ABSTRACT
The supposed antistress effect of vitamins-alpha-tocopherol, pyridoxine and dexpanthenol (pantothenic acid precursor)--was followed on the model of nociceptive stress in laboratory rats. The decrease of the stress enhancement of nonesterified fatty acids (NEFA), estimated in the brain cortex, hypothalamus and the brain stem, was taken for the indicator of the antistress effect. Nonesterified fatty acids were determined with the help of gas chromatography following the separation performed by thin layer chromatographic method. Five-day application of alpha-tocopherol acetate (per os, 300 mg.kg-1) led to a decrease of the stress enhancement of arachidonic acid level in the brain stem.
Subject(s)
Brain Chemistry/physiology , Fatty Acids, Nonesterified/metabolism , Pantothenic Acid/analogs & derivatives , Pyridoxine/pharmacology , Stress, Psychological/metabolism , Vitamin E/pharmacology , Animals , Brain Chemistry/drug effects , Male , Pantothenic Acid/pharmacology , Rats , Rats, WistarSubject(s)
Anabolic Agents/pharmacology , Central Nervous System/metabolism , Fatty Acids, Nonesterified/metabolism , Nandrolone/pharmacology , Stress, Psychological/metabolism , Animals , Brain Stem/drug effects , Brain Stem/metabolism , Central Nervous System/drug effects , Cerebral Cortex/drug effects , Cerebral Cortex/metabolism , Hypothalamus/drug effects , Hypothalamus/metabolism , Male , Pain/metabolism , Rats , Rats, WistarABSTRACT
In the brain tissue there exists a highly active "pool" of nonesterified fatty acids (NEFA). The greatest part of NEFA comes from the fraction of nerve endings. It was evidenced that the model convulsive activity provoked by Bemegrid increased NEFA in the brain cortex, hypothalamus and brain stem. Cinnarizine (StugeronR) markedly decreases the convulsive increase of NEFA. The greatest inhibitory effect was observed in the brain cortex. Cinnarizine has an objective stabilizing and anticonvulsive effect on the brain tissue.
Subject(s)
Brain/metabolism , Cinnarizine/pharmacology , Fatty Acids, Nonesterified/metabolism , Seizures/metabolism , Animals , Bemegride , Male , Rats , Rats, Inbred Strains , Seizures/chemically inducedABSTRACT
The authors observed biphasic changes of dopamine, norepinephrine and serotonin in the rat brain stem after a single application of physostigmine (1 mg/kg of body weight). The results confirm the hypothesis of "labilization and stabilization" of membranes.
Subject(s)
Brain Stem/drug effects , Physostigmine/pharmacology , Animals , Brain Stem/metabolism , Dopamine/metabolism , Male , Norepinephrine/metabolism , Rats , Rats, Inbred Strains , Serotonin/metabolismABSTRACT
The levels of NEFA (oleic acid, palmitic acid, stearic acid, arachidonic acid) were studied in the brain cortex, hypothalamus and the brain stem of rat brain. Inhibition of phospholipase A2 by Delagil (Mepacrinium dichloratum CsL 3) decreased statistically significantly the values of arachidonic aci (-5.5%) in the brain cortex and the values of stearic acid (-11.2%) in the hypothalamua. The cyclooxygenase inhibition by aspirin led to a significant increase of palmitic acid (+12.7%), oleic acid (+18.7%) and arachidonic acid (+14.3%) in the hypothalamus. Total NEFA increased by 11.2%. A significant increase of palmitic acid (+26.9%), arachidonic acid (+33.9%) and of total NEFA (+22.9%) was evidenced in the brain stem. Delagil administered in combination with acetylsalicylic acid suppressed the NEFA increase observed after the application of acetylsalicylic acid alone. A statistically significant decrease was found in stearic acid (-12.6%) in the hypothalamus and in all studied NEFA in the brain stem (palmitic acid, -14.2% stearic acid -11.7%, oleic acid -3.8%, arachidonic acid -16.6% and total NEFA -11.8%).
Subject(s)
Brain/metabolism , Fatty Acids/metabolism , Phospholipases A/physiology , Phospholipases/physiology , Prostaglandin-Endoperoxide Synthases/physiology , Animals , Aspirin/pharmacology , Brain/drug effects , Enzyme Inhibitors/pharmacology , Male , Phospholipases A/metabolism , Phospholipases A2 , Prostaglandin-Endoperoxide Synthases/metabolism , Rats , Rats, Inbred StrainsABSTRACT
An acute 30 min exposure to toluene vapours (0.32 mmol/l of the air) provoked in the rat brain a decrease of total nonesterified fatty acids (arachidonic acid -21.7%, oleic acid -18.3%, stearic acid -7.9% in the brain cortex and arachidonic acid -6.8% in the hypothalamus). The results are in harmony with the hypothesis of the NEFA decreasing effect of the inhibitory substances in the brain.
Subject(s)
Brain/metabolism , Fatty Acids/metabolism , Psychotropic Drugs/pharmacology , Toluene/pharmacology , Animals , Brain/drug effects , Male , Rats , Rats, Inbred StrainsABSTRACT
The administration of physostigmine (0.3 mg/kg s.c.) compensated toluene intoxication in rats together with NEFA return toward the normal values. This interaction of toluene and physostigmine supports the hypothesis of NEFA functioning as moderators of the cerebral activity.
Subject(s)
Physostigmine/pharmacology , Poisoning/drug therapy , Toluene/toxicity , Animals , Brain/drug effects , Brain/metabolism , Fatty Acids/metabolism , Male , Rats , Rats, Inbred StrainsABSTRACT
A survey of experimental studies dealing with physostigmine in the course of seventeen years is completed by authors' own experience with physostigmine application in practice.
Subject(s)
Physostigmine/therapeutic use , Aged , Analgesics , Animals , Cats , Central Nervous System/drug effects , Female , Humans , Physostigmine/pharmacologyABSTRACT
There was studied the effect of repeated administration of delta-9-THC (10 mg/kg per os for two days) on the level of nonesterified fatty acids (NEFA) in the brain structures of laboratory rats. Palmitic acid, stearic acid, oleic acid and arachidonic acid were estimated with the help of gas chromatography after preliminary separation by TLC. After administration of delta-9-THC, the levels of NEFA decreased in the brain cortex, the brain stem and most in the hypothalamus. The NEFA decrease after delta-9-THC administration is in harmony with the functional inhibition of CNS, provoked by this substance.
