Effect of Nifedipine on Morphine-Induced Analgesia

Carta, F; Bianchi, Mauro; Argenton, Stefano; Cervi, Daniele; Marolla, Giampaolo; Tamburini, M. C.; Breda, Massimo; Fantoni, A; Panerai, Alberto E.

doi:10.1213/00000539-199005000-00005

Cited by 48 publications

(14 citation statements)

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“…In particular, the extracellular calcium influx and release from stores were larger in IL‐6 treated neurons compared with controls. Since it has been demonstrated that morphine exerts an inhibitory effect on cellular calcium (North 1986) and that calcium plays an important role in modulating the analgesic effect of morphine in both experimental animals and humans (Carta et al . 1990; Kuzmin et al .…”

Section: Discussionmentioning

confidence: 99%

Presence of a reduced opioid response in interleukin‐6 knock out mice

Bianchi¹,

Maggi²,

Pimpinelli³

et al. 1999

Eur J of Neuroscience

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Cytokines are known to influence neuronal functions. The purpose of this study was to investigate the putative role of the cytokine interleukin-6 (IL-6) in the pathways involved in opioid-mediated responses, by using IL-6-deficient mice. We reported that with a thermal stimulus IL-6-knock-out (IL-6KO) mice presented nociceptive thresholds similar to those measured in their controls. However, they showed a reduced analgesic response both to the restraint stress and to the administration of low doses of morphine. Hypothalamic levels of the opioid peptide beta-endorphin were significantly higher in IL-6KO mice than they were in their controls. The development of tolerance to the analgesic effect of morphine was more rapid in IL-6-deficient mice than in wild-type controls. Binding experiments showed that the number of opioid receptors in the midbrain, but not in the hypothalamus, decreased in IL-6KO mice. Autoradiographic binding analysis revealed that the density of mu receptors diminished while the delta-opioid receptors did not. These results suggest that IL-6 is necessary for a correct development of neuronal mechanisms involved in the response to both endogenous and exogenous opiates.

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Section: Discussionmentioning

confidence: 99%

Presence of a reduced opioid response in interleukin‐6 knock out mice

Bianchi¹,

Maggi²,

Pimpinelli³

et al. 1999

Eur J of Neuroscience

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“…However, the on-demand iv infusion of fentanyl for the control of pain after elective hysterectomy was not significantly different in groups of patients double-blindly assigned to the administration of an additional infusion of either placebo or nimodipine (51). Oral administration of slow-release tablets of nifedipine given 18, 9 and 1 h before the beginning of surgery significantly potentiated the analgesic effect of morphine slowly infused by the iv route in patients submitted to elective hysterectomy or orthopedic surgery (30). However, slow-release nifedipine given orally 12 and 1 h before surgery did not change significantly the postoperative pain relief produced by epidural fentanyl (52).…”

Section: Clinical Studiesmentioning

confidence: 98%

Involvement of calcium in pain and antinociception

2001

Braz J Med Biol Res

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Calcium ions are widely recognized to play a fundamental role in the regulation of several biological processes. Transient changes in cytoplasmic calcium ion concentration represent a key step for neurotransmitter release and the modulation of cell membrane excitability. Evidence has accumulated for the involvement of calcium ions also in nociception and antinociception, including the analgesic effects produced by opioids. The combination of opioids with drugs able to interfere with calcium ion functions in neurons has been pointed out as a useful alternative for safer clinical pain management. Alternatively, drugs that reduce the flux of calcium ions into neurons have been indicated as analgesic alternatives to opioids. This article reviews the manners by which calcium ions penetrate cell membranes and the changes in these mechanisms caused by opioids and calcium antagonists regarding nociceptive and antinociceptive events.

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“…[10] In the study by Carta et al, a slow release preparation of nifedipine was used (half-life of 15.2 ± 4.3 h), which might have delayed its antianalgesic action. [11]…”

Section: Discussionmentioning

confidence: 99%

L-type calcium channel blockers, morphine and pain: Newer insights

Kumar¹,

Mehra²,

Ray³

2010

Indian J Anaesth

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Earlier, we had reported that co-administration of opioids and L-type calcium channel blockers (L-CCBs) like diltiazem could prove useful in the treatment of cancer pain. Much of this report was based upon earlier published work involving animal models of pain exposed to brief periods of noxious radiant heat without any tissue injury. However, pain in clinical situations usually result from tissue injury. Thus, the aim of the current investigation was to study the analgesic effect of this combination of drugs in the rat formalin test which is associated with actual tissue injury. Wistar rats (n=60) received either L-CCB (nifedipine/nimodipine/verapamil/diltiazem i.p.) or morphine (s.c.) or both drugs. The formalin test was done 30 min after morphine or placebo injection. The naloxone reversal test was also done. Administration of L-CCBs alone, particularly diltiazem, increased pain in the formalin test. In contrast, co-administration of these L-CCBs with morphine led to decreased pain response, though statistically significant decrease was noted only with nimodipine + morphine. Naloxone reversed this analgesic effect, indicating that it was primarily an opioid-mediated effect. The results show that administration of L-CCBs alone may prove counterproductive in the therapeutic management of pain (anti-analgesic effect). However, co-administration of both drugs (morphine and nimodipine) in quick succession could lead to adequate pain relief.

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Effect of Nifedipine on Morphine-Induced Analgesia

Cited by 48 publications

References 0 publications

Presence of a reduced opioid response in interleukin‐6 knock out mice

Presence of a reduced opioid response in interleukin‐6 knock out mice

Involvement of calcium in pain and antinociception

L-type calcium channel blockers, morphine and pain: Newer insights

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