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Department of Anesthesia, University of Iowa College of Medicine, Iowa City, Iowa 52242
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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We hypothesized that
the response of cerebral blood flow (CBF) to changing viscosity would
be dependent on "baseline" CBF, with a greater influence of
viscosity during high-flow conditions. Plasma viscosity was adjusted to
1.0 or 3.0 cP in rats by exchange transfusion with red blood cells
diluted in lactated Ringer solution or with dextran. Cortical CBF was
measured by H2 clearance. Two groups of animals remained
normoxic and normocarbic and served as controls. Other groups were made
anemic, hypercapnic, or hypoxic to increase CBF. Under baseline
conditions before intervention, CBF did not differ between groups and
averaged 49.4 ± 10.2 ml · 100 g
1 · min1 (±SD). In control
animals, changing plasma viscosity to 1.0 or 3.0 cP resulted in CBF of
55.9 ± 8.6 and 42.5 ± 12.7 ml · 100 g1 · min1, respectively (not
significant). During hemodilution, hypercapnia, and hypoxia with a
plasma viscosity of 1.0 cP, CBF varied from 98 to 115 ml · 100 g1 · min1. When plasma viscosity
was 3.0 cP during hemodilution, hypercapnia, and hypoxia, CBF ranged
from 56 to 58 ml · 100 g1 · min1 and was significantly
reduced in each case (P < 0.05). These results support
the hypothesis that viscosity has a greater role in regulation of CBF
when CBF is increased. In addition, because CBF more closely followed
changes in plasma viscosity (rather than whole blood viscosity), we
believe that plasma viscosity may be the more important factor in
controlling CBF.
brain; hemodilution; hypercapnia; hypoxia; oxygen
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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IT HAS BEEN SUGGESTED THAT blood viscosity is an important independent regulator of cerebral blood flow (CBF). In rigid tubes, flow and viscosity are inversely related. If the cerebral circulation behaves as a rigid tube, and if perfusion pressure remains constant, CBF should increase as blood viscosity is reduced. However, CBF may be actively regulated in response to change in viscosity; reduction of shear force applied to the endothelium as viscosity falls may result in vasoconstriction (13).
Hemodilution, which decreases plasma viscosity, whole blood viscosity, and arterial O2 content (CaO2), increases CBF. We (30) and others (14) have reported that both viscosity and CaO2 play important roles in the CBF response to hemodilution; reduced blood viscosity accounts for approximately one-half of the increase in CBF, with the remainder caused by the change in CaO2. However, other studies have reported that when CBF is normal, selective alteration of viscosity (without changing CaO2) results in little or no change in CBF (3-5, 25). This leads to the possibility that baseline CBF (or vascular tone) may play an important role in determining the response to viscosity change. We therefore hypothesized that manipulation of plasma viscosity in animals with normal CBF would have little effect on CBF, whereas similar viscosity changes would have a much greater impact on CBF when flow is elevated.
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MATERIALS AND METHODS |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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Animal Preparation
The University of Iowa Animal Care and Use Committee approved all experiments. Male Sprague-Dawley rats (n = 64; Harlan Sprague-Dawley, Indianapolis, IN) weighing 320-390 g were anesthetized with 4-5% halothane in 100% O2 in a plastic box. They were then removed from the box, 1% lidocaine was infiltrated subcutaneously into the anterior neck, and a tracheotomy was performed. Animals were ventilated with an inspired gas mixture of 1.0% halothane in 40% O2-60% N2. Ventilator settings were adjusted to achieve normocarbia. Bilateral femoral arterial and venous catheters (PE-50) were surgically inserted after infiltration of lidocaine. Arterial blood pressure was thereafter measured continuously, and arterial blood was intermittently sampled for the determination of pH, blood gas tension (Instrumentation Laboratory System 1306, Lexington, MA), hemoglobin concentration, CaO2 (Radiometer OM3), hematocrit (Hct), and both whole blood and plasma viscosity. Hct was determined by microcapillary tube centrifugation. Rectal temperature was maintained at 37-38°C with a heating pad.After preparation (~45 min), the halothane was discontinued. A
loading dose of pentobarbital sodium (50 mg/kg iv) was administered, followed by a maintenance infusion (18 mg · kg1 · h1 iv). The
animals were then turned prone, and the head was fixed in a stereotaxic
frame (David Kopf Instruments, Tujunga, CA). The scalp was reflected
(after lidocaine infiltration), and two frontoparietal burr holes, ~5
mm in diameter, were created using a high-speed drill. The posterior
margin of the holes was located ~5 mm anterior to the coronal suture,
and the medial margin was located ~1-2 mm lateral to the
midline. During drilling, the craniectomy site was irrigated with
saline to avoid thermal injury to the cortex. The dura was incised with
the aid of a microscope, and, avoiding dural and pial vessels,
25-µm-diameter wire electrodes were inserted bilaterally
~0.5-1.0 mm into the cortex using micromanipulators. The
electrodes were constructed from 90% platinum-10% iridium wire
(Medwire, Mt. Vernon, NY) insulated with glass, leaving an exposed 2-mm
tip. An Ag/AgCl reference electrode was placed subcutaneously in the
tissue of the posterior scalp and neck. The platinum electrodes were
polarized to +250 mV relative to the Ag/AgCl reference.
Calculations
For measurement of CBF, H2 was added to the inhaled gas mixture while the voltage output of the polarization amplifier was recorded on a Grass model 79 polygraph. When a plateau had been achieved (after 5-10 min), H2 administration was stopped, and the washout curve was recorded. CBF was calculated from the clearance curve using the T1/2 method (32)
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, the
partition coefficient for H2, is taken to be 1. CBF
values from each hemisphere were averaged to yield a single value for
each animal at each measurement point.
Experimental Protocols
After preparation and stabilization, baseline CBF was measured in all animals. Rats were then randomly assigned to 1 of 8 groups: group 1, control with normal Hct and reduced plasma viscosity (n = 8); group 2, control with normal Hct and increased plasma viscosity (n = 8); group 3, hemodilution (Hct
15%,
CaO2 8 ml O2/dl) with reduced
plasma viscosity (n = 8); group 4,
hemodilution with increased plasma viscosity (n = 8);
group 5, hypercapnia [arterial PCO2
(PaCO2) 80 mmHg] with reduced plasma
viscosity; group 6; hypercapnia with increased plasma
viscosity; group 7, hypoxia [arterial
PO2 (PaO2) 35 mmHg,
CaO2 8 ml O2/dl] with reduced
plasma viscosity; and group 8, hypoxia with increased plasma viscosity.
Groups 1 and 2: controls. In the control groups with normal Hct, plasma viscosity was manipulated by plasma exchange with either lactated Ringer solution (LR) or 9% dextran (average mol wt 2,000,000; Sigma Chemical, St. Louis, MO). To reduce plasma viscosity (group 1), 4 ml of whole blood were withdrawn and 2 ml of donor red blood cell (RBC) concentrate (see Preparation of Donor RBCs) in 12-16 ml of LR were infused; 7 ml of blood were then withdrawn and replaced with 3.5 ml of RBC concentrate in 21-28 ml of LR. This process was repeated four times, with the goal being to achieve a target plasma viscosity of 1 cP with an unchanged Hct (the exact volumes of blood and fluid used were determined in preliminary studies). After the last blood exchange, LR was infused intravenously at 0.5-1.0 ml/min to maintain a constant Hct. In animals with normal Hct and increased viscosity (group 2), 4 ml of blood were withdrawn, and 2 ml of donor RBC concentrate and 2 ml of 9% dextran were infused; 1 ml of whole blood was then withdrawn, followed by the infusion of 0.5 ml of donor RBC concentrate and 0.5 ml of 9% dextran. This process was repeated four times with the goal of a plasma viscosity of 3.0 cP. Hct was adjusted to baseline by additional administration of the donor RBC concentrate or 9% dextran as needed. Blood pressure was maintained at baseline values in both groups by methoxamine infusion. CBF was then measured a second time in both groups, and blood was withdrawn for whole blood and plasma viscosity measurements. The interval between CBF measurements was ~1.5 h.
Groups 3 and 4: hemodilution.
Two groups of animals underwent hemodilution rather than simple plasma
exchange. In the reduced-viscosity hemodiluted group (group
3), baseline CBF and viscosity measurements were performed. CaO2 was decreased to a target value of 8.0 ml
O2/dl (Hct 15%) by blood withdrawal and infusion
of LR at a 5:1 ratio. After hemodilution, LR was infused intravenously
at 1.0-1.5 ml/min to maintain constant Hct and
CaO2. In the hemodiluted group with increased plasma
viscosity (group 4), CaO2 was decreased to
a target value of 8.0 ml O2/dl by blood withdrawal and
replacement with an equal volume of 7% dextran (average mol wt
413,000; Sigma Chemical) in LR. Blood pressure was maintained by
infusion of methoxamine, CBF was again measured, and a final blood
sample was drawn to determine viscosity.
Groups 5 and 6: hypercapnia.
In the two hypercapnic groups, a PaCO2 of 80 mmHg was achieved by adding CO2 to inhaled gases. During
CO2 adjustment, plasma viscosity was decreased (group
5) or increased (group 6) by plasma exchange as in
groups 1 and 2. Before initiation of the
CO2 inhalation, skeletal muscle paralysis was produced with
pancuronium bromide (0.25 mg/kg iv), and mean arterial pressure (MAP)
was maintained by infusion of methoxamine. CBF was measured after
target PaCO2 had been achieved, and a final blood
sample was drawn to determine viscosity.
Groups 7 and 8: hypoxia. Hypoxia was achieved by incremental reductions in inspired O2 concentration (produced by changing the O2-to-N2 ratio) until a target PaO2 of ~35 mmHg (CaO2 of 8.0 ml O2/dl) was reached. Plasma viscosity was decreased or increased by plasma exchange as in groups 1 and 2. Before reduction of the O2 concentration, skeletal muscle paralysis was produced with pancuronium bromide (0.25 mg/kg iv), and methoxamine was used to maintain MAP. Because the O2 concentration increased when the inhalation of the H2 was terminated, the flow of O2 was adjusted to maintain PaO2 at target values during H2 washout.
Blood Viscosity Measurement
One milliliter of blood was used to determine whole blood viscosity, and one milliliter of plasma was separated by centrifugation at 3,000 rpm for 10 min and used for plasma viscosity measurement. Viscosity was measured in a Brookfield LVDV-I+ viscometer (Brookfield, Stoughton, MA) at shear rates of 100, 20, and 5 s1 at
37°C. However, unless specifically noted, all reported viscosity values were determined at a shear rate of 20 s1.
Preparation of Donor RBCs
A donor RBC concentrate was prepared on the day of the experiment. Donor rats were anesthetized with halothane, and femoral arterial and venous catheters (PE-50) were inserted. Seven milliliters of whole blood were withdrawn and anticoagulated with heparin sulfate. Five milliliters of LR were infused, and blood was again withdrawn and anticoagulated. This process was repeated four times. The harvested blood was centrifuged at 1,000 rpm for 10 min to separate RBCs and plasma.Statistics
All results are expressed as means ± SD. Values were compared using ANOVA with a Duncan's post hoc test. A value of P < 0.05 was accepted as significant.| |
RESULTS |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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Systemic Variables
Under baseline conditions, there were no significant differences between groups in any systemic variable. Global means of baseline values are shown in Table 1. After intervention, Hct, CaO2, PaCO2 and PaO2 differed among groups as intended (Table 2). Hypoxia and hemodilution reduced CaO2 to equivalent levels. A greater rate of methoxamine infusion rate was required in the hypoxic groups (Table 2).
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Whole Blood and Plasma Viscosity
Baseline plasma and whole blood viscosity were not different among groups. After plasma exchange or hemodilution, plasma viscosity differed as intended between the hypo- and hyperviscosity groups (Table 2). Because plasma viscosity is an important contributor to whole blood viscosity, whole blood viscosity also varied between groups. As anticipated, whole blood viscosity was reduced to a greater degree in groups that underwent hemodilution. Viscosity measurements were similar at shear rates of 5 and 100 s1 (data not shown).
Cerebral Blood Flow
Baseline CBF before intervention did not differ among groups and averaged 49.4 ± 10.1 ml · 100 g1 · min1. CBF after
interventions is shown in Fig. 1.
Manipulation of plasma viscosity did not significantly affect CBF in
normocapnic, normoxic animals with a normal Hct (Fig. 1). However, when
CBF was elevated by hemodilution, hypoxia, or hypercarbia, increasing viscosity significantly reduced CBF (P < 0.05).
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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This study demonstrates that viscosity significantly influenced flow only when CBF was elevated. Under normal conditions, a threefold variation in plasma viscosity with a twofold variation in whole blood viscosity did not significantly alter CBF. However, when hemodilution, hypercapnia, or hypoxia elevated CBF, increasing viscosity significantly reduced CBF.
Previous investigations of the role of viscosity in the regulation of CBF have yielded inconsistent results. A number of studies report that blood viscosity can influence CBF (23, 24, 26). These studies were conducted with models in which CaO2 and plasma viscosity were simultaneously altered, most commonly by hemodilution. Because a change in both viscosity and CaO2 can affect CBF, this study design makes it difficult to determine the specific role of either variable. To better delineate the role of viscosity, we selectively manipulated plasma viscosity under normal conditions and when CBF was increased.
Our findings are consistent with studies conducted in animals and humans with normal CBF, i.e., the independent alteration of plasma viscosity alone had little or no effect on CBF (3-5), and independent alteration of whole blood viscosity without change in CaO2 did not affect CBF (25). Our findings are also consistent with most previous studies carried out in the face of elevated flows. For example, in humans with paraproteinemia and anemia, CBF is lower than in anemic humans with normal plasma viscosity (15). In dogs, increasing plasma viscosity limits the increase in CBF during hypercapnia (11). In contrast, one study reported that independent manipulation of plasma viscosity did not affect CBF when CBF was elevated by exchange transfusion with a cell-free hemoglobin solution (33). The nonphysiological conditions of this study may have affected the cerebral vascular response to viscosity and produced contradictory results.
In rigid tubes, viscosity and flow are inversely related if perfusion pressure remains constant. Because CBF was not influenced by viscosity in control animals with normal baseline CBF, Hct, and PaCO2, it is clear that the cerebral circulation does not respond as a rigid tube. Under normal conditions, the circulation exhibits an active regulatory response to viscosity. In the noncerebral circulation, increasing plasma viscosity results in dilatation of blood vessels, reducing flow velocity and thereby maintaining shear stress (the product of flow velocity and viscosity) at near-constant values (6, 17). Similar measurement of blood vessel diameter and shear stress during isolated change in viscosity has not been undertaken in the cerebral circulation. However, during hemodilution, when both CaO2 and viscosity are reduced, cerebral arteries and pial arterioles constrict (13, 20). This suggests an active regulatory response to change in viscosity.
Because alteration of plasma viscosity also altered whole blood viscosity, we cannot fully separate their roles in the CBF response. Some data suggest that plasma viscosity may be more important than blood viscosity in regulation of CBF. In the two groups that underwent hemodilution, because of the reduction in Hct, whole blood viscosity was significantly lower than in similar hypercapnic or hypoxic groups. However, the effect of plasma viscosity manipulation on CBF was very similar between the hemodiluted, hypercapnic, and hypoxic groups, with CBF more closely following changes in plasma than whole blood viscosity. The importance of plasma viscosity in the regulation of flow is not surprising. Because of the axial migration of RBCs in flowing blood, plasma is the principal interface with the blood vessel wall (1). Shear stress of plasma moving at the endothelial surface influences vessel diameter, modulating the release of autocoids (prostacyclin, nitric oxide).
In contrast to normal conditions, we found that when hypercapnia, hypoxia, or hemodilution increased CBF, increased plasma viscosity significantly reduced CBF. To maintain constant flow with increased viscosity, cerebral arteries and arterioles must dilate. Similar to our findings, hypoxia, hemodilution, and hypercapnia have been shown to impair pressure-mediated regulation (autoregulation) of CBF (10, 16, 19). The inability to maintain constant CBF under high-flow conditions suggests that cerebral blood vessels were unable to dilate further. However, the stimuli used to increase CBF do not produce maximal increase in CBF, and this would suggest that some vasodilatory capacity remains in the cerebral circulation. The mechanisms responsible for failure of viscosity-mediated CBF regulation under high-flow conditions are currently unknown.
We selected hypercapnia, hypoxia, and hemodilution to increase CBF because these stimuli likely differ in some mechanisms of vasodilatation. Our goal was to evaluate the effect of change in viscosity during a variety of vasodilator stimuli. Although a full understanding of how hypercapnia, hypoxia, and hemodilution produce cerebrovasodilatation is lacking, some information is available. During hypercapnia, nitric oxide, cGMP, and potassium channels contribute to cerebrovasodilatation (2). During hypoxia, nitric oxide, potassium channels, and adenosine contribute to vasodilatation (8, 29). After hemodilution, reduced viscosity and CaO2 are responsible for increased CBF (14, 30). However, after hemodilution, potassium channels and nitric oxide do not contribute to increased CBF (27, 29). Thus, although there is overlap of the mechanisms that increase CBF during hypercapnia, hypoxia, and hemodilution, other mechanisms differ. Because we saw a similar effect of increased viscosity on CBF during all three vasodilator stimuli, this implies that the effect of viscosity does not depend on the underlying vasodilator mechanism.
Consideration of Methods
For this study, we selected target plasma viscosities of 1.0 and 3.0 cP to represent relevant change in viscosity. A plasma viscosity of 1.0 cP is consistent with plasma viscosity in humans during hemodilution with a crystalloid solution. A plasma viscosity of 3.0 cP is within the range of values found in humans with abnormal plasma viscosity caused by increased plasma proteins (4, 22).We previously reported (27, 28) that when CaO2 is reduced to equal values, hypoxia increases CBF more than hemodilution. In both prior studies, global CBF was measured with radiolabeled microspheres. In the current study, hypoxia and hemodilution resulted in equivalent CBF. Consistent with our current study, other investigators (17a) have reported that hypoxia and hemodilution result in equal CBF when CBF is measured by H2 clearance. As used in the current study, H2 clearance only measured cortical CBF. It is possible that the discordant results from the current and prior studies are caused by measurement of CBF in different brain compartments.
We measured CBF by H2 clearance, which requires insertion of an electrode into the brain. Electrode insertion into rat brain can initiate spreading depression, which reduces baseline CBF and impairs cerebral vascular response to some stimuli (7, 18). However, insertion of electrodes of <50-µm diameter does not initiate spreading depression in rats (31). In our model, we used a 25-µm electrode. Insertion of the H2 electrode is associated with some tissue injury, and CBF values determined by H2 electrodes may be less than CBF values determined by other, noninvasive methods. However, CBF measured with an acutely placed 50-µm electrode correlates closely with [3H]nicotine-measured CBF (31).
We considered whether dextran solutions might alter CBF independently of viscosity. In the cremaster circulation, low-molecular-weight dextran exchange transfusion that maintains constant plasma viscosity does not alter vascular diameter (6). This suggests that there is no independent, direct effect of dextran on vascular tone. High-molecular-weight dextrans can cause RBC aggregation, which could also affect blood flow. However, high-molecular-weight dextran-induced RBC aggregation does not appear to be important in regulation of blood flow in the cerebral and peripheral circulation (5, 9).
We used methoxamine, an 
-agonist, to maintain constant blood
pressure during interventions. Methoxamine constricts the peripheral circulation and alters regional blood flow. However, when the blood-brain barrier is intact, direct intracarotid infusion of -agonists does not alter CBF (12, 21). Furthermore,
similar methoxamine infusion rates were required in both hyper- and
hypoviscosity animals within a given group (e.g., hypoxia group),
indicating that the observed differences cannot be the result of
vasopressor use.
In conclusion, our results indicate that under normal conditions, the cerebral circulation responds to change in viscosity and maintains constant flow. In contrast, when CBF was increased, there was failure of flow regulation when viscosity increased. Plasma viscosity may be more important than whole blood viscosity, because change in flow more closely followed plasma viscosity. When viscosity increases during high-flow conditions, cerebral arterioles must further dilate to maintain constant CBF. We speculate that the failure to maintain constant CBF with increased viscosity during high-flow conditions may be caused by failure of dilatation in cerebral arteries and arterioles. In addition, because increased viscosity reduced CBF by approximately one-half, O2 delivery was also reduced to a similar degree. Under some conditions, this could be detrimental to brain O2 supply.
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ACKNOWLEDGEMENTS |
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Present address of Y. Tomiyama: Department of Anesthesiology, Tokushima University School of Medicine, 3-18-15 Kuramoto, Tokushima, Tokushima 770-8503, Japan.
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FOOTNOTES |
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Address for reprint requests and other correspondence: J. E. Brian, Jr., Dept. of Anesthesia, Univ. of Iowa Health Center, 6 JCP, 200 Hawkins Dr., Iowa City, IA 52242 (E-mail: eddie-brian{at}uiowa.edu).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Received 27 December 1999; accepted in final form 23 May 2000.
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
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P < 0.05 compared with respective control
group.