic (EEG) activity and exerts part of its anesthetic effect in the spinal cord. The authors hypothesized that isoflurane would indirectly depress the EEG and subcortical response to noxious stimulation in part by a spinal cord action. Methods Depth electrodes were inserted into the midbrain reticular formation (MRF) and thalamus of six of seven isoflurane-anesthetized goats, and needle-electrodes were placed into the skull periosteum. In five of seven goats, an MRF microelectrode recorded single-unit activity. The jugular veins and carotid arteries were isolated to permit cranial bypass and differential isoflurane delivery. A noxious mechanical stimulus (1 min) was applied to a forelimb dewclaw at each of two cranial-torso isoflurane combinations: 1.1+/-0.3%-1.2+/-0.3% and 1.1+/-0.3-0.3+/-0.1% (mean +/- SD). Results When cranial-torso isoflurane was 1.1-1.2%, the noxious stimulus did not alter the EEG. When torso isoflurane was decreased to 0.3%, the noxious stimulus activated the MRF, thalamic, and bifrontal-hemispheric regions (decreased high-amplitude, low-frequency power). For all channels combined, total (-33+/-15%), delta(-51+/-22%), theta (-33+/-19%), and alpha (-26+/-16%) power decreased after the noxious stimulus (P<0.05); beta power was unchanged. The MRF unit responses to the noxious stimulus were significantly higher when the spinal cord isoflurane concentration was 0.3% (1,286+/-1,317 impulses/min) as compared with 1.2% (489+/-437 impulses/min, P<0.05). Conclusions Isoflurane blunted the EEG and MRF-thalamic response to noxious stimulation in part via an action in the spinal cord.


1974 ◽  
Vol 52 (6) ◽  
pp. 1207-1211 ◽  
Author(s):  
O. Calvillo ◽  
J. L. Henry ◽  
R. S. Neuman

Morphine, applied by microiontophoresis to functionally identified dorsal horn neurones in segments L5–L7 of cats (chloralose anaesthetized, decerebrated or high spinal), produced primarily a depression of the discharge of neurones responding to noxious radiant heat applied to the skin. It depressed on-going activity (12 out of 20 neurones), glutamate-evoked excitation (8/8) and the response to the noxious stimulus (13/21). The response of two additional neurones to heat was potentiated. The effects began 10–30 s from the onset of application, reached a maximum in up to 8 min and outlasted application by up to 10 min. Morphine had relatively little effect on on-going activity and glutamate-evoked excitation of neurones responding to non-noxious stimuli (n = 18). Naloxone (intravenously and iontophoretic) reversed these depressions (4/11). It is suggested that morphine may produce analgesia, at least in part, by a direct action on a specific morphine receptor in the spinal cord.


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