1995 Fiscal Year Final Research Report Summary
Inhibitory effect of intravenous anesthetics and magesium on vascular and airway smooth muscles of the guinea-pig.
| Project/Area Number |
06671549
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | Jchi Medical School |
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Principal Investigator |
KASUDA Haruyuki Jichi Medical School, Dept of Anesthesiology, Associate Professor, 医学部, 助教授 (20090590)
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| Co-Investigator(Kenkyū-buntansha) |
YAMASHIRO T Jichi Medical School, Dept of Anesthesiology, Research fellow, 医学部, 助手 (70265271)
TSUKAMOTO N Jichi Medical School, Dept of Anesthesiology, Research fellow, 医学部, 助手
TOGASHI H Jichi Medical School, Dept of Anesthesiology, Research fellow, 医学部, 助手 (80301456)
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| Project Period (FY) |
1994 – 1995
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| Keywords | vascular smooth muscle / airway smooth muscle / intravenous anesthetics / propofol / ketamine / thiopetal / magnesium / relaxation |
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| Research Abstract |
We examined the direct effect of propofol on contractile response and the modulating effect of propofol on electrically induced neurogenic contractions, using the guinea pig vascular and airway smooth muscles. Results indicate that, in a nonspecific way, propofol exhibited the relaxant effect on vascular and airway smooth muscles, and that the mechanism may mainly be on interference with opening of voltage-operated Ca^<2+> channels in the sarcolemma. It is suggested that propofol inhibited autonomic neurotransmission by decreasing norepinephrine released on postsynaptic membrane in vascular smooth muscle, whereas by decreasing neuropeptides released on presynaptic membranein airway smooth muscle.
We compared the direct effects of intravenous anesthetics and Mg on contractile response and the modulating effects them on electrically induced neurogenic contractions, using the guinea pig airway smooth muscles. Results indicate that, in a nonspecific way, they exhibited the relaxant effect on airway smooth muscle, and that the mechanisms may mainly be on interference with opening of voltage-operated Ca^<2+> channels when propofol, with Ca^<2+>-Releasing from SR when ketamine, and with the both when thiopental or Mg^<2+>. It is suggested that they inhibited autonomic neurotransmission. Mg^<2+>, ketamine and thiopental inhibited cholinergic, nonadrenergic and noncholinergic neurotransmisson, whereas propofol did not inhibit cholinergic neurtransmission.
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