Neuromuscular blocking activity of dibekacin, a new semisynthetic aminoglycoside antibiotic.
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Biomedical subjects
Publications and source records attributed to C Triantaphyllidis.
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The aminoglycoside antibiotics possess neuromuscular blocking activity; the potency of those antibiotics tested appears to be as follows: gentamicin greater than streptomycin greater than amikacin greater than sisomicin greater than kanamycin = tobramycin greater than kanendomycin = dibekacin. The neuromuscular blockade produced by these antibiotics is not reversed by neostigmine, whereas it is reversed by calcium. Calcium not only has the ability to restore the neuromuscular transmission but also to exert protective action against the neuromuscular blocking activity of aminoglycoside antibiotics; these antibiotics are also potentially capable of interacting with non-depolarizing muscle relaxant drugs (d-tubocurarine, pancuronium) or propranolol, a beta-adrenergic receptor blocking agent. This interaction results in respiratory depression and/or prolonged apnoea. Our findings lead to the assumption that amino-glycoside antibiotics are involved in the process of acetylcholine release by nerve impulses, antagonizing calcium ions.
Analysis at 20 genetic loci by starch gel electrophoresis of a population from Greece shows that contrary to most accepted views, the outdoor Eastern Mediterranean Short-tailed Mouse (i) does not belong to the same species as the House Mouse (Mus musculus), (ii) is not less distant from the Eastern European semi-species of House Mouse (biochemical group 2) than from the Western and Mediterranean European semi-species (group 1), and (iii) is not more closely related to the outdoor Western Mediterranean Short-tailed Mouse Mus spretus (group 3), than to M. musculus. It represents a new biochemical group (group 4) and deserves a species rank (Mus spicilegus).
Aminodeoxykanamycin (Kaneudomycin) as well as other members of the aminoglycoside antibiotics, has an action at the neuromuscular junction. Kanendomycin was found to be five times less potent than gentamycin, as far as their neuromuscular blocking action on the rat diaphragm is concerned. The neuromuscular blocking action on the rat diaphragm is concerned. The neuromuscular blockade produced by Kanendomycin is not reversed by neostigmine but only by calcium chloride.
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The genetic polymorphism of two salivary enzymes (esterase and alpha-amylase) was studied in individuals from eight districts of Greece. The pooled gene frequencies were: SetS = 0.63, SetF = 0.37, AMY1 = 0.87, AMY2 = 0.10, AMY3 = 0.02, and AMY4 = 0.01. There was no intrapopulation heterogeneity, while there was a significant difference between the Greeks and the few other European populations studied.
An expected response in a hypoglycemic patient to a muscle relaxant formed the basis for the research presented in this study. There was no information available in the accessible literature and references gave no data on this subject. But because perioperative hypoglycemia is not unusual, we scheduled this experimental work. Four groups of 6 white adult Wistar albino rats were used in the study. Group A was the normoglycemia control group, with blood glucose levels of 80-120 mg/dl. Groups B, C and D were made hypoglycemic by i.v. injection of insulin 1 IU/100 g b.w. Blood glucose levels were reduced to 50% of the control values in hypoglycemic animals, which were sacrificed 40 min later. Phrenic nerve-hemidiaphragm preparations were placed in a 100 ml bath containing Paradelis-Zaimis solution, 37 degrees C, pH 7.2, aerated with O2/CO2:95/5%. After stabilization and recording of neuromuscular activity, pancuronium bromide was administered in doses of 1.5 x 10(-9) M in groups A and B, 3 x 10(-9) M in group D. Statistical analysis between A-B, A-C, A-D groups was done with Student's paired t test. Results showed that under hypoglycemic conditions the amount of pancuronium bromide needed for complete neuromuscular blockade was 2.5-fold greater than that needed in normoglycemic conditions. These findings suggest that the integrity of the neuromuscular junction is altered during hypoglycemia.