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Abstract
Effect of intraperitoneally (i.p.) injected sub-anesthetic (8x10^sup -5^-8x10^sup -2^ mg/g) and anesthetic (0.125mg/g) doses of ketamine on rats' pain sensitivity and tissue hydration of different organs were studied. Determination of water content of tissue was performed by Adrian's traditional "tissue drying" experimental procedure. The number of functionally active receptors were determined by counting the number of [3H]-ouabain in tissues. Latent period of pain sensitivity was defined by means of "hot plate" test.
Ketamine in sub-anesthetic doses (8x10^sup -5^-8x10^sup -2^ mg/g i.p.) had depressing effect on rats' latent period of pain sensitivity which was accompanied by dehydration of tissues and decrease of the number of [3H]-ouabain receptors in membrane of tissues of different organs. The ouabain influence on brain cell hydration was characterized by dose dependent (10^sup -9^-10^sup -4^M) three phases and this fact was accompanied by corresponding changes of number of ouabain receptors in membrane.
Ketamine anesthetic dose had reversing effect on all three phases of ouabain - induced cell hydration. It was suggested that ketamine - induced cell dehydration leading to decrease of number of functional active proteins in membrane serves as a powerful mechanism through which an analgesic and anesthetic effects of ketamine on organisms were realized.
Article (J Int Dent Med Res 2011; 4: (1), pp. 42-49)
Keywords: rat, ketamine, [3H]-ouabain receptor, pain sensitivity, cell hydration.
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Introduction
It is assumed that ketamine administration causes "dissociative anesthetic state" characterized by profound analgesic, moderate hypnotic properties and by marked sympathomimetic reactions.
Important adverse effects are hallucinations and hypersalivation. Pharmacological profile of ketamine influence can not be explained by a single mechanism. Analgesic, anesthetic and sympathomimetic effects are mediated by different sides of action. It is suggested that N-methyl-D-aspartate (NMDA)-receptor antagonism accounts for most of the amnestic, analgesic, psychotomimetic and neuroprotective effects of ketamine1,2.
It is also known that ketamine blocks an NMDA receptor-mediated component of synaptic transmission in a voltage-dependent manner3-7. At the same time it is well established that ketamine has depressing effect on variety of receptors: nicotinic8,9, muscarinic10 and opioid ones10-12 as well as on voltage sensitive Na+ 9, 13, K+ 13-15 and Ca2+ channels16 of nerve cell membrane in peripheral and central nervous system. At present it is known that influence of ketamine is...