1992 Fiscal Year Final Research Report Summary
Mechanisms of Anesthesia-related drugs on Cerebral Microcirculation - A In Vivo Study Using Intravital Microscope
| Project/Area Number |
02454350
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
麻酔学
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| Research Institution | Gifu University School of Medicine |
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Principal Investigator |
DOHI Shuji M.D.,Professor and Chairman, Department of Anesthesiology & Critical Care Medicine Gifu University School of Medicine, 医学部・麻酔・蘇生学講座, 教授 (40155627)
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| Project Period (FY) |
1990 – 1992
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| Keywords | Cerebral Microcirculation / Spinal Agents / Cocaine / Nicorandil / Dexamedetomidine / コカイン |
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| Research Abstract |
Background and Purpose: In order to know mechanisms of anesthesia related drugs' effects on cerebral microcirculation, the investigator studied pharmacological responses to topical application of K-channel opener(nicorandil), local anesthetic(cocaine), endotheline, alpha adrenergic agonist(dexamedetomidine) on vasomotor tone of pial vessel.
Methods: In dogs and cats anesthetized lightly with pentobarbital and prepared with a parietal cranial window, each agent dissolved in artificial cerebrospinal fluid were applied under the window. The pial arteriolar and venular diameters were measured ateach concentration by a videomicrometer with television attached to a microscope. After effects of each drug were obtained, a known antagonist was pretreated and then the drug was administered and followed the measurements.
Results: Cocaine (10^<-4>-10^<-8>) and nicorandil (10^<-3>-10^<-7>) produced pial arteriolar vasodilation in a dose related fashion, and the effects were blocked with the pretreatment of propranolol and methylene blue, respectively. Dexmedetomidine (10^<-4>-10^<-7>) produced pial arteriolar vasoconstriction in a dose related fashion and this effect was completely blocked with yohimbine. End theline administered into lumbar subarachnoid space caused significant decrease in spinal cord blood flow but not in cerebral blood flow. The decreased spinal cord blood flow was partially antagonized with nicardipine.
Conclusion: The results of the present in vivo studies suggest that pharmacological responses of cerebral microcirculation to potential spinal agents were similar to the responses obtained in vitro study using with peripheral vessels, and thus mechanism(s) of the act ioncould be similar with some difference in sensitivity.
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