| The effects of isoflurane pretreatment on cerebral blood flow, capillary permeability, and oxygen consumption in focal cerebral ischemia in rats. | |
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MedLine Citation:
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PMID: 20304986 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: We performed experiments to test whether isoflurane pretreatment produces vascular effects, especially at the levels of arterioles and capillaries affecting regional cerebral blood flow (rCBF), O(2) supply and consumption, or capillary permeability in focal cerebral ischemia. Because inducible nitric oxide synthase (iNOS) was implicated as one of the mechanisms of isoflurane preconditioning, the effect of iNOS inhibition on rCBF was also studied. METHODS: Twenty-four hours before middle cerebral artery (MCA) occlusion, rats were pretreated with 2% isoflurane for 30 minutes using an endotracheal tube and mechanical ventilation for the isoflurane preconditioned (IsoPC) group. For the group of iNOS inhibition, aminoguanidine 200 mg/kg was injected IP 30 minutes before isoflurane pretreatment. One hour after MCA occlusion, rCBF was measured using (14)C-iodoantipyrine autoradiography. Alternate slices of the tissue were used to determine arteriolar and venular O(2) saturation using cryo microspectrophotometry. Capillary permeability was determined by measuring the transfer coefficient (Ki) of (14)C-alpha-aminoisobutyric acid. Additional measurements of rCBF were performed at 3 hours after MCA occlusion. RESULTS: MCA occlusion decreased rCBF and O(2) consumption and increased Ki in both the control and the IsoPC groups at 1 hour after MCA occlusion. In the ischemic cortex (IC), the rCBF and O(2) consumption were significantly greater in the IsoPC group than in the control group (+40% and +41%, respectively), but they were similar in the contralateral cortex between the 2 groups. There was no difference in Ki between the groups in the IC or in the contralateral cortex. The increase of rCBF in the IC (+50%) was sustained in the IsoPC group at 3 hours after MCA occlusion. With iNOS inhibition, the increase of rCBF in the IC with isoflurane pretreatment became insignificant. CONCLUSIONS: Our data demonstrate that isoflurane pretreatment improved rCBF and increased the regional O(2) supply and consumption in the focal ischemic area but did not affect capillary permeability during the early stage of focal cerebral ischemia. The isoflurane-induced increase in rCBF in the ischemic area became insignificant with inhibition of iNOS. |
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Authors:
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Oak Z Chi; Christine Hunter; Xia Liu; Harvey R Weiss |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-03-19 |
Journal Detail:
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Title: Anesthesia and analgesia Volume: 110 ISSN: 1526-7598 ISO Abbreviation: Anesth. Analg. Publication Date: 2010 May |
Date Detail:
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Created Date: 2010-04-26 Completed Date: 2010-05-13 Revised Date: 2010-05-28 |
Medline Journal Info:
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Nlm Unique ID: 1310650 Medline TA: Anesth Analg Country: United States |
Other Details:
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Languages: eng Pagination: 1412-8 Citation Subset: AIM; IM |
Affiliation:
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Department of Anesthesia, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, New Brunswick, NJ 08901-1977, USA. chi@umdnj.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Aminoisobutyric Acids
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diagnostic use Anesthetics, Inhalation / pharmacology* Animals Antipyrine / analogs & derivatives, diagnostic use Arterioles / drug effects Blood Gas Analysis Blood Pressure / drug effects Brain Ischemia / metabolism, physiopathology* Capillary Permeability / drug effects* Cerebrovascular Circulation / drug effects* Functional Laterality / drug effects Heart Rate / drug effects Ischemic Preconditioning / methods* Isoflurane / pharmacology* Male Middle Cerebral Artery / physiology Nitric Oxide Synthase Type II / metabolism Oxygen Consumption / drug effects* Rats Rats, Wistar |
| Chemical | |
Reg. No./Substance:
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0/Aminoisobutyric Acids; 0/Anesthetics, Inhalation; 129-81-7/iodoantipyrine; 26675-46-7/Isoflurane; 60-80-0/Antipyrine; 62-57-7/2-aminoisobutyric acid; EC 1.14.13.39/Nitric Oxide Synthase Type II |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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