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In a series of fifty-two patients undergoing abdominal surgery the listed below agents for postoperative analgesia are used: moradol (M), dipidolor (D), droperidol--DNBP, fentanyl (F). The control group is given analgin. During the first six hours, M and D show optimal effect in terms of postoperative pain syndrome relief, without suppression of the hemodynamics and respiration.
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The study was undertaken to study the functional relations between the overall electric activities of smooth muscles in 3 gastric portions (cardial and pyloric antrums, and the body of the stomach) and that of duodenal muscles during their direct electric stimulation, followed by the recording of potentials evoked in the feline cerebral cortex. There was an ambiguous correlation of the amplitudes of the electric activity of 4 portions of the gastroduodenal complex during opiate receptor activation and after vagotomy. The central and intraorgan components were found to play a combined role in displaying responses of gastroduodenal smooth muscles to opiate receptor stimulation and block.
60 parturients were given the following drugs on purpose to achieve painless postoperative period--group 1--moradol--M, group 2--tramal--T, group 3--lydol--L, and group 4--promedol--P. Preparations M and T compared with L and P proved to be with better analgetic effect with no suppression on the contractile activity of the uterus, no blockade of hypothalamus-hypophysis-adrenal system and no influence on the respiration, pulse, blood pressure, acid-base balance and interchange of gases.
The central mechanisms of analgesic action of phentanyl and moradol are compared using analysis of changes in the early and late components of somatosensory evoked potentials (SSEP) of the brain in normal volunteers in response to pain stimulation. Phentanyl and moradol differently affect the changes in the early components of SSEP: phentanyl reduces their amplitude, whereas moradol increases it. Both drugs similarly influenced changes in the late components of SSEP. Specific effects of the drugs on the sensory and psychoemotional components of pain perception by man are discussed.
Moradol was used for analgesia in 154 patients with unstable angina pectoris and small- and large-focal myocardial infarction and noubain in 69 patients aged 46 to 83. Moradol was found to be an effective analgesic for patients with acute myocardial infarction, exerting a hyperdynamic effect on the circulation, which was easily eliminated if the drug was combined with droperidol or relanium. Noubain is also effective in myocardial infarction, but exerts no hyperdynamic effect on the circulation.
Beforal was used for anesthesia in 21 children aged 4 to 14 years and weighing 15 to 65 kg. Surgical interventions lasted for 2.5 to 9 hours. The basic dose of beforal was 0.5 to 1 mg/kg. Anesthesia was maintained with half or third of the basic dose in combination with inhalations of nitrogen oxide and relanium (diazepam) in a dose of 0.3 to 0.4 mg/kg. Beforal as the only analgesic component of anesthesia effectively protected the organism of a child from surgical shock and its use was associated with stability of the studied hemodynamic parameters.
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The binding characteristics of the kappa opioid ligands [3H]U69,593 and [3H]bremazocine, the mu opioid ligand [3H][D-ala2,N-Me-Phe4,glycol5]enkephalin and the delta opioid ligand [3H]p-Cl-[D-pen2,5]enkephalin were studied in rhesus monkey brain membranes in saturation binding experiments and were followed by competition binding experiments with a variety of peptidic and nonpeptidic opioid ligands. The [3H]U69,593 sites appeared to be a subset of kappa opioid receptors (kappa-1 receptors: Kd, 1.2 nM; Bmax, 66 fmol/mg). [3H]Bremazocine (in the presence of mu and delta receptor-masking agents), bound to a larger population of kappa receptors (kappa-all: Kd, 0.39 nM; Bmax, 227 fmol/mg), which presumably included the aforementioned kappa-1 sites. Competition binding experiments revealed that the presently defined kappa-1 sites were similar to previously reported sites in other mammalian species, particularly in terms of the higher kappa-1 selectivity observed with arylacetamide (e.g., U50,488) vs. benzomorphan kappa agonists (e.g., ethylketocyclazocine). The kappa-selective antagonist norbinaltorphimine (nor-BNI) displayed a very small (2.3-fold) selectivity for kappa-1 vs. kappa-all sites. This led to the prediction that in rhesus monkeys (n = 3), systemically administered nor-BNI (10 mg/kg s.c.) should have a very moderate degree of antagonist selectivity for the antinociceptive effects of a putative kappa-1-agonist, the arylacetamide U50,488 (0.1-3.2 mg/kg s.c.), vs. those of the benzomorphan kappa agonist ethylketocyclazocine (0.01-056 mg/kg s.c.). This prediction was confirmed in vivo because nor-BNI (10 mg/kg) caused a robust and long lasting (up to 21 days) antagonism of the antinociceptive effects of U50,488 and a small but significant antagonism of ethylketocyclazocine. The arylacetamide congener Cl-977 (enadoline), which displayed an 11-fold kappa-1 vs. kappa-all binding selectivity, was not sensitive to nor-BNI pretreatment. This indicates that the kappa subtype-binding profile of an agonist is not necessarily predictive of its sensitivity to nor-BNI in vivo. Overall, the present results suggest that at least two functional kappa receptor populations may be present in rhesus monkey brain.
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