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© 1999 International Anesthesia Research Society
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Abstract |
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We examined the cerebral response to changing hematocrit during hypothermic cardiopulmonary bypass (CPB) in 18 adults. Cerebral blood flow (CBF), cerebral metabolic rate for oxygen (CMRO2), and cerebral oxygen delivery (CDO2) were determined using the nitrous oxide saturation technique. Measurements were obtained before CPB at 36°C, and twice during 27°C CPB: first with a hemoglobin (Hgb) of 6.2 ± 1.2 g/dL and then with a Hgb of 8.5 ± 1.2 g/dL. During hypothermia, appropriate reductions in CMRO2 were demonstrated, but hemodilution-associated increases in CBF offset the reduction in CBF seen with hypothermia. At 27°C CPB, as the Hgb concentration was increased from 6.2 to 8.5 g/dL, CBF decreased. CDO2 and CMRO2 were no different whether the Hgb was 6.2 or 8.5 g/dL. In eight patients in whom the Hgb was less than 6 g/dL, CDO2 remained more than twice CMRO2.
Implications: This study suggests that cerebral oxygen balance during cardiopulmonary bypass is well maintained at more pronounced levels of hemodilution than are typically practiced, because changes in cerebral blood flow compensate for changes in hemoglobin concentration.
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Introduction |
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During cardiopulmonary bypass (CPB), patients may experience acute changes in both hemoglobin (Hgb) concentration and temperature. Management of CPB has largely evolved empirically, so there are few guidelines for manipulating these variables. Regardless, the physiology of the anesthetized patient during CPB is not qualitatively different from the anesthetized patient under nonbypass conditions. For the central nervous system, cerebral metabolic rate for oxygen (O2) (CMRO2) is primarily dependent on brain temperature and anesthetic depth, whereas cerebral blood flow (CBF) and cerebral O2 delivery (CDO2) vary with the CMRO2, PaCO2, and the hematocrit (Hct). Although the interaction of these variables may be complex, particularly during periods of temperature change, the independent effect of each can be predicted.
Patients are hemodiluted during cardiac surgery, but the limits of hemodilution, particularly as determined by patient temperature, are not well characterized. At its most extreme, in congenital heart surgery, the Hct during profound hypothermia may vary from 5% to 30% between institutions (1,2). both practically and physiologically, these values represent a very broad range.
Under both bypass and nonbypass conditions, hemodilution is associated with increases in CBF (3–5). It is unclear if these flow increases are the passive result of changes in blood viscosity (4), or if CDO2 is also actively regulated outside the hypoxic range (6). Ultimately, these increases in CBF offset decreases in arterial O2 content (CaO2), and CDO2 is supported (5,7). However, there is a limit to this compensatory response and for a tissue, or the body as a whole, a critical Hct will be reached where increases in flow cannot compensate for the decreasing CaO2 so that O2 delivery is compromised. If CaO2 is reduced further, ischemia will result in a decrease in O2 consumption (8–11). The critical Hct should therefore be a function of tissue metabolic rate and indirectly of temperature.
A previous report in animals suggested that, at 27°C, CDO2 is sufficient to maintain CMRO2 with a Hgb of 5 g/dL (10). The purpose of this study was, first to demonstrate the adequacy of CDO2 in patients undergoing CPB, with a Hgb of approximately 6 g/dL. Second, we proposed to demonstrate that CDO2 was independent of a Hgb concentration between 6 and 8.5 g/dL during hypothermic CPB.
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Methods |
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After institutional approval and written informed consent, 20 patients undergoing elective cardiac surgery for coronary artery bypass grafting and/or valve replacement were enrolled. The following patients were excluded from the study: female patients of childbearing age, patients with clinical or laboratory evidence of cerebrovascular disease, patients with allergy to radiographic contrast dye, and those with uncontrolled hypertension. The typical study patient was moderately anemic, had a clinical history consistent with an increased intravascular volume, and was undergoing a multiple valve or valve-coronary revascularization procedure with an expected cross-clamp time of >90 min.
Anesthesia consisted of fentanyl (25–50 µg/kg), midazolam (75–100 µg/kg), and isoflurane maintained at 0.5%–1% throughout the study. Inspired O2 fraction and ventilation were regulated to maintain a PaO2 > 150 mm Hg and PaCO2 of 35–40 mm Hg. Heart rate, blood pressure (including arterial, pulmonary arterial, and right atrial), end-tidal CO2 and nasopharyngeal (NP) temperature were continuously assessed. After anesthetic induction, a 16G single lumen catheter was placed into the right jugular bulb to allow sampling of cerebral venous blood for determination of CBF and CMRO2 by the Kety-Schmidt technique (12) a modified for use during CPB (5). Catheter position was confirmed by fluoroscopy.
During CPB, a nonpulsatile flow of 2.2–2.4 L · m-1 · m-2 was established and PaCO2 was adjusted to 35–40 mm Hg using 
-stat management. Flow adjustments and sodium nitroprusside (SNP) infusion were used during CPB to maintain a mean arterial blood pressure (MAP) of 60–80 mm Hg. With the onset of CPB, patients were immediately cooled to 27°–28°C and maintained at this temperature, during which CBF measurements were obtained.
CBF and cerebral arteriovenous O2 content difference (AVDO2) were measured during three periods: 1) prebypass between sternotomy and aortic cannulation, 2) hypothermic CPB (27°C) with a Hgb of approximately 6 g/dL, and 3) hypothermic CPB with a Hgb concentration of approximately 8.5 g/dL. MAP, pump flow rate during CPB, and NP temperature were stable at least 15 min before measurements were made. A minimum of 30 min elapsed between the end of the previous and the beginning of the subsequent measurement. During CPB, the systemic venous Hgb and O2 saturation were continuously monitored (CDI 100, 3M, Minneapolis, MN). The cerebral venous O2 saturation (SjvO2) was determined from a jugular bulb blood sample by blood-gas tension analysis. Measurement of CBF and cerebral AVDO2 allowed subsequent calculation of CMRO2 and CDO2.
To achieve the target Hgb concentrations during CPB, a variety of interventions were used. First, an attempt was made to select moderately anemic patients with a clinical history or physical exam consistent with an elevated blood volume. Second, a subset of patients underwent normovolemic hemodilution removing up to 750 mL of whole blood prior to incision and replacing at 1:1 with 5% albumin. Third, when necessary, patients underwent further hemodilution during CPB cooling to achieve the target Hgb concentration of 6–6.5 g/dL for the first measurement at 27°C. After measurements at the lower Hgb were completed, the Hgb concentration was increased by one or more of the following techniques: hemofiltration (HPH 1000TS Minntech, Minneapolis, MN), diuresis, and retransfusion of autologous blood. Homologous blood was never administered for the purpose of the investigation, although we targeted a Hgb value of at least 7.5 g/dL during rewarming in all patients.
CBF was measured using the nitrous oxide (N2O) washing of technique of Kety and Schmidt (12) according to previously established methods (5). Briefly, 10% N2O was introduced into the ventilator or oxygenator fresh gas flow with an air-O2 mixture. Timed collections of arterial and jugular bulb venous blood were drawn on the following schedule (arterial) at 1.25, 2.25, 3.25, 5.25, 7.25, 9.25, 11.25, and 14.25 min of N2O exposure; and (venous) at 0, 1.5, 2.5, 3.5, 5.5, 7.5, 9.5, 11.5, and 14.5 min of N2O exposure. Each 2-mL sample was drawn anaerobically over 30 s into heparinized syringes. The samples were placed immediately on ice, and the N2O concentration (ppm) in each sample was measured with an infrared N2O analyzer (Trace N2O Monitor, Dynatech Electro-optics, Saline, MI) (resolution 1 ppm, calibrated with 87 ppm span gas). The CBF was calculated from arterial and jugular venous uptake curves fit to the measured N2O concentrations and integrated to 14 min (5). 
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The reported value for 
of 1.06 was used in the prebypass period, and during hypothermia a solubility coefficient of 0.94 was used (13,14).
Cerebral Metabolism Measurement
The CMRO2 was determined from the product of the AVDO2 and the CBF, using the equation:
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Arterial and jugular bulb blood-gas tensions and saturations were determined (IL-BGE Analyzer, IL 4-286 CO-Oximeter, Instrumentation Laboratories, Inc., Boston, MA) during each CBF measurement period. The arterial and venous O2 content (CxO2), CDO2, and CMRO2 at 27°C were calculated as follows:
arterial or internal jugular venous content (CxO2):
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Cerebral arteriovenous O2 content difference (AVDO2):
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Repeated-measures analysis of variance followed by the Bonferroni correction was used to compared CBF, CDO2, CMRO2, and other physiologic values between the three study periods. P < 0.05 was considered significant. A regression curve of the form y = a + b (lnx) was generated for the 36 CBF–Hgb pairs at 27°C. The Spearman-rank order correlation was used to determine the significance of the Hgb–CBF relationship at 27°C. All data are reported as mean ± SD.
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Results |
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Twenty patients were enrolled, but the study was completed in 18 patients for technical reasons. In one patient, the CPB time was too short to complete the study and in the second patient no change in Hgb concentration was achieved between the two measurement periods. The mean age of the 18 patients was 68 ± 13 yr, and their body surface area was 1.9 ± 0.2 m2. The mean CPB time was 170 ± 56 min.
In the prebypass period, the MAP at the time of the first cerebral physiologic measurement was 74 ± 16 mm Hg. The Hgb concentration, PaCO2, and patient temperature were 10.1 ± 1.6 g/dL, 35 ± 3 mm Hg, and 35.5 ± 0.5°C, respectively (Table 1). At this time, 5 of 18 patients required (SNP) at a mean dose of 0.42 ± 0.84 µg · kg-1 · min-1 to control MAP. In the prebypass period, the mean CBF was 43 ± 19 mL · 100 g-1 · min-1; CDO2 and CMRO2 were 5.93 ± 2.37 and 2.74 ± 1.12 mL O2 · 100 g-1 · min-1, respectively. The mean SjvO2 was 55 ± 8% (Table 2).
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At the first 27°C CPB measurement, the mean Hgb concentration was 6.2 ± 1.2 g/dL. The PaCO2 was 35 ± 3 mm Hg, the CPB flow was 2.0 ± 0.2 L · min-1 · m-2, and the MAP was 66 ± 11 mm hg. To achieve this MAP, 11 patients received a SNP infusion at a mean dose of 0.99 ± 1.01 µg · kg-1 · min-1. The MAP and PaCO2, in the first CPB period did not differ from that in the pre-CPB period. Temperature, Hgb, and PaO2 differed from the pre-CPB period (Table 1).
During CPB at 27°C with a mean Hgb of 6.2 ± 1.2 g/dL, the CBF was 42 ± 20 mL · 100 g-1 · min-1, whereas the CDO2 and CMRO2 were 3.38 ± 1.17 and 0.95 ± 0.32 mL O2 · 100 g-1 · min-1, respectively. The SjvO2 was increased (72 ± 6%) relative to the pre-CPB period. CBF was unchanged from pre-CPB whereas CDO2 and CMRO2 were both reduced (Table 2). Figure 1 plots the CDO2 against CMRO2 during this study period. Points above the dashed line in Fig. 1 have an ordinal value more than twice the corresponding abscissal value; thus, in every patient under this condition, CDO2 was more than twice cerebral O2 demand.
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.During the first CPB period, 8 of 18 patients had Hgb concentrations less than 6 g/dL (mean 5.2 g/dL). In these patients, the mean SjvO2 was 74 ± 7%, and the mean CDO2 and CMRO2 were 4.0 mL O2 · 100 g-1 · min-1 and 1.08 ± 0.38 mL O2 · 100 g-1 · min-1, respectively. The CDO2–CMRO2 relationship of these eight patients is indicated separately in Fig. 1.
Before the second set of CPB measurements, the Hgb was increased from a mean of 6.2–8.5 ± 1.2 g/dL. Temperature, PaO2, and CPB flow rate remained unchanged from the first CPB period. The PaCO2 at this time was 39 ± 4 mm Hg and higher (4 mm Hg) than the two previous measurement periods. The MAP during the second CPB measurement period was 69 ± 10 mm Hg and was achieved by a mean SNP infusion of 1.21 ± 1.13 µg · kg-1 · min-1 in 14 of 18 patients (Table 1). Neither the MAP nor SNP dose differed from the first CPB measurement period, although the SNP dose was higher in the second CPB period than in the prebypass period.
With the increase in Hgb concentration, CBF decreased in the second CPB period, although the CMRO2 was unchanged and the PaCO2 was higher. The SjvO2 at the higher Hgb concentration (70 ± 11%) did not differ from that at the lower Hgb concentration (Table 2). In the second CPB period, the decrease in CBF associated with the increased Hgb concentration resulted in a CDO2 (3.40 ± 1.33 mL O2 · 100 g-1 · min-1) that was nearly identical to the CDO2 in the first CPB period (3.38 ± 1.17 mL O2 · 100 g-1 · min-1) (Table 2, see also Fig. 3). In Fig. 2, the mean CDO2 is plotted for each of the three study periods. Figure 3 demonstrates the relationship between Hgb concentration and CBF during CPB at 27°C.
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Discussion |
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This is the first study in humans to determine the cerebral response to a stepwise change in Hgb concentration during CPB. CPB offers an unusual opportunity for this type of investigation because during CPB, systemic physiology can be tightly controlled. More importantly, CPB represents a clinical situation wherein patients routinely undergo large changes in Hgb concentration, with a requirement for decision-making about absolute levels of hemodilation.
This investigation makes two primary observations. First, during hypothermic (27°C) CPB, global brain oxygenation is maintained at a Hgb concentration 6.2 g/dL. Second and related, with stable MAP, cerebral oxygenation is unchanged during hypothermic CPB, with a Hgb concentration between approximately 6 and 8.5 g/dL. This captures most of the range of hemodilution typically experienced during adult cardiac surgery and includes the range in which most decisions about transfusions must be made. These findings complement previous clinical measurements of cerebral O2 balance during normothermia where we found that cerebral oxygenation was independent of Hct between Hgb concentrations of 8.1 and 11 g/dL (6).
Certain caveats must be applied to the interpretation of our findings. First, we are not advocating a Hgb of 6.2 g/dL during hypothermic CPB. Clinical investigations of this type are rigorously controlled. Patients are carefully selected, physiologic control is strict, and there is a protocol for the management of CPB. Although this level of control is possible outside a clinical investigation, it is more difficult to achieve. Second, whereas a Hgb of 6.2 g/dL is tolerated in this group of patients at 27°C, there is physiologic evidence in animal models that the Hgb concentration should be 
7 g/dL as the patient is rewarmed (10,15). We have characterized the brain and body’s requirement for Hgb at different CPB temperatures in an animal model and found that healthy animals require a greater Hgb concentration greater than 6.2 g/dL at normothermia (10,15).
Our data must also be viewed with the critical lens provided by Dexter and Hindman (16), who emphasized the important effect of hypothermia on the P50 of Hgb. They have observed that the SjvO2 value indicative of adequate cerebral oxygenation should increase as temperature is reduced. Their mathematical model indicates that, with -stat management at 27°C, a SjvO2 of 70% is required to be confident that the CMRO2 is at least 90% predicted. With these observations in mind, our data still indicate an adequacy of global cerebral oxygenation with a mean Hgb of 6.2 g/dL. Under this CPB condition, the mean SjvO2 was 72%, even in patients with the lowest Hct values. More important, SjvO2, CDO2, and CMRO2 were unchanged as the Hgb concentration was increased by more than 2 g/dL. If O2 delivery at a Hgb of 6.2 g/dL was inadequate, we would have expected that SjvO2, CDO2, and CMRO2 would have increased as the Hgb was increased, but this did not occur.
A better design for this study would have been to initially study half the patients at the higher Hgb during CPB. Because we felt it was clinically important to have a higher Hgb during rewarming, this was not practical. A potential criticism of our design is that the decrease in CBF seen with an increase in Hgb concentration could be interpreted to be a function of CPB time or continued brain cooling rather than the change in Hgb. Whereas two clinical reports have indicated that CBF decreases during the course of CPB (17,18), there is evidence to suggest that other factors were responsible for their observation (19–21).
Hindman et al. (21) were unable to document an effect of CPB duration on CBF in a rabbit model and speculated that the clinical findings of decreasing CBF over time during CPB were a function of brain cooling not reflected in NP temperature. Similar results were obtained in baboons (19) and dogs (20). The study by Johnston et al. (20) is particularly notable in that blood flow to cerebral cortex and cerebellum were measured in 30, 90, and 150 min of hypothermic CPB, and no decline in CBF was demonstrated under either - or pH-stat conditions. Subsequent clinical studies have also failed to show a decrease in CBF with CPB time (5,22).
Although we did not document cerebral temperature, our study was designed to minimize the potential effect of brain cooling on CBF. We incorporated a 15-min delay after achievement of target temperature before initiating our first CBF measurement. Furthermore, data do not suggest a decrease in brain temperature with time. A decrease in brain temperature not reflected in the NP temperature should be associated with a decrease in CMRO2, and this was not observed. There is good evidence that the decrease in CBF seen in the second CPB period is attributable to the increase in Hgb concentration. The decrease in CBF that we document with hemoconcentration is similar to what has been reported with Hct change under nonbypass conditions in both animal (3,23) and human studies (24,25). Finally, and most importantly, our study documented CDO2 stability in the context of an unchanged cerebral O2 demand. For this combination of reasons, we believe our study has generated reliable results, even given this weakness in design.
In summary, we found that adult cardiac surgical patients without known cerebral vascular disease can tolerate a Hgb concentration of 6.2 g/dL during CPB at 27°C. Specifically, at this level of hemodilution, with a MAP of 65 mm Hg, CDO2 is more than twice cerebral O2 demand. Furthermore, the brain is equally well oxygenated whether the Hgb is 6.2 or 8.5 g/dL. This would suggest we can be more conservative in our transfusion decisions under hypothermic conditions. Although we do no advocate hemodilution to a Hgb of 6.2 g/dL during hypothermic CPB, it can be tolerated under well-defined conditions. A variety of clinical situations would dictate a higher bypass Hgb, and Hgb concentration should probably be increased as patients are rewarmed. Nonetheless, data presented increase our understanding of cerebral physiology during CPB.
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References |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Eke CC, Gundry SR, Baum MF, et al. Neurologic sequelae of deep hypothermic circulatory arrest in cardiac transplant infants. Ann Thorac Surg 1996;61:783–8.
[Abstract/Free Full Text] -
Nicolas F, Daniel JP, Bruniaux J, et al. Conventional cardiopulmonary bypass in neonates. A physiological approach—10 years of experience at Marie-Lannelongue Hospital. Perfusion 1994;9:41–8.
[Abstract/Free Full Text] -
Todd MM, Wu B, Maktabi M, et al. Cerebral blood flow and oxygen delivery during hypoxemia and hemodilution: role of arterial oxygen content. Am J Physiol 1994;267:H2025–31.
[Abstract/Free Full Text] -
Horosue K, Heros RC. Mechanism of cerebral blood flow augmentation by hemodilution in rabbits. Stroke 1992;23:1487–92.
[Abstract/Free Full Text] -
Cook DJ, Oliver WC Jr, Orszulak TA, et al. Cardiopulmonary bypass temperature, hematocrit, and cerebral oxygen delivery in humans. Ann Thorac Surg 1995;60:1671–7.
[Abstract/Free Full Text] -
Brown MM, Wade JP, Marshall J. Fundamental importance of arterial oxygen content in the regulation of cerebral blood flow in man. Brain 1985;108:81–93.
[Abstract/Free Full Text] -
Fan FC, Chen RY, Schuessler GB, Shien S. Effects of hematocrit variations on regional hemodynamics and oxygen transport in the dog. Am J Physiol 1980;238:H545–22.
[Abstract/Free Full Text] -
Cain SM. Oxygen delivery and uptake in dogs during anemic and hypoxic hypoxia. J Appl Physiol 1977;42:228–34.
[Abstract/Free Full Text] -
Adams RP, Dieleman LA, Cain SM. A critical value for O2 transport in the rat. J Appl Physiol 1982;53:660–4.
[Abstract/Free Full Text] - Cook DJ, Orszulak TA, Daly RC. Minimum hematocrit at differing cardiopulmonary bypass temperatures in dogs. Circulation 1998;98:II-170–5.
-
van Woerkens EC, Trouwborst A, van Lanschot JJ. Profound hemodilution: what is the critical level of hemodilution at which oxygen delivery-dependent oxygen consumption starts in an anesthetized human? Anesth Analg 1992;75:818–21.
[Free Full Text] -
Kety SS, Schmidt CF. The determination of cerebral blood flow in man by the use of nitrous oxide in low concentrations. Am J Physiol 1945;143:53–66.
[Free Full Text] -
Kety SS, Harmel MH, Broomell HT, Rhode CB. The solubility of nitrous oxide in blood and brain. J Biol Chem 1948;173:487–96.
[Free Full Text] -
Allott PR, Steward A, Flook V, Mapleson WW. Variation with temperature of the solubilities of inhaled anaesthetics in water, oil and biological media. Br J Anaesth 1973;45:294–300.
[Free Full Text] -
Liam BL, Plochl W, Cook DJ, et al. Hemodilution and whole body oxygen balance during normothermic cardiopulmonary bypass in dogs. J Thorac Cardiovasc Surg 1998;115:1203–8.
[Abstract/Free Full Text] - Dexter F, Hindman BJ. Theoretical analysis of cerebral venous blood hemoglobin oxygen saturation as an index of cerebral oxygenation during hypothermic cardiopulmonary bypass. A counterproprosal to the "luxury perfusion" hypothesis. Anesthesiology 1995;83:405–12.[Web of Science][Medline]
- Prough DS, Rogers AT, Stump DA, et al. Cerebral blood flow decreases with time whereas cerebral oxygen consumption remains stable during hypothermic cardiopulmonary bypass in humans. Anesth Analg 1991;72:161–8.[Web of Science][Medline]
- Rogers AT, Stump DA, Gravlee GP, et al. Response of cerebral blood flow to phenylephrine infusion during hypothermic cardiopulmonary bypass: influence of PaCO2 management. Anesthesiology 1988;69:547–51.[Web of Science][Medline]
- Schwartz AE, Kaplon RJ, Young WL, et al. Cerebral blood flow during low-flow hypothermic cardiopulmonary bypass in baboons. Anesthesiology 1994;81:959–64.[Web of Science][Medline]
- Johnston WE, Vinten-Johansen J, DeWitt DS, et al. Cerebral perfusion during canine hypothermic cardiopulmonary bypass: effect of arterial carbon dioxide tension. Surg 1991;52:479–89.
- Hindman BJ, Dexter F, Cutkomp J, et al. Brain blood flow and metabolism do not decrease at stable brain temperature during cardiopulmonary bypass in rabbits. Anesthesiology 1992;77:342–50.[Web of Science][Medline]
-
Croughwell ND, Reves JG, White WD, et al. Cardiopulmonary bypass time does not affect cerebral blood flow. Ann Thorac Surg 1998;65:1226–30.
[Abstract/Free Full Text] -
Hudak ML, Koehler RC, Rosenberg AA, et al. Effect of hematocrit on cerebral blood flow. Am J Physiol 1986;251:H63–70.
[Abstract/Free Full Text] -
Tu YK, Liu HM. Effects of isovolemic hemodilution on hemodynamics, cerebral perfusion, and cerebral vascular reactivity. Stroke 1996;27:441–5.
[Abstract/Free Full Text] -
Hino A, Ueda S, Mizukawa N, et al. Effect of hemodilution on cerebral hemodynamics and oxygen metabolism. Stroke 1992;23:423–6.
[Abstract/Free Full Text]
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