[Morphine antibodies in the mechanisms of morphine resistance, morphine tolerance and of the action of an antagonist]. / Antitela k morfinu v mekhanizmakh morfinnoi rezistentnosti, morfinnoi tolerantnosti i deistviia antagonista.

It was found that the absence of the analgesic effect of morphine, as determined by the tail-flick test, in morphine-resistant and morphine-tolerant rats, as well as in naloxane blockade of morphine analgesia in morphine-sensitive rats was attended with a four- to eight-fold increase in morphine antibodies in the plasma, as determined by the ELISA method. It is suggested that a pharmacokinetic factor mediated through immune reactions of morphine antibodies formation is one of the mechanisms of such conditions.

[Clinical and experimental analysis of the use of the Analgedent electrostimulator for dental analgesia]. / Klinicheskii i éksperimental'nyi analiz primeneniia élektrostimuliatora "Analgedenta" dlia dental'nogo obezbolivaniia.

Clinical studies and animal experiments have demonstrated an antinociceptive effect of auricular electrostimulation (AE), 15 Hz, 300 microA, 25 min, on toothache. Perceptual and emotional vegetative components of the painful reaction were reduced by AE in 60 percent of patients and 64 percent of animals. Intravenous naloxone (0.2 mg/kg) abolished AE analgetic effect. The absence of AE analgetic effect in 40 percent of patients and 36 percent of animals can be explained by individual features of the endogenic opioid system functioning. Prospects of AE clinical application with various stimulation frequencies are discussed.

[Angiotensin mechanism of auriculo-acupuncture dental analgesia]. / Angiotenzinovyi mekhanizm aurikulo-akupunkturnoi dental'noi analgezii.

In unanaesthetized rabbits auriculo-acupuncture electrostimulation with frequency of 15 Hz decreased the amplitude of somatosensory EP second component in response to the tooth pulp electrostimulation which was blocked by intravenous injection of naloxone but not by intraventricular injection of saralasin. The same effect of auriculo-acupuncture electrostimulation with frequency 100 Hz was blocked by saralasin, was increased by angiotensin II, was diminished by methysergide but wasn't changed by naloxone. It's suggested that there is angiotensinergic antinociceptive mechanism of dental pain which is activated by auriculo-acupuncture electrostimulation with frequency 100 Hz.

New peptide mechanism of auriculo-acupuncture electro-analgesia: role of angiotensin II.

In rabbits, auriculo-acupuncture electrostimulation with frequencies of 15 and 100 Hz induced an analgesic effect expressed by a decrease in the amplitude of a cortical somatosensory evoked potential in response to tooth pulp electrostimulation. Intracerebroventricular saralasin injection abolished or blocked the effect of auriculo-acupuncture stimulation at 100 Hz, but not at 15 Hz frequency. Intravenous injection of naloxone abolished the effect of auriculo-acupuncture stimulation at 15 Hz but not at 100 Hz frequency. Methysergide or D,L-p-chlorophenylalanine injection diminished but did not entirely block the effect of auriculo-acupuncture stimulation at 100 Hz. This suggests that the neuropeptide angiotensin II is a antinociceptive factor in dental peptide analgesic mechanisms induced by auriculo-acupuncture stimulation at 100 Hz frequency.

[Selective analgetic effects of angiotensin and bombesin during the action of dental and cutaneous nociceptive irritants]. / Izbiratel'nost' analgeziruiushchikh éffektov angiotenzina i bombezinapri deistvii dental'nykh i kozhnykh notsitseptivnykh razdrazhitelei.

In non-anesthesized rabbits intraventricular injection of angiotensin II reduced the amplitude of somatosensory evoked potential to nociceptive tooth pulp, but not to nociceptive electrocutaneous stimulation. The same injection of bombesin induced the contrary analgetic effect. The systemic naloxone (0.1 mg/kg) injection didn't reverse the peptides analgetic effects. It's suggested that selective analgetic effects of angiotensin II and bombesin are determined by the presence of the specific different peptide mechanisms for nociception with the different pain genesis.

[Effect of angiotensin II and naloxone on the nociceptive sensitivity of rabbits undergoing electrostimulation of the skin and dental pulp]. / Vliianie angiotenzina II i naloksona na notsitseptivnuiu chuvstvitel'nost' krolikov pri élektrostimuliatsii kozhi i pul'py zuba.

In unanesthetized rabbits intraventricular and intravenous administration of angiotensin II resulted in a decrease of the somatosensory evoked potential amplitude in response to nociceptive electrodental stimulation but not nociceptive electrocutaneous stimulation. Saralasin administered intraventricularly abolished the effect of angiotensin II. Naloxone injected by the same route increased the evoked potential amplitude in response to electrodental but not to electrocutaneous stimulation and also reversed the analgesic effect of angiotensin II. The selectivity of the antinociceptive effect of angiotensin II is probably due to the presence of different specific peptide pain mechanisms of varying origin.

Angiotensin II, bombesin and naloxone in tooth pulp and cutaneous nociceptive mechanisms in rabbits.

The effects of angiotensin II (A II), bombesin (B) and naloxone (N) on the amplitude of the late component of the evoked potentials of the cortex (EP) were studied by electrocutaneous (ECS) and tooth pulp (ETS) stimulation. An intraventricular (50 ng/kg) or intravenous (5 micrograms/kg) injections decreased the amplitude of the negative-positive component with a 20-40 ms latency (NP20-40) EP to ETS, but not to ECS. Saralasin (A II antagonist) injected intraventricularly (130 ng/kg) abolished this effect of A II in response to ETS. N intraventricular injections (30 micrograms/kg) increased the amplitude of NP20-40 EP to ETS, but not to ECS. B (intraventricular injection 20 ng/kg decreased the amplitude of NP20-40 EP to ECS, but not to ETS. This suggests there are the specific mechanisms in analgesia induced by A II and B in the pathways activated by ECS and ETS.