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At least 19 recordsLinked to original sources
PubMed1989

A pharmacological approach to cellular mechanisms of PGI2-induced gastric cytoprotection on ethanol-induced gastric mucosal damage in rats.

The aims of this study were as follows: 1. to analyse the effects of drugs with different subcellular mechanisms on the PGI2-induced gastric cytoprotection in a non acid dependent (ethanol-induced) gastric ulcer model; 2. to identify the affinity and intrinsic activity curves on the PGI2-induced gastric cytoprotection; 3. to evaluate the main cellular mechanisms of PGI2-induced gastric mucosal defence. The observations were carried out on both sexes of CFY-strain rats, weighing 180 to 210 g. The gastric mucosal damage was produced by intragastric administration of 96% ethanol. The animals were killed at 1 hr after administration of ethanol, and the number and severity of gastric mucosal lesions (ulcers) was noted. Atropine, actinomycin D, cimetidine, mannomustine, dinitrophenol, epinephrine, pentagastrin, histamine, ouabain, tetracycline were given intraperitoneally (in different doses) at 30 min before administration of ethanol. The effects of these drugs were tested on the PGI2-induced (5 micrograms/kg was given intragastrically) gastric cytoprotection. It has been found that: 1. atropine, actinomycin D, cimetidine, epinephrine, ouabain, tetracycline and mannomustine inhibited the PGI2-induced gastric cytoprotection; 2. histamine, pentagastrin and 2,4-dinitrophenol enhanced the PGI2-induced gastric cytoprotection; 3. the molar concentrations of these drugs modifying the PGI2-induced gastric cytoprotection differed significantly. It has been concluded that: 1. the drugs stimulating or inhibiting the cell functions are capable to modify the extent of PGI2-induced gastric cytoprotection; 2. different subcellular mechanisms (oxidative phosphorylation, increased synthesis of proteins, ribonucleic and deoxyribonucleic acids, modifications of membrane-bound ATP-dependent energy systems) are involved in the development of PGI2-induced gastric cytoprotection.

Animals↗
PubMed1980

Effects of perineurally applied cytostatic, cytotoxic and chelating agents upon peripheral and central processes of primary nociceptive neurons.

After perineural application, the effects of mannomustine, cyclophosphamide, tetrameskylmannite, 6-mercaptopurine, azathioprine and d-penicillamine upon structure of peripheral nerves and the substantia gelatinosa Rolandi were studied by means of neurohistochemical techniques and compared to those of the microtubule inhibitors Vinblastine, Vincristine and colchicine. While the cytostatic and cytotoxic drugs induced only sporadic degeneration in the structure of the peripheral nerve and, accordingly, caused only a minor extent of transganglionic degenerative atrophy in the Rolando substance, the chelating agent d-penicillamine causes massive Wallerian degeneration after perineural application and, consequently, induces an extensive degenerative atrophy in the Rolando substance. The destructive effect of d-penicillamine upon conduction properties of the impaired nerve has been established also by means of electrophysiological recording. All the drugs studied differ fundamentally from microtubule inhibitors like the Vinca alcaloids that, by virtue of their blocking effect of axoplasmic transport, induce degenerative atrophy in the Rolando substance after perineural application without causing Wallerian degeneration in the peripheral nerve. Accordingly Vinca alcaloids are the most promising candidates as locally applied therapeutics in intractable pain.

Action Potentials↗
PubMed1975

Functional and fine structural characteristics of the sensory neuron blocking effect of capsaicin.

In the eye of rats the long-lasting specific desensitization induced by local or systemic capsaicin treatment is characterized by three phases: 1. complete insensitivity, 2. decreased sensitivity and a tendency to rapid adaptation, 3. normal initial sensitivity with a tendency to rapid adaptation to chemical pain stimuli. A low density of nicrovesicles and swollen mitochondria were found after local capsaicin treatment in certain nerve endings of the cornea of rats, but no signs of axonal degeneration or alteration in fine structure of non-neural elements were seen. Systemic capsaicin desensitization induced selective mitochondrial swelling in B type of neurons of the trigeminal ganglion which was demonstrable even 60 days after the pretreatment. Actinomycin-D, 8-azaguanine, 6-azauracil, aminopterin, mannomustin or cycloheximide in high doses did not alter the desensitizing effect of systemic capsaicin treatment. However, pretreatment of rats with colchicine or vinblastine prolonged the desensitizing effect of local capsaicin application, probably by inhibiting the axonal flow. It is concluded that capsaicin is a specific sensory neuron blocking agent having a practically irreversible effect in rats and guinea-pigs.

Analgesia↗
PubMedDate not supplied

The effect of alkylating agents on the synaptic transmission in the frog's isolated sympathetic ganglion.

The effect of four alkylating agents, such as dibenamine, phenoxybenzamine, mannomustine and cyclophosphamide, was studied on the isolated sympathetic ganglion of the frog. It has been established that all of these agents were able to bind to the nicotinic receptors through the formation of the reactive ethylenimonium ion not only in the frog ganglion but also in the motor end-plate of the rat skeletal muscle. The binding to the ganglionic receptors showed reversible and irreversible phases being dependent not only on the drug concentrations and the incubation time used but the temperature of the medium as well.

Action Potentials↗
PubMed1978

Prolongation of rat cardiac allograft survival by donor pretreatment. Screening of antineoplastic drugs.

We have made preliminary investigations into the effect of 33 different drugs on the survival of rat cardiac allografts, the drugs being administered to the allograft donor. All drugs were administered at LD50 i.v. to the graft donor 6 hr prior to removal of the organ. Especially effective were alkylating agents and antimetabolites. Pretreatment with cyclophosphamide, busulfan, methotrexate, azauridine, or bromodeoxyuridine prolonged the survival from 7 to more than 20 days. Pretreatment with chlorambusil, mannomustine, mannosulfan, 1-(2-chlorethyl)-3-cyclohexyl-1-nitrosourea, DTC, fluoruracil, or hudroxyurea prolonged the survival to more than 14 days. Several other alkylating agents and antimetabolites prolonged the survival moderately, i.e., to approximately 10 days or more. Purine antagonists, mercaptopurine and azathioprine, were totally ineffective as were also anticancer antibiotics and vinca alkaloids. Pretreatment with procarbazine or methylprednisolone alone increased the survival only moderately, whereas pretreatment with both of these drugs together increased the survival up to 27 days.

Alkylating Agents↗