Dissertation
Dissertation > Medicine, health > Surgery > Surgical operation > Anesthesiology

Anesthetics on hippocampal pyramidal neurons sodium channel current and its mechanism

Author HeShaoMing
Tutor ZengYinMing
School China Medical University
Course Anesthesiology
Keywords Mechanism Propofol Isoflurane Lidocaine Hippocampal pyramidal neurons Sodium channel
CLC R614
Type PhD thesis
Year 2002
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Foreword anesthesia anesthesiology principle is the most important basic theories, but the exact mechanism of action of anesthetics is still unknown. Inhalation anesthetics generally considered more complex mechanism of action, which may bear with intravenous anesthetics mechanism. Regardless of inhalation anesthetics role of macro and micro level of how parts can now be sure that the site of action at the molecular level in the nerve cell membrane. More and more evidence suggests that volatile anesthetics exert its effect on the cell membrane is the site of ion channels. In many of the ion channel, anesthetics on n-acetylcholine receptor (nAChR) and r-aminobutyric acid A receptor (GABA_AR) channel affected the most studied, due to experimental conditions and different factors such as drug dose, mixed results . Generally believed that the role of nAChR channel is not the main target for anesthetics. Although GABA_A receptor channel is generally accepted that the main target of anesthetics in clinical anesthetic concentration of the major enhancements in GABA receptor channel effects, but has found that many of the role of the channel can not be explained by the phenomenon, so anesthetics other excitatory ion channels has been attached. In the central nervous system (CNS) major excitatory ion channels, sodium channels as the major excitatory voltage-gated ion channels, are excitable cells generate action potentials and conduction of nerve impulses and determinants of key parts, although the previous It was found that squid giant axon sodium channel model is not sensitive to anesthetics, but later studies have shown that clinical concentrations of anesthetics on rat brain sodium channels in alveolar type Ⅱ cells and cardiac myocytes sodium channel Na channel has significant inhibition , and follow the Meyer-Overton rule. Therefore, general anesthetics on the brain sodium channels and this affects the position of general anesthesia is worth studying. The three-part research project propofol (intravenous anesthetic), isoflurane (inhalation anesthetics) and lidocaine (local anesthetic) acutely isolated CNS sodium channels. The first part of propofol on hippocampal pyramidal neurons sodium channel currents in Materials and Methods 10 * 4d SD rats of either sex, weighing 20-309, by the Experimental Animal Center of Xuzhou Medical College. The rats were quickly decapitated, placed 0-4 ℃ oxygen saturation of artificial cerebrospinal fluid (ACSF) isolated hippocampus, hand cut into thick slices about 500pm. The slices were incubated release floating tank with ACSF for 60 plus n, continuous communication with 95% O. +5 Does CO. Maintain the pH at 7.35 -7.40. Using H-step enzymatic digestion, respectively, with 10 InL dubbed the ACSF 0.05% and 0.05% TyPsin Pronase, have been digested in the incubation fine root 2 ℃, 30 min each person's brain slices after digestion washed two times with ACSF incubation continued. Experiment, each taking two slices release about 1InL filled with ACSF in a small glass, heat-treated successively with a tip diameter of about 400 pm and 150pm Pasteur pipette gently pipetting through 400 mesh steel mesh filter into the cell perfusion tank, placed on an inverted microscope stand for 15-20min to adherent cells with extracellular fluid lavage three times made after whole-cell patch clamp recording. Choose the right under the microscope pyramidal neurons as experimental subjects, there is a hard core glass tube two-step drawing rough recording electrode, with the microelectrode manipulator slowly toward the electrode cell, when the cell membrane electrode tip stick gently attract so sealing, sealing impedance is greater than IGfl when when negative pressure rupture, series resistance compensation capacitor current and whole-cell state. With EPC-9 patch-clamp amplifier at room temperature (24-26T) recorded under sodium current, electrical stimulation pulses per capita output and electrical signals collected by the commercial software through the computer to complete the Pulse 8.02, are digitized and then stored in a computer hard drive. Were divided into seven groups, propofol h, Pro) by adding in the concentration of extracellular fluid wide 0,30,50,100 Pmol / L) corresponding to the divided Pro;. Group, Pro. . Group, u. Groups and PrO;. Group, head fat emulsion Ontralwid, Iry) by PrO. . Groups and Pro;. Group corresponds to the same concentration ILPw groups and ILP;. Control group administered still perfused with extracellular fluid. 6 cells each, were recorded before administration and after administration of 2 dn 2 dn after washing the sodium channel current. Inhibition reduced the maximum inward currents calculated using the percentage of control values ??based. · 2 · Results group and control group * LPro ILPl. Group peak sodium current rate of decline was 4. Two L 3.2% 3.7 ± 46% and in three soil 3. Two mail, the difference was not significant (P> o.05 * depresses peak sodium current density was positively correlated with the degree k = 0.993, P Propofol is a fat-soluble drugs, there are experimental reports dissolve fat emulsion of propofol on myocardial contractile function to a certain extent. The experimental results show that fat emulsion on paved channel current had no significant effect, indicating that the effects of propofol on hippocampal neurons?

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