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Updated: Jul 29, 2026
Assessment of Morphine-induced Hyperalgesia and Analgesic Tolerance in Mice Using Thermal and Mechanical Nociceptive Modalities
Published on: July 29, 2014
[Metabolic and immune response to spinal vs intravenous morphine for analgesia after radical prostatectomy]
J Longás Valién1, J M Abengochea Beisty, J R Martínez Ubieto
1Servicio de Anestesiología, Reanimación y Terapia del Dolor, Hospital Clínico Universitario Lozano Blesa, Zaragoza. jalonva@terra.es
Objective:
To study differences between the endocrine-metabolic and immune cell responses to spinal or intravenous administration of morphine for analgesia after radical prostatectomy.
Material And Methods:
Prospective study of 60 patients randomized to 2 groups: in group A (n=30) morphine for postoperative analgesia was infused intravenously and in group B (n=30) morphine was infused into the spinal canal. Changes in leukocyte populations and lymphocyte subpopulations in peripheral blood and blood from surgical drains (local) were analyzed to study immune cell response to morphine administration. Cortisol, corticotropin, growth hormone, glucose, and immunoglobulin levels in peripheral blood were measured as indicators of metabolic and humoral immune responses.
Results:
Both groups developed lymphopenia in peripheral blood. The group treated with spinal morphine had significantly lower CD4+ cell counts in peripheral blood P<0.05. No differences were found in the local leukocyte response in either group. Significant differences were found in natural killer and CD4+ cell counts both locally and in peripheral blood P<0.05. There was humoral immune response suppression in both groups; however, it was more marked in the group treated with spinal morphine and the difference was significant P<0.05. The metabolic response was greater in the group treated with intravenous morphine.
Conclusion:
Patients who received morphine by spinal infusion had a less marked endocrine-metabolic response. Although local cell responses were similar in the 2 groups, the response in peripheral blood was different, possibly reflecting different mechanisms of central modulation of the inflammatory response to stress.
