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Biomedical subjects

L V Kaliuzhnyĭ

Publications and source records attributed to L V Kaliuzhnyĭ.

At least 19 recordsLinked to original sources
PubMed1994

[Enkephalinase mechanisms of tolerance of analgetic action of opioids. Effects of D-phenylalanine and naloxone].

The paper reviews the data available in the literature and the authors own data demonstrating the differences in the levels of endogenous opioids and in the effects of enkephalinase inhibitor and naloxone in morphine-responsive and morphine-resistant and -tolerant animals. In the morphine-tolerant animals, a single administration of enkephalinase inhibitor or some doses of naloxone was found to produce an analgesic effect leading to a short-term analgesic effect of morphine. Chronic administration of naloxone causing a gradual decrease in and subsequent cessation of its analgesic effect leads to recovery of morphine's analgesic effect in the drug-resistant and -tolerant animals. It is suggested that the morphine-resistant animals have a congenital high activity of enkephalinase, while the drug-tolerant ones have its acquired high activity. Naloxone in certain doses with the high activity of enkephalinase act as its inhibitor, but in high doses acts as its opioid antagonist.

Animals↗
PubMed1993

[The enkephalinase mechanisms of the resistance and tolerance to the analgesic effect of morphine in rats. Differences in the effects of the action of D-phenylalanine in morphine-sensitive, morphine-tolerant and morphine-resistant rats].

In morphine-sensitive (s.c. 1.5 mg/kg) Wistar rats (60%) i.p. inoculation of 300-600 mg/kg d-Phenylalanine (d-Pha) did not change the nociception (tail-flick test), but in morphine-resistant rats (40%) evoked a dose-dependent analgetic effect. In morphine-sensitive rats (40%) chronic morphine administration induced the tolerance and d-Pha injection evoked analgetic effect. Morphine injection just after d-Pha analgesia was over evoked analgetic effect in morphine-resistant and -tolerant rats. It is suggested that morphine-resistant rats have a congenital and morphine-tolerant rats an acquired high level of enkephalinase activity which blocked the morphine analgetic action.

Analgesia↗
PubMed1993

[The enkephalinase mechanisms of the resistance and tolerance to the analgesic effect of morphine in rats. Differences in the effects of naloxone in morphine-sensitive, morphine-resistant and morphine-tolerant rats].

In morphine-sensitive (s. c. 1.5 mg/kg) Wistar rats i.p. injection of 0.3 mg/kg naloxone either did not change nociception (tail-flick test) or induced hyperalgesia. In morphine-resistant rats 0.2-0.7 mg/kg naloxone injection induced analgetic effect but 1.0 mg/kg induced hyperalgesia. In morphine-sensitive rats chronic morphine administration induced the tolerance and naloxone injection evoked analgetic effect. Morphine inoculation just after naloxone analgesia was over induced analgetic effect. In morphine-resistant and -tolerant rats chronic naloxone administration induced gradual decrease and subsequent disappearance of its analgetic effect and subsequent morphine injections induced analgetic effect for some days. It is suggested that naloxone in morphine-resistant and -tolerant rats with high level of enkephalinase activity functions as its inhibitor. Chronic naloxone administration evoked progressive inhibition of enkephalinase activity that induced the morphine analgetic effect in morphine-resistant and -tolerant rats.

Analgesia↗
PubMed1992

[Extracellular pH, [K+] and synaptic transmission in the dorsal horn of spinal cord of rats in hypercapnia].

In rats anaesthetized with +-chloralose the changes in extracellular pH and K+ in spinal cord dorsal horn were studied using pH and K+ ion-selective electrodes. The addition of 20% CO2 into inhaled air decreased the basal level of [pH]0 from 7.35 +/- 0.01 to 6.78 +/- 0.09 pH units and increased the basal level of [K+]0 from 3.1 +/- 0.1 to 5.14 +/- 0.8 mM. Electrocutaneous supramaximal (10 mA) simulation of both hind paws with the frequency 30 and 100 Hz induced the shift in the concentration of H+ and K+ by 0.15-0.2 unit and 2-2.5 mM, respectively. Under hypercapnia this shift of pH decreased by 36.9 +/- 8.5% at 30 Hz frequency of electrocutaneous stimulation and by 41.9 +/- 6.1% at 100 Hz frequency. The K+ shift decreased by 11.5 +/- 1.3% and by 17.3 +/- 1.5% under similar conditions. Hypercapnia induced by addition of 20% CO2 into inhaled air decreased also the focal potential amplitude by 16.8 +/- 4%. Thus, hypercapnia induces the increase of [K+]0 and [pH]0 and the decrease of recorded indicators in response to electrocutaneous stimulation. Total depression of synaptic transmission and analgetic effect occur due to these changes of ions distribution.

Animals↗
PubMed1991

[Action of an enkephalinase blocker on the effect of acupuncture in acupuncture sensitive and resistant rabbits].

In unanaesthetized acupuncture-sensitive rabbit d-phenylalanine injection didn't change the EP in response to tooth pulp electrostimulation, but prolonged the analgetic effect of auriculo-acupuncture stimulation 15 Hz expressed by decreasing of the amplitude of N1P2 component EP. In acupuncture-resistant rabbit d-phenylalanine injection induced analgetic effect which was enhanced and prolonged by auriculo-acupuncture stimulation. It's suggested that the recovery of pain sensibility after acupuncture analgesia is determined by enkephalinase's mechanism activation which is activated permanently in acupuncture-resistant rabbits.

Acupuncture Analgesia↗
PubMed1990

[Angiotensin mechanism of auriculo-acupuncture dental analgesia].

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.

Acupuncture Analgesia↗
PubMed1989

[The biphasic selective effect of an antiserum to beta-endorphin on pain sensitivity in rats].

In rats beta-endorphin antiserum systemic injection decreased during 1-2 days the threshold of tail-shock and latency of tail-flick tests, and during subsequent 85 days increased the threshold of tail shock, but not changed the latency of tail-flick tests. Naloxone injection blocked the increasing of thresholds, but not changed the latency of tail tests. It is suggested that antiserum evokes the first inhibition and the second selective activation of endogenous antinociceptive opioid system with affinity to electric nociception.

Animals↗
PubMed1988

[Selective analgetic effects of angiotensin and bombesin during the action of dental and cutaneous nociceptive irritants].

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.

Analgesics↗
PubMed1985

[Effect of beta-neo-endorphin--an agonist of chi-opiate receptors on the neuronal activity of the cerebral cortex].

Experiments on cats were made to examine the neuronal responses (the first zone of the somatosensory cortex and the 5th region of the parietal associative cortex) to microapplications of beta-neo-endorphine (an agonist of kappa-opiate receptors), morphine (an agonist of mu-opiate receptors), leuenkephalin (an agonist of delta-opiate receptors) and beta-endorphine (an agonist of mu, delta, epsilon-opiate receptors). beta-Neo-endorphine and other opioid peptides produced similar depressive changes in spontaneous activity. Naloxone in doses which block the depressive reactions of morphine, leu-enkephalin and beta-endorphine did not remove the depressive reactions of beta-neo-endorphine. Opioid peptides and morphine produced different changes in nociceptive-stimulated neuronal activity in the first zone of the somatosensory cortex and photostimulated neuronal activity in the 5th region of the parietal cortex. It is assumed that the different types of opiate receptors and their endogenous ligands (opioid peptides) play different functional roles in the preparation of the nociceptive and visual information in the cortex.

Animals↗
PubMed1983

[Significance of the hypothalamus opioid system in the mechanism of morphine analgesia].

It has been demonstrated in experiments on conscious rabbits that microinjections of nalorphine to the paraventricular area of the hypothalamus blocked morphine analgesia assessed from the tail-flick test and evoked potential variation in the sensorimotor area of the brain cortex in response to nociceptive electrocutaneous stimulation. An analogous but less powerful effect was produced by nalorphine injected into the large raphe nucleus. It is assumed that morphine analgesia is primarily mediated by opioid structures of the hypothalamus.

Analgesia↗
PubMed1981

[Effect of motropin and naloxone on electroacupuncture analgesia].

It was demonstrated in experiments on awake rabbits that electroacupuncture increases the pain threshold (the tail-flick-test) and suppresses the second positive wave of evoked potential in the somatosensory cortex in response to nociceptive electrocutaneous stimulation. Naloxone, the typical antagonist of narcotic analgetics, in doses of 0.05-0.1 mg/kg completely blocks the effects induced by electroacupuncture. The similar effects were produced by motropin, a new antagonist of narcotic analgetics, belonging to the tropan series, administered in doses of 10-20 mg/kg.

Acupuncture Therapy↗
PubMed1981

[Changes in pain sensitivity during electric stimulation of emotiogenic zones of the rabbit hypothalamus].

Electrical stimulation of 80% of negative and 82% of positive sites of the rabbit hypothalamus increased the latent period of thermal nociceptive stimulus avoidance and diminished the evoked potential amplitude in the parafascicular complex of the thalamus in response to electrical nociceptive stimulation of the skin. The opposite effects were evoked by subthreshold stimulation of the negative rather than positive sites. Electrical stimulation of neutral sites had not effect on the test parameters of pain sensitivity.

Animals↗
PubMed1980

[Disappearance of the electroacupuncture effect in rabbits following destruction of the dorsomedial hypothalamus].

In ten experiments on 10 awake rabbits it was shown that the lesion of dorsomedial hypothalamic nuclei induced blocking of the suppression effect of the evoked potential of the thalamus median center on electrocutaneous stimuli under electroacupuncture. At the same time the lesion of the nucleus raphe magnus did not influence the electroacupunture effect. It is suggested that the electroacupuncture is mediated by the hypothalamic analgesic system.

Acupuncture Therapy↗