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Neuronal Nitric Oxide Synthase Mediates Halothane- Induced Cerebral Microvascular Dilation Michael Staunton, M.B., F.F.A.R.C.S.I.,* Cathy Drexler, M.D.,† Phillip G

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Neuronal Nitric Oxide Synthase Mediates Halothane- Induced Cerebral Microvascular Dilation Michael Staunton, M.B., F.F.A.R.C.S.I.,* Cathy Drexler, M.D.,† Phillip G 125 Anesthesiology 2000; 92:125–32 © 2000 American Society of Anesthesiologists, Inc. Lippincott Williams & Wilkins, Inc. Neuronal Nitric Oxide Synthase Mediates Halothane- induced Cerebral Microvascular Dilation Michael Staunton, M.B., F.F.A.R.C.S.I.,* Cathy Drexler, M.D.,† Phillip G. Schmid III, M.D.,‡ Heather S. Havlik, B.S.,§ Antal G. Hudetz, B.M.D., Ph.D.,i Neil E. Farber, M.D., Ph.D.# Downloaded from http://pubs.asahq.org/anesthesiology/article-pdf/92/1/125/399507/0000542-200001000-00023.pdf by guest on 03 October 2021 Background: The causes of volatile anesthetic-induced cere- tered and vasodilation was calculated as a percentage of pre- bral vasodilation include direct effects on smooth muscle and constriction. indirect effects via changes in metabolic rate and release of Results: Halothane caused significant, dose-dependent dila- mediators from vascular endothelium and brain parenchyma. tion of hippocampal microvessels (halothane group). Inhibi- The role of nitric oxide and the relative importance of neuronal tion of nNOS by 7-NINA or nNOS 1 eNOS by L-NAME similarly and endothelial nitric oxide synthase (nNOS and eNOS, respec- attenuated halothane-induced dilation at 0.6, 1.6, and 2.6% halo- tively) are unclear. thane. The dilation (mean 6 SEM) at 1.6% halothane was 104 6 Methods: Rat brain slices were superfused with oxygenated 10%, 65 6 6%, and 51 6 9% in the halothane, 7-NINA 1 halo- 1 artificial cerebrospinal fluid. Hippocampal arteriolar diameters thane and L-NAME halothane groups, respectively. The spec- were measured using computerized videomicrometry. Vessels ificity of 7-NINA was confirmed by showing that acetylcholine- induced dilation was not inhibited by 7-NINA but was converted were preconstricted with prostaglandin F2a (PGF2a; halothane group) or pretreated with 7-nitroindazole sodium (7-NINA, spe- to constriction by L-NAME. Conclusions: At clinically relevant concentrations, halothane cific nNOS inhibitor, 7-NINA 1 halothane group) or N-nitro-L- potently dilates intracerebral arterioles. This dilation is medi- arginine methylester (L-NAME; nonselective NOS inhibitor, ated, in part, by neuronally derived nitric oxide. Endothelial L-NAME 1 halothane group) and subsequently given PGF a to 2 NOS does not play a major role in halothane-induced dilation of achieve the same total preconstriction as in the halothane hippocampal microvessels. (Key words: Anesthesia; cerebral group. Increasing concentrations of halothane were adminis- blood flow; hippocampus; microcirculation.) * Visiting Assistant Professor, Department of Anesthesiology, Medi- VOLATILE anesthetics cause cerebral vasodilation, cal College of Wisconsin. which may lead to increased cerebral blood flow (CBF), † Resident, Department of Anesthesiology, Medical College of Wis- cerebral blood volume, and intracranial pressure.1,2 consin. When there is decreased intracranial compliance or al- ‡ Instructor, Department of Anesthesiology; and Fellow, Neuroanes- thesiology Research, Medical College of Wisconsin. ready established intracranial hypertension, further in- creases in intracranial pressure may cause cerebral isch- § Medical Student, Medical College of Wisconsin. emia and herniation of brain tissue. The mechanisms of i Professor, Departments of Anesthesiology and Physiology, Medical College of Wisconsin. volatile anesthetic-induced cerebral vasodilation are un- derstood incompletely and may include direct effects on # Associate Professor, Departments of Anesthesiology, Pharmacol- ogy and Toxicology, and Pediatrics; and Director, Pediatric Anesthesi- vascular smooth muscle and indirect effects via release ology Research, Medical College of Wisconsin and the Children’s of mediators from endothelial and parenchymal cells and Hospital of Wisconsin. changes in neuronal activity or cerebral metabolic Received from the Departments of Anesthesiology, Physiology, Phar- rate.1–3 The relative importance of these factors is un- macology and Toxicology, and Pediatrics, the Medical College of Wis- known. In particular, the role of nitric oxide (NO) and consin and the Children’s Hospital of Wisconsin, Milwaukee, Wiscon- the relative importance of NO derived from neuronal sin. Submitted for publication March 11, 1999. Accepted for publication June 29, 1999. Supported in part by RO1 grants and endothelial NO synthases (NOS; nNOS, type I NOS; no. GM56398 (to Drs. Hudetz and Farber) and 2T32GM08377 (to Dr. eNOS, type III NOS, respectively) are unclear. In vitro Schmid) from the National Institutes of Health, Bethesda, Maryland; studies using isolated large cerebral arterial rings have and by the Foundation for Anesthesia Education and Research, Roch- shown that vascular relaxation caused by volatile anes- ester, Minnesota; Ohmeda, Tewksbury, Massachusetts; and the Society thetics does not depend on the presence of an intact for Pediatric Anesthesia, Richmond, Virginia (Dr. Farber). endothelium.4,5 In contrast, in vivo studies of the pial Address reprint requests to Dr. Farber: Department of Anesthesiol- ogy, MEB, 462C, Medical College of Wisconsin, 8701 Watertown Plank circulation have shown that inhibition of NOS with the Road, Milwaukee, Wisconsin 53226. Address electronic mail to: nonselective NOS inhibitor, N-nitro-L-arginine methyl- [email protected] ester (L-NAME), decreases volatile anesthetic-induced di- Anesthesiology, V 92, No 1, Jan 2000 126 STAUNTON ET AL. lation.3,6–8 A study that evaluated laser Doppler flow in achieving sufficient anesthesia, a midline thoracotomy the parietal cortex of nNOS gene-deficient mice and was performed and 20 ml NaCl, 0.9%, was infused into wild-type controls suggested that eNOS may be involved the left ventricle while simultaneously making a right in isoflurane-induced hyperemia at low anesthetic con- atrial incision for blood drainage. The animals were then centrations (1.2 and 1.8%), with nNOS involved at higher decapitated and the brains rapidly removed and rinsed concentrations (2.4%).9 These studies described changes with nutrient medium (artificial cerebrospinal fluid, in large cerebral arteries and superficial cerebral vessels, aCSF) of the following composition (mM): NaCl: 124; Downloaded from http://pubs.asahq.org/anesthesiology/article-pdf/92/1/125/399507/0000542-200001000-00023.pdf by guest on 03 October 2021 but did not provide information about the mechanism of KCl: 5; CaCl2: 2.4; MgCl2: 1.3; glucose: 10; KH2PO4: anesthetic-induced effects on intraparenchymal arte- 1.24; NaHCO3: 26. Nutrient medium was prepared daily rioles specifically. and equilibrated with 95% oxygen and 5% carbon diox- We previously used an in vitro rat brain slice prepara- ide (95% O –5% C ) to achieve a pH of 7.4. All mea- 2 O2 tion to show that halothane causes potent, dose-depen- surements of cerebral microvessel diameters were per- dent dilation of hippocampal arterioles10 and that halo- formed within5hofthetissue slice preparation. thane and isoflurane cause dilation that is region-specific Brains were cut freehand into blocks containing the and agent-specific.11 At equipotent doses, the two agents hippocampus. A vibratome mechanical tissue slicer cause similar dilation in hippocampal, but not in neocor- (OTS-3,000-03; FHC, Brunswick, ME) was used to imme- tical, vessels, in which halothane produces a greater diately section the block into coronal slices approxi- degree of dilation.11 mately 280-mm thick. Throughout the slicing procedure, The objectives of this investigation were to assess the tissues were continuously bathed in the oxygenated contribution of NO to the resting tone of hippocampal aCSF at room temperature. Subsequently, the slices were intraparenchymal arterioles, to define the role of NO in transferred to a Plexiglas holding chamber (M & G Plastic the mechanism of halothane-induced microvascular dila- Specialists, West Allis, WI) and maintained at interface tion, and to determine the relative importance of NO with oxygenated aCSF at the same temperature. Individ- derived from eNOS and nNOS. An in vitro rat brain slice ual slices were then transferred for evaluation to a preparation was used to assess the effects of halothane recording chamber mounted on an inverted halogen on hippocampal arterioles in the presence and absence transillumination microscope (Nikon Diaphot 200; of NOS inhibition. The NOS inhibitors used were the Yokohama, Japan). nonselective NOS inhibitor L-NAME and the selective The recording chamber consisted of a central record- nNOS inhibitor 7-nitroindazole sodium (7-NINA). ing–superfusion compartment and a laterally placed ele- vated chamber to allow gentle vacuum suction. Nylon mesh beneath the brain slice allowed for circulation of Materials and Methods superfusate under and around the slice. Flow through the recording chamber was at a rate of 2.0 ml/min, All experimental procedures used in this investigation completely exchanging the volume in the chamber in were reviewed and approved by the Animal Use and less than 2 min. The chamber temperature was contin- Care Committee of the Medical College of Wisconsin, uously monitored and maintained at 34°C using a ther- with protocols completed in accordance with the Guid- moelectric Peltier device coupled to a sensing ther- ing Principles in the Care and Use of Laboratory Animals mistor. The slices were maintained in this chamber, of the American Physiologic Society and in accordance continuously superfused with the oxygenated aCSF for with National Institutes of Health (NIH) guidelines. All approximately 1 h before initiation of the experimental animals used in this
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