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doi: 10.1097/ALN.0b013e31816c8a30
Laboratory Investigations

Effects of Anemia and Hypotension on Porcine Optic Nerve Blood Flow and Oxygen Delivery

Lee, Lorri A. M.D.*; Deem, Steven M.D.†; Glenny, Robb W. M.D.‡; Townsend, Ian B.A.§; Moulding, Jennifer B.S.§; An, Dowon B.S.∥; Treggiari, Miriam M. M.D., M.P.H.*; Lam, Arthur M.D., F.R.C.P.C.#

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Background: Perioperative ischemic optic neuropathy occurs after major surgical procedures, which are often associated with hypotension, anemia, or venous congestion. However, the effects of these conditions on optic nerve (ON) blood flow are unknown and cannot be studied adequately in humans.
Methods: Farm-raised pigs were anesthetized with isoflurane, kept normocapnic and normothermic, and subjected to conditions of euvolemic or hypovolemic hypotension (mean arterial pressure 50–55 mm Hg), anemia (hematocrit 17%), venous congestion, and combinations thereof. Control animals were kept euvolemic and normotensive for the entire experiment. Fluorescent microspheres were used to measure cerebral blood flow (CBF) and ON blood flow at baseline and after experimental conditions, and to calculate oxygen delivery (DO2).
Results: No significant changes in CBF or ON blood flow or DO2 occurred with euvolemic hypotension (n = 5), compared with controls (n = 12). Hypovolemic hypotension (n = 4) resulted in stable CBF and cerebral DO2, but significant reductions in ON DO2 (P = 0.032). The significant increase in CBF associated with anemia (n = 6) resulted in stable cerebral DO2. In contrast, ON blood flow did not significantly change with anemia, with (n = 5) or without (n = 6) euvolemic hypotension, resulting in significant reductions in ON DO2 (P < 0.01).
Conclusion: Compensatory mechanisms for porcine CBF maintain stable DO2 under specified conditions of hypotension or anemia, whereas ON compensatory mechanisms were unable to maintain blood flow and to preserve DO2. The authors conclude that the porcine ON is more susceptible to physiologic perturbations than the brain.
VISUAL loss from ischemic optic neuropathy (ION) is one of the most devastating complications that can occur perioperatively and is most commonly associated with spine surgery in the prone position, coronary artery bypass operations, and head and neck procedures.1–3 Data from the American Society of Anesthesiologists’ Postoperative Visual Loss Registry examining 83 cases of ION associated with spine surgery demonstrated that 94% of these cases had an anesthetic duration of 6 h or longer, and 82% had an estimated blood loss of 1 l or greater, with a mean nadir hematocrit of 26 ± 5%.2 The majority of these patients were relatively healthy (two thirds American Society of Anesthesiologists physical status I or II), and the youngest patient was only 16 yr old.2 These findings suggest that perioperative ION associated with spine surgery may be secondary to extreme physiologic perturbations of optic nerve (ON) perfusion, rather than an atherosclerosis-related complication.
The highest reported incidence of ION associated with spine surgery is 0.1%,4 which makes a randomized controlled study impractical because it would require a large number of centers over a long period of time. Moreover, there are significant ethical issues to randomizing patients to a treatment arm that has been suggested to be associated with ION. Examining the intraoperative effects of transient or mild hemodynamic changes on human ON function or blood flow is not feasible with the current technology.5,6 Consequently, an animal model is needed to examine the effects of physiologic changes that occur intraoperatively in these high-risk cases on optic nerve blood flow (ONBF). Intraoperative conditions that are frequently encountered during operations associated with perioperative ION are (1) hypotension, either deliberate or caused by hypovolemia; (2) anemia caused by blood loss and hemodilution; and (3) increased venous pressures from the prone position and/or obstruction of venous outflow from the head.1–3 This study examines the effects of each of these physiologic conditions, and their combined effect, on ONBF and calculated ON oxygen delivery (DO2). Cerebral blood flow (CBF) was also measured, and cerebral DO2 was calculated, to compare the compensatory responses of the brain and ON to different physiologic stresses.
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Materials and Methods

After approval from the University of Washington Animal Care Committee, Seattle, Washington, nonfasted, farm-raised pigs (19–21 kg) were anesthetized by mask induction with 5% isoflurane (Webster Veterinary, Sterling, MA), given intramuscular succinylcholine (400 mg; Hospira, Inc., Lake Forest, IL) and pancuronium bromide (10 mg; Hospira, Inc.); and endotracheally intubated. Animals were kept normothermic (37°–38°C) using a temperature-controlled heat lamp (YSI Tele-Thermometer; Yellow Springs Instrument Co., Inc., Yellow Springs, OH). They were mechanically ventilated (Ohmeda 7000; Ohmeda, Madison, WI) and kept normocapnic (37–42 mm Hg), and maintained on 0.7–1.5% isoflurane in 100% oxygen. Continuous end-tidal carbon dioxide was measured using a POET IQ (Criticare Systems, Inc., Waukesha, WI). Bilateral femoral arterial catheters and a femoral venous catheter were inserted for withdrawal of blood, for administration of intravenous fluid and drugs, and for continuous monitoring of arterial and venous pressures (Abbott, North Chicago, IL). A median sternotomy was performed for insertion of a left ventricular catheter for fluorescent microsphere (FMS) injections. A bolus of 300 ml normal saline (NS) was administered via a pump (LifeCare Pump; Abbott Laboratories) to compensate for the estimated 75–100 ml of blood loss with surgical procedures before baseline blood gas measurements on an ABL 5 (Radiometer America, Inc., Westlake, OH) and hematocrit measurements (Micro-capillary centrifuge; International Equipment Co., Boston, MA). Maintenance intravenous fluid (NS) was administered at an approximate rate of 120 ml/h to account for basic fluid requirements and insensible losses.
All FMS injections consisted of 7 ml of 106/ml 15 μm FMS (Invitrogen Corp., Eugene, OR). FMS colors (blue–green, yellow–green, orange, and crimson) were selected to avoid any spillover between adjacent colors. FMS vials were sonicated and vortexed to prevent microsphere aggregation and to achieve a uniform concentration before each use. Two baseline FMS injections were performed 5 min apart, and then a third FMS injection was performed at the end of the experimental conditions. FMS were injected over 1 min, and 15 ml of arterial blood was withdrawn from each femoral arterial catheter over 3 min using a Harvard Apparatus 22 pump at a withdrawal rate of 5 ml/min (Harvard Apparatus, South Natick, MA). After the final FMS injection, animals were killed during general anesthesia via exsanguination or injection of 10 ml saturated potassium chloride intravenously. Bilateral sections of brain, ONs, and kidneys were obtained and weighed, along with a section of lumbar spinal cord. The fluorescent signals for each color were determined by digesting the tissues and extracting the fluorescent dyes from each tissue piece with an organic solvent (Cellosolve AE; Sigma-Aldrich, St. Louis, MO) and then measuring the concentration of fluorescence in each sample.7 Fluorescent intensities were determined at fixed wavelengths and by synchronous scanning using a Perkin-Elmer LS-50B spectrofluorometer (Perkin Elmer Corp., Norwalk, CT) equipped with an automated sampler and WINFAC software.8** At the beginning of each sample set, blank solvent and pure color reference solutions with 500 FMS/ml were measured to determine the spillover matrix (to correct for spillover between colors)9 and to convert fluorescent intensities to numbers of microspheres. Femoral arterial blood samples were analyzed separately and then averaged to determine the reference organ sample fluorescence. Flow rates for each tissue were determined by comparing its fluorescence to the fluorescence of the reference arterial blood samples with a known flow rate of 5 ml/min, after correction for background and spillover. When two ONs from the same animal were available for FMS analysis, the average flow of the two ONs was used.
Fig. 1
Fig. 1
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For the first set of control experiments (n = 14), an additional fourth FMS injection was performed 5 min after the third injection to determine the effect of repeated FMS injections over time. These control experiments were conducted for 2–4 h, with mean arterial pressure (MAP) maintained between 75 and 95 mm Hg. Based on results from these control experiments, the second FMS injection was used as the baseline flow, and the third FMS injection was used as the final flow for analysis of the second set of controls and the experimental animals (fig. 1). The second set of control experiments (n = 12) was conducted for 6 h, with MAP maintained between 75 and 95 mm Hg.
Table 1
Table 1
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Experimental groups consisted of the following conditions (table 1): group 1, euvolemic deliberate hypotension (Eu-DH, n = 5); group 2, hypovolemic hypotension (Hypo-DH, n = 4); group 3) euvolemic anemia (Eu-Anemia, n = 6); group 4, combined Eu-Anemia + DH (n = 5); group 5, venous congestion (VC, n = 8); and group 6, combined VC + Eu-Anemia + DH (n = 8). Experimental conditions were maintained for 6 h, except for the Eu-DH group, which had experimental conditions maintained for 1 h.
Group 1: In the Eu-DH group, induction of deliberate hypotension to a goal MAP of 50–55 mm Hg was accomplished within 30 min of the second baseline FMS injection with an approximate dose of 15–25 mg/kg intravenous labetalol. Thereafter, labetalol was administered to maintain the target MAP of 50–55 mm Hg, reaching a total dose of approximately 30–40 mg/kg over the duration of the experiment. The final FMS injection was performed 1 h after the MAP had been reduced to 50–55 mm Hg. Group 2: In the Hypo-DH group, induction of hypovolemic hypotension to a MAP of 50–55 mm Hg was initiated after the second baseline FMS injection by rapid exsanguination via the femoral arterial catheter of approximately 30% of the estimated blood volume in the first hour. To prevent reflex tachycardia and provide more consistent hemodynamics at a goal MAP of 50–55 mm Hg, approximately 10–20 mg labetalol was administered during the first hour of exsanguination. Further exsanguination occurred throughout the experiment to maintain a goal MAP of 50–55 mm Hg. Approximately 50% of estimated blood volume was shed for the duration of the experiment with 1:1 volume replacement with NS. The final FMS injection was performed 1 h after the MAP had been reduced to 50–55 mm Hg. Group 3: In the Eu-Anemia group, anemia was achieved by exsanguination after the second baseline FMS injection with replacement of shed blood with NS in a ratio of 1 ml blood:3–4 ml NS for a goal hematocrit of 17%. The rate of exsanguination and fluid administration were adjusted to maintain normotension. Hematocrit values were checked every 1–2 h, and additional blood was shed with NS replacement to maintain the target hematocrit of 17%. Total blood shed in these experiments was approximately 40–50% of estimated blood volume. The final FMS injection was performed 6 h after initiation of anemic conditions. Groups 4 and 6: Induction of deliberate hypotension with labetalol in the Eu-Anemia + DH group and the VC + Eu-Anemia + DH group was initiated after the second baseline FMS injection during the exsanguination for anemia (described in Materials and Methods, paragraph 5) and venous ligation (described in Materials and Methods, paragraph 5) procedures. Initial doses of labetalol in these experiments ranged from approximately 3 to 15 mg/kg, with subsequent administration throughout the experiments reaching an approximate total dose of 5–30 mg/kg. The final FMS injection was performed 6 h after goal MAP and hematocrit ± venous ligation was accomplished. Group 5: In the VC group, venous congestion was induced by ligation of the bilateral internal and external jugular veins after the second baseline FMS injection, and placing the head down approximately 45°. The final FMS injection was performed 6 h after venous ligation and head-down position was initiated.
Oxygen delivery was derived by the formula DO2 (ml · 100 g−1 · min−1) = Cao2 × Q, where Cao2 = arterial oxygen content (ml O2/100 ml) = [(1.39 × hemoglobin × Sao2) + (0.003 × Pao2)] and Q = tissue flow (ml · 100 g−1 · min−1).
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Statistical Analysis
Table 2
Table 2
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Results are presented as mean and SE, unless otherwise specified. The longitudinal effect of repeated FMS injections over time in the initial set of control experiments was analyzed using generalized estimating equations (fig. 1). Differences between baseline and final intraoperative variables within each group were analyzed using one-sample paired t tests (table 2). To explore differences in baseline blood flow and DO2 variables for ON and brain between experimental and control conditions, we used two-sample Student t test. Some of the experiments demonstrated significant differences in baseline between groups. To account for baseline differences, linear regression of relative change from baseline to the end of study was carried out with robust variance estimation. A P value less than 0.05 was considered statistically significant. All analyses were performed using the statistical software STATA version 9.2 (StataCorp, College Station, TX).
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Table 3
Table 3
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Table 4
Table 4
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The number of microspheres lodged in the ONs of animals ranged from 45 to 507, with an average of 173 ± 14 (SE) microspheres at baseline (all groups). The number of microspheres lodged in the tissues from brains of animals ranged from 758 to 10,078, with an average of 3,405 ± 242 (SE) microspheres at baseline (all groups). The number of FMSs collected in the reference arterial blood sample was at least 8,000 in all animals. The first set of control experiments (n = 14) to determine the effect of repeated FMS injections over time demonstrated no statistically significant difference between any of the CBF measurements (fig. 1). However, there was a statistically significant decrement in ONBF between the first injection and all subsequent injections (P < 0.05; fig. 1). ONBF values for the second through fourth injections were not statistically significantly different from each other. The second FMS injection was therefore used as the baseline ONBF measurement, and the third FMS injection was used as the final injection. The second set of control experiments (n = 12; table 2) had no significant change in blood flow or DO2 for the ON or brain between the baseline and final FMS injections performed 6 h apart (table 3 and 4). Baseline ONBF values for Eu-DH, Hypo-DH, and Eu-Anemia groups were significantly higher than controls (P < 0.05), and baseline DO2 was significantly higher for Hypo-DH and Eu-Anemia groups compared with controls (P < 0.05; tables 3 and 4).
Fig. 2
Fig. 2
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The Eu-DH group (n = 5) had a significant decrease in average MAP using labetalol alone (P = 0.005; table 2) for 1 h, but had no significant change in blood flow or DO2 for either the ON or brain compared with control animals (figs. 2A and B). The Hypo-DH group had a significant decrease in average MAP using exsanguination and small-dose labetalol for 6 h (P = 0.001; table 2). Compared with control animals, the Hypo-DH animals had a significant decrease in ON DO2 (P < 0.05; fig. 2B). There was no significant change in CBF or cerebral DO2 in Hypo-DH animals compared with controls (figs. 2A and B).
Fig. 3
Fig. 3
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Eu-Anemia animals (n = 6) had a significant decrease in mean hematocrit (P ≤ 0.001; table 2) over 6 h. There was a significant increase in CBF with Eu-Anemia compared with controls (P = 0.007; fig. 3A) resulting in no significant change in cerebral DO2 (fig. 3B). In contrast, ONBF did not significantly change with Eu-Anemia (fig. 3A) resulting in a significant reduction in ON DO2 compared with controls (P = 0.005; fig. 3B). When Eu-Anemia was combined with Eu-DH (n = 5), CBF did not significantly increase in response to anemia, thereby resulting in a significant decrease in cerebral DO2 under these conditions compared with controls (P = 0.011; fig. 3B). Eu-Anemia + Eu-DH experiments exhibited a significant decrement in ON DO2 compared to controls (P = 0.009; fig. 3B).
The VC group (n = 8) demonstrated no significant change in blood flow or DO2 to the ON or brain (table 3 and 4). Intraocular pressures minimally increased from 16 ± 2 (SE) to 19 ± 3 mm Hg (data not shown; P = 0.053) during these 6-h experiments. The combination of Eu-Anemia + Eu-DH conditions to VC (n = 8) resulted in no significant changes in CBF and ONBF (table 3), but significant decrements in cerebral and ON DO2 compared with controls (P = 0.046 and 0.045, respectively; table 4), similar to the experiments with Eu-Anemia + DH without VC. Intraocular pressures in this group increased from 18 ± 1 (SE) to 21 ± 1 mm Hg (P = 0.038).
The correlation coefficient for isoflurane concentration versus ONBF (for baseline and final control values, and baseline values in all experimental groups) was 0.001, and that for isoflurane concentration versus ON DO2 was 0.0003.
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These experiments examine the effects on ONBF and ON DO2 of several intraoperative changes in hemodynamic conditions encountered during procedures considered high risk for perioperative ION. By simultaneously examining ON and brain hemodynamics, the differences in compensatory responses of the two organs to different physiologic stresses could be compared. These comparisons may provide insight into the paradox of why perioperative ION usually occurs without other organ ischemia, even in the presence of known cerebrovascular or cardiac disease.2
Euvolemic deliberate hypotension with labetalol to a MAP of 50–55 mm Hg was associated with stable CBF and cerebral DO2, as has been demonstrated previously.10 Similarly, the ON maintained stable blood flow and DO2 under these conditions, suggesting that it may have some degree of autoregulatory capacity as well. These results are consistent with most previous studies demonstrating that the ON can autoregulate to some degree in both humans and animals, although it may vary between individuals.11,12 Alternatively, labetalol may cause vasodilation of the ON vasculature, with a resultant increase in ONBF. Beta blockade was used to induce deliberate hypotension in these experiments because it was the most common technique used in the American Society of Anesthesiologists’ Postoperative Visual Loss Registry cases for this purpose.2 In contrast, when hypovolemia was the primary means of inducing hypotension, ON DO2 decreased significantly. However, the effects of euvolemic and hypovolemic hypotension on ONBF cannot be directly compared in these experiments because the duration of the conditions differed. Animals were exposed to Eu-DH with labetalol for 1 h to determine the immediate effect of this condition, because some clinicians advocate using deliberate hypotension for a brief period of time during spine surgery when bleeding is greatest. Further experiments with incremental increases in duration of Eu-DH would be useful to assess whether further prolongation of this condition affects ONBF.
The goal hematocrit of 17% for the anemia experiments resulted in a 37% decrease from baseline hematocrit and was based on the 35% mean decrease in hematocrit (40% to 26% hematocrit) observed in the Postoperative Visual Loss Registry cases.2 The effects of anemia (hematocrit 17%) on the brain demonstrated that the cerebrovasculature was able to maintain stable DO2 by increasing CBF. Increased CBF with hemodilution seems to be a result of both active regulatory mechanisms (stable cerebral DO2) and passive changes induced by reduced blood viscosity (Poiseuille's law).13,14 It is controversial as to which mechanism has the greater effect. The addition of a second physiologic stress, euvolemic hypotension, to euvolemic anemia, resulted in a significant decrease in cerebral DO2 (figs. 3A and B). Hemodilution has previously been shown to impair cerebral autoregulation and narrow the range of blood pressure over which the brain can autoregulate.15,16 These findings are consistent with the theory that the cerebral vasculature may be maximally vasodilated with either anemia or hypotension alone and that it cannot compensate (dilate) any further when the second physiologic stress is added.
In contrast, ONBF did not show a compensatory increase in the presence of anemia, with or without hypotension, thereby resulting in significant reductions in ON DO2. Anemia with or without hypotension has frequently been associated with ION cases reported after spine surgery, cardiac bypass procedures, head and neck operations, and gastrointestinal hemorrhage.1–3,17,18 The fact that reduced blood viscosity did not increase ONBF is somewhat surprising, but might be explained by a vascular “steal” phenomenon where blood flow from the ophthalmic vasculature is shunted away in favor of the cerebral supply when cerebral DO2 is inadequate. The ophthalmic vasculature provides a conduit between extracranial and intracranial vessels in both pigs and humans, although it arises off the extracranial circulation in the former species and the intracranial circulation in the latter.19–21 Blood flow in the human ophthalmic artery can move in retrograde direction intracranially under conditions of severe carotid artery stenosis or occlusion.22,23 Similarly, we have previously demonstrated increased ophthalmic artery blood flow velocity in awake subjects during moderate hypocapnia, suggesting the existence of a dynamic shunt from the intracranial to extracranial circulation via the ophthalmic artery.24 Moreover, approximately 3.4% of the population either have their ophthalmic artery originate from the extracranial middle meningeal artery or have greatly enlarged anastomoses between these vessels.25 It is possible that these variant ophthalmic to middle meningeal artery connections may predispose the ophthalmic artery to behave more similarly to the extracranial circulation and be more likely to provide collateral flow to the brain when DO2 is compromised. Although it is conjecture at present, this cerebral-protective physiologic response of the ophthalmic vasculature to provide collateral flow to the brain when DO2 is insufficient would explain why the majority of cases of ION occur in the absence of cerebral or cardiac ischemia.2
Animal studies with microspheres were originally constrained by the estimate of Buckberg et al.26 that a minimum of 400 FMSs must be impacted into an organ to obtain accurate measurements with less than 20% error. However, several groups have determined that accurate measurements can be obtained in organs with low blood flow with only 49–60 FMSs as long as the reference blood sample has greater than 400 FMSs, and that the differences between compared groups are large enough.27,28 Lin and Roth29 successfully used 15-μm FMSs in rats examining retinal blood flow in the postischemic period with as few as 39 FMSs lodged into both retina combined. However, because of these concerns, we chose a pig model because the larger size of the ON and its blood flow allows a larger number of FMSs to lodge in the porcine ON compared with rodents. We were able to obtain twice the number of FMSs in the tissue of interest using approximately one tenth the number of FMSs injected in rodent retinal studies when relative weights of the rodent and pig were considered.29
Although analysis of the ON by anterior or posterior portions may have provided more detailed information on ONBF by region, the number of FMSs lodged would be significantly lower and would lead to less accurate measurements. Despite the fact that anterior ION is more often associated with cardiac bypass operations, and posterior ION with spine surgery in the prone position, there is significant overlap in ophthalmologic diagnoses and suggested risk factors for both procedures.1,2 This overlap makes it unclear whether perioperative anterior and posterior ION have distinct etiologies or are a continuum of the same pathophysiologic process. To control for any microcirculatory changes induced by repeated injections of FMSs, we performed control experiments to assess the effects of time and repeat FMS injections on flow, and compared our experimental conditions to the control values obtained at the same time point with the same number of FMS injections. The variability in baseline flow between groups may be explained by the high variability with large SDs in ONBF between animals with relatively small numbers in some groups. There was no temporal relation between high- or low-flow baseline values making the possibility of a technical change in microsphere injections remote. No effect of isoflurane concentration on ONBF measurements was observed (correlation coefficient 0.001). The high variability in minimum alveolar concentration of isoflurane for swine has been previously documented.30
Our animal model of venous congestion produced only a modest increase (19%) in intraocular pressures from baseline compared with the documented 100% or more increase in humans during prone spine surgery.31 It is possible that supplemental venous channels in the porcine neck prevent simulation of the clinical scenario of venous congestion of the head and neck during prone spine surgery or bilateral radical neck dissection. Consequently, these results may not apply to the clinical setting, and this current model cannot be used to simulate the effects of venous congestion on ONBF encountered during prone spine surgery in humans. Because of limitations and expense with microsphere injections, continuous ONBF measurements were not possible, thus limiting the assessment of time as a variable. Future experiments examining the effect of time on ONBF will be useful because the development of ION in patients in the American Society of Anesthesiologists’ Postoperative Visual Loss Registry seems to require a critical window of time of 5–6 h in the prone position to develop in the majority of patients.2
In conclusion, we have found that porcine ON DO2 is significantly decreased during hypovolemic hypotension induced by exsanguination. Euvolemic anemia (hematocrit 17%) resulted in an increase in porcine CBF with stable cerebral DO2. Despite the lower viscosity with euvolemic anemia, there was no significant change in porcine ONBF resulting in a significant reduction in ON DO2. The compensatory mechanisms of the porcine ON to maintain stable DO2 during physiologic stress induced by hypotension and anemia are unable to ensure the same homeostatic conditions as the brain.
The authors thank Steve Roth, M..D. (Associate Professor, Department of Anesthesiology and Critical Care, University of Chicago, Chicago, Illinois), for helpful discussion of experimental design; Christopher Bernards, M.D. (Clinical Professor, Department of Anesthesiology, University of Washington, Seattle, Washington, and Staff Anesthesiologist, Virginia Mason Medical Center, Seattle, Washington), for assistance with the animal experiments and design; and Kenneth Mackie, M.D. (Linda and Jack Gill Chair of Neuroscience and Professor, Department of Psychological and Brain Sciences, Indiana University, Bloomington, Indiana), for thoughtful discussion and feedback on experiments.
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