| ||||||||||||||
|
|
|||||||||||||


*Division of Pharmacology, School of Pharmacy, University of Missouri-Kansas City, Kansas City, Missouri; and
Department of Pharmacology, School of Medicine, Tulane University Health Sciences Center, New Orleans, Louisiana
Address correspondence and reprint requests to Bradley K. Taylor, PhD, Department of Pharmacology, SL83, Tulane University School of Medicine, 1430 Tulane Ave., New Orleans, LA 70112. Address e-mail to taylorb{at}tulane.edu
Several studies have emphasized an opioidergic link between the central regulation of cardiovascular function and acute noninflammatory pain. By contrast, relatively few studies have investigated the relationships between opioids, hypertension, and inflammatory pain. We used the formalin model of acute inflammatory pain to compare morphine antinociception among spontaneously hypertensive (SHR) rats, their genetic normotensive controls, Wistar-Kyoto (WKY) rats, and Sprague-Dawley (SD) rats. Measures of nociception included both behavioral and cardiovascular end-points (increased mean arterial blood pressure and heart rate). Morphine (3.0 mg/kg subcutaneously) produced greater hypotension and bradycardia in SHR than in WKY or SD rats. We next administered formalin (5%; 50 µL) and observed greater nociception during both Phase 1 and Phase 2 in SHR controls than in WKY controls. The morphine-treated groups did not differ, suggesting that morphine attenuates hypersensitivity to formalin pain in the SHR. Morphine inhibited edema but not paw hyperthermia to a greater degree in SHR, whereas Phase 1 remifentanil produced a relatively shorter delay in the onset of Phase 2 in SHR. We suggest that the presentation of essential hypertension be considered when opioid regimens are planned both during surgery (to minimize cardiovascular complications) and during the postoperative period (to optimize analgesic effects).
IMPLICATIONS: Presentation of essential hypertension should be considered when opioid regimens are planned both during surgery (to minimize cardiovascular complications) and during the postoperative period (to optimize analgesic effects).
This article has been cited by other articles:
![]() |
D. Fraga, R. R. Machado, L. C. Fernandes, G. E. P. Souza, and A. R. Zampronio Endogenous opioids: role in prostaglandin-dependent and -independent fever Am J Physiol Regulatory Integrative Comp Physiol, February 1, 2008; 294(2): R411 - R420. [Abstract] [Full Text] [PDF] |
||||
![]() |
D. Cozzolino, F. C. Sasso, D. Cataldo, D. Gruosso, A. Giammarco, A. Cavalli, C. Di Maggio, G. Renzo, T. Salvatore, D. Giugliano, et al. Acute Pressor and Hormonal Effects of {beta}-Endorphin at High Doses in Healthy and Hypertensive Subjects: Role of Opioid Receptor Agonism J. Clin. Endocrinol. Metab., September 1, 2005; 90(9): 5167 - 5174. [Abstract] [Full Text] [PDF] |
||||
|