PubMed · 11413694
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H A Adams, E Kochs, C Krier. 2001. [Current anesthesia techniques--an attempt at classification].. https://doi.org/10.1055/s-2001-14470
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The Ca(2+) channel blocker, nimodipine, increases the chronic naltrexone-induced supersensitivity to morphine analgesia in mice without affecting the density of up-regulated mu-opioid receptors. In the present study, the change in dihydropyridine-sensitive Ca(2+) channels associated with chronic naloxone-induced supersensitivity to morphine analgesia was studied in rat whole-brain membranes using a radiolabeled Ca(2+) channel blocker, [3H]PN200-110 [isopropyl 4-(2,1,3-benzoxadiazol-4-yl)-1,4-dihydro-2,6-dimethyl-5-methoxycarbonylpyridine-3-carboxylate] (0.02-1.0 nmol/l). Rats were chronically treated with naloxone (1 mg/kg, i.p.), nimodipine (1 mg/kg, i.p.) or their respective vehicles twice daily for 10 days. On the 11th day, 16 h after the last injection of either nimodipine or naloxone, morphine (2 mg/kg, i.p.)-induced tail-flick analgesia was determined or rats were killed for the binding study. Chronic naloxone significantly potentiated (+84%) the morphine-induced analgesia. Chronic nimodipine also potentiated (+76%) morphine analgesia. In rats treated with nimodipine and naloxone, there was an additive increase (206%) in morphine analgesia. In binding studies, chronic naloxone resulted in a significant decrease (-39%) in the density (B(max)) of [3H]PN200-110 binding with no change in K(d) value when compared to the effect of chronic vehicle. Chronic nimodipine resulted in a slight but significant (+14.5%) increase in the B(max) of [3H]PN200-110. However, when nimodipine was co-administered with naloxone, it not only reversed the down-regulation but actually up-regulated (+25%) [3H]PN200-110 binding with no change in K(d) value. Our results show significant down-regulation of [3H]PN200-110 binding in association with naloxone-induced analgesic supersensitivity to morphine. The supersensitivity was also observed following chronic blockade of up-regulated Ca(2+) channels by nimodipine. These results indicate an important role of L-type Ca(2+) channel regulation in naloxone-induced analgesic supersensitivity to morphine.
Millimeter wave treatment (MWT) is based on those biological effects that develop following skin exposure to low power electromagnetic waves. This method of treatment is in wide clinical use in several Eastern European countries for treatment of a variety of conditions, including pain syndromes. However, most treatment modes of MWT were developed empirically, and certain indications and contraindications for the use of MWT remain to be established. In our previous blind experiments we have shown that the hypoalgesic effect of MWT may be quantitatively evaluated, and most probably mediated by the neural system in general, and the system of endogenous opioids in particular. Taking in consideration a well-known ability of opioids to cause gastrointestinal disturbances, which could limit clinical application of MWT, the main aim of the present study was to investigate whether a single MWT, that can produce opioid-related hypoalgesia, may also retard gut transit and colorectal passage in mice. The charcoal meal test was used to quantitatively evaluate upper gastrointestinal transit, and the glass bead test was employed to examine colonic propulsion in mice. MWT was applied to the nose area of mice. The MWT characteristics were: frequency = 61.22 GHz; incident power density = 15 mW/cm(2); and duration = 15 min. The results obtained have shown that MWT does not significantly change small intestinal or colonic transit in mice, and thus suppression of gastrointestinal motility should not be a setback in the clinical use of MWT.
The effects of diltiazem, an L-type calcium channel blocker, and MK-801, a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist on morphine analgesia and pharmacokinetics were examined in mice. Mice received a subcutaneous injection of morphine (3.2 mg/kg) 30 min after a subcutaneous injection of diltiazem or MK-801. Diltiazem (20-60 mg/kg) potentiated morphine analgesia and increased serum morphine levels in a dose-dependent manner. MK-801 (0.3 mg/kg) significantly attenuated morphine analgesia but had no significant effect on serum or brain morphine levels. These results suggest that a modification of morphine metabolism is involved, at least in part, in the ability of diltiazem to enhance morphine analgesia, whereas MK-801 attenuates morphine analgesia without affecting morphine pharmacokinetics.