| Effect of Isoflurane Anesthesia on Local Cerebral Glucose Utilization and Local Cerebral Blood Flow in Rats. |
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Hee Soon Kim, Chong Min Park |
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Department of Anesthesiology, Catholic University Medical College, Seoul, Korea. |
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| Abstract |
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The influence of isoflurane on local cerebral glucose utilization and local cerebral blood fiow was studied by quantitative autoradiography using 23 male Sprague-Dawley rats. rats had both the femoral artery and vein cannulated and were anesthetized with 0.5 MAC and 1.0 MAC isoflurane.
Local cerebral glucose utilization and local cerebral blood flow were compared between conscious controls and isofiurane anesthetized rats. The results were as follows: 1) There was a slight decrease of blood pressure in the anesthetized group but it was within the range of autoregulation. The PaO2 and PaCO2 were influenced by artificial ventilation in the anesthetized group but were in the normal range. 2) 1-CM-Rg was decreased in most regions and there was no significant difference between the 0.5 MAC and 1.0 MAC isoflurane anesthesia groups. 3) Some regions had increased glucose utilization. They were the cerebellum nucleus, vestibular nucleus, substantia nigra pars compacta, and hippocampus molecular layer. 4) Some regions had prominent glucose utilization in the anesthetized rats which did not appear in coscious controls. They were the havenula, havenulo-interpedunculus nucleus and fornix. 5) The order of decreased glucose utilization was cerebral association area>auditory system> visual system > sensory motor system > limbic system > extrapyramidal system = myelinated fiber.
This means most of the cerebral cortex and auditory system had decreased glucose utilization but extrapyramidal system was well preserved by isoflurane anesthesia. 6) The order of decreased glucose utilization according to anatomical region was telencephalone> diencephalone > mesencephalone > metencephalone > mylencephalone, which means there is rostraI to caudal gradient of glucose utilization. In other words, forebrain was more affected than the hindbrain, so unconsciousness can be achieved with isoflurane with no specific effect on respiration, blood pressure or temperature. 7) Local cerebral blood flow was significantly increased in anesthetized group, and was especiaBy more increased in 0.5 MAC anesthetized group, but some regions (cerebellum white, thalamus) showed decreased blood flow. 8) The order of increased cerebral blood flow was visual system > sensory motor system > auditory system= limbic system > extrapyramidal system) myelinated fiber> cerebral association area in the 0.5 MAC group; but in the 1.0 MAC group, it was visual system>limbic system>extrapyramidal system>sensorymotor system auditory system>myelinated fiber>cerebral association are. 9) The order of increased cerebral blood flow according to the anatomical region was mesencephalon>myelencephalon>diencephalon>telencephalon Metencephalone in 0.5 the MAC group but in the 1.0 MAC group, it was myelencephalon>mesencephalon>diencephalon>telencephalon>metencephalon.
10) There was flow-metabolism uncoupling, although much less than with other inhalation anesthetics, with low metaholism and high blood flow by isoflurane anesthesia. The ratio (1-CBF/ 1-CMRg) was four times greater than control group in the 0.5 MAC group, and three times greater in the 1.0 MAC.
11) Some nucleus of limbic system were prominent in glucose utilization with no significant eidence of limbic seizure but may have some degree of protective effect in the hypoxic or ischemic brain. |
| Key Words:
Isoflurane; Cerebral glucose utilization; CBF |
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