Effect of verapamil on development of the pain syndrome in rats after sciatic nerve division

Laboratory of Pathophysiology of Pain and Laboratory of General Pathology of the Microcirculation, Research Institute of General Pathology and Pathological Physiology, Russian Academy of Medical Sciences, Moscow. Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 114, No. 9, pp. 229–231, September, 1992.     

Effect of lamotrigin on the development of neurogenic pain syndrome in rats

Analgesic activity of a new anticonvulsive agent lamotrigin was studied on the model of neurogenic pain syndrome produced in rats by penicillin applied to the dorsal surface of the spinal cord and by dissection of the sciatic nerve. Lamotrigin was shown to have a profound analgesic activity. It can be used as an efficient prophylactic agent for prevention of chronic pain syndromes by suppression of the generators of pathologically enhanced excitation in the nociceptive structures which are the pathophysiological basis of the chronic pain syndromes. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 125, No. 5, pp. 517–521, January, 1998.     

Pathological forms of brain electrical activity and localization of its sources in patients with trigeminal neuralgia

No significant differences from the typical electroencephalogram were observed in patients with trigeminal neuropathy. In patients with typical trigeminal neuralgia, the electroencephalogram variations were detected both in the changes of dominant activity and in the appearance of individual pathological phenomena. The three-dimensional localization of pathological activity generators points to the involvement of the median nonspecific brainstem structures into pathological process evoked by trigeminal neuralgia. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 124, No. 9, pp. 275–279, September, 1997     

Synthesis and acid ionization constants of cyclic cystine peptides

Cyclic peptide disulfides of the general formula were synthesized from the corresponding peptide derivatives [Boc-Cys(Trt)(Gly)-_n-Cys(Trt)-OBu^t] by oxidation with iodine in methanol and by subsequent removal of the terminal groups with trifluoroacetic acid. Acid ionization constants of the obtained peptides were determined by potentiometric titration in aqueous KCl (0.1 mol/L) medium. All compounds have two dissociable hydrogens, corresponding to carboxyl (pK¹= 2.35–2.84) and to terminal amino group (pK₂= 5.61–6.93); pK₁, values show first an upward and then a downward trend with the increase in ring size; the opposite is true for pK₂, values. These trends could be tentatively attributed to the intramolecular salt bridge (-COO——-NH⁺₃-) formation.     

Epileptiform activity in the somatosensory cortex of rats with trigeminal neuralgia

Laboratory of Pathophysiology of Pain, Research Institute of General Pathology and Pathological Physiology, Russian Academy of Medical Sciences, Moscow. Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 114, No. 8, pp. 126–128, August, 1992.     

Counseling Fathers (2010) by C.Z. Oren and D.C. Oren

No abstract available for this article.     

Reperfusion injury after critical intestinal ischemia and its correction with perfluorochemical emulsion ＂perftoran＂

AIM: To investigate the anti-ischemic properties of perfluorochemical emulsion "perftoran" in mesenteric region. METHODS: Experiments were conducted on 146 nonlinear white male rats weighing 200-350 g. Partial critical intestinal ischemia was induced by thorough atraumatic strangulation of 5-6 cm jejunal loop with its mesentery for 90 min. Global critical intestinal ischemia was made by atraumatic occlusion of the cranial mesenteric artery (CMA) for 90 min also. Perftoran (PF, 0.8-1.0 mL per 100 g) in experimental groups or 0.9% sodium chloride in control groups was injected at 75 min of ischemic period. Mean systemic arterial blood pressure (BPM) registration, intravital microscopy and morphological examination of ischemic intestine and its mesentery were performed in both groups. RESULTS: During 90 min of reperfusion, BPM progressively decreased to 27.3±7.4% after PF administration vs 38.6±8.0% in the control group of rats with partial intestinal ischemia (NS) and to 50.3±6.9% vs 53.1±5.8% in rats after global ischemia (NS). During the reperfusion period, full restoration of microcirculation was never registered; parts with restored blood flow had leukocyte and erythrocyte stasis and intra-vascular clotting, a typical "non-reflow" phenomenon. The reduction of mesenteric 50-400 μm feeding artery diameter was significantly less in the PF group than in the control group (24±5.5% vs 45.2±3.6%, P<0.05) 5 min after partial intestinal ischemia. This decrease progressed but differences between groups minimized at the 90th min of reperfusion (41.5±4.2% and 50.3±2.8%, respectively). In reperfusion of rat's intestine, a significant mucosal alteration was registered. Villous height decreased 2.5-3 times and the quantity of crypts decreased more than twice. In the group of rats administered PF, intestinal mucosal layer was protected from irreversible post-ischemic derangement during reperfusion. Saved cryptal epithelial cells were the source of regeneration of the epithelium, which began to cover renewing intestinal villi after 24 h of blood flow restoration. View of morphological alterations was more heterogeneous in CMA groups. CONCLUSION: Systemic administration of perftoran promotes earlier and more complete structural regeneration during reperfusion in rats after partial and global critical intestinal ischemia.