Effect of hemodilution on cerebral hemodynamics and oxygen metabolism.

Hino, Akihiko; Ueda, Satoshi; Mizukawa, Nobuyoshi; Imahori, Yoshio; Takahashi, Hiroshi

doi:10.1161/01.str.23.3.423

Cited by 76 publications

(31 citation statements)

References 24 publications

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“…In the two studies that recorded the systemic temperature of the subjects before, during, and after hemodilution, no temperature changes were reported during the procedure (5, 42). In the other seven studies, temperature data were not reported (13,19,20,46,59,61,65); it was thus assumed that the CBF change can be attributed solely to hematocrit changes. Linear fitting of Eq.…”

Section: Resultsmentioning

confidence: 99%

A theoretical model of selective cooling using intracarotid cold saline infusion in the human brain

Konstas¹,

Neimark²,

Laine³

et al. 2007

Journal of Applied Physiology

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Konstas AA, Neimark MA, Laine AF, Pile-Spellman J. A theoretical model of selective cooling using intracarotid cold saline infusion in the human brain. J Appl Physiol 102: 1329 -1340, 2007. First published December 14, 2006; doi:10.1152/japplphysiol.00805.2006.-A threedimensional mathematical model was developed to examine the transient and steady-state temperature distribution in the human brain during selective brain cooling (SBC) by unilateral intracarotid freezing-cold saline infusion. To determine the combined effect of hemodilution and hypothermia from the cold saline infusion, data from studies investigating the effect of these two parameters on cerebral blood flow (CBF) were pooled, and an analytic expression describing the combined effect of the two factors was derived. The Pennes bioheat equation used the thermal properties of the different cranial layers and the effect of cold saline infusion on CBF to propagate the evolution of brain temperature. A healthy brain and a brain with stroke (ischemic core and penumbra) were modeled. CBF and metabolic rate data were reduced to simulate the core and penumbra. Simulations using different saline flow rates were performed. The results suggested that a flow rate of 30 ml/min is sufficient to induce moderate hypothermia within 10 min in the ipsilateral hemisphere. The brain with stroke cooled to lower temperatures than the healthy brain, mainly because the stroke limited the total intracarotid blood flow. Gray matter cooled twice as fast as white matter. The continuously falling hematocrit was the main time-limiting factor, restricting the SBC to a maximum of 3 h. The study demonstrated that SBC by intracarotid saline infusion is feasible in humans and may be the fastest method of hypothermia induction. therapeutic hypothermia; ischemic stroke; spatial and temporal brain temperature distributions THE CENTRAL NERVOUS SYSTEM is vulnerable to focal and global ischemia resulting from acute ischemic stroke (63) and cardiac arrest (21). Therapeutic hypothermia has been repeatedly shown to be effective in limiting the damage of global and focal ischemia in animal models and clinical studies (6,21).In most clinical studies, hypothermia is induced by surface cooling. Although this is the simplest and most cost-effective option for inducing hypothermia (14), it has two major drawbacks. 1) Several hours are required to reach the target body core temperature. All studies report a 3-to 7-h period for cooling to 32-34°C (26, 52); however, endovascular systemic cooling may be able to accelerate the rate of cooling and improve the efficacy of hypothermia (15).2) The incidence of adverse effects, such as impaired immune function, decreased cardiac output, pneumonia, and cardiac arrhythmias/bradycardias, is high (14, 31). Selective brain cooling (SBC) without reducing body core temperature can theoretically address both problems of whole body cooling.Different methods for SBC have been reported (18). Noninvasive methods most commonly used are cooling caps and helmets. However, th...

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Section: Resultsmentioning

confidence: 99%

A theoretical model of selective cooling using intracarotid cold saline infusion in the human brain

Konstas¹,

Neimark²,

Laine³

et al. 2007

Journal of Applied Physiology

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“…Another limitation is that the glucose content measured in a region reflects the glucose present in both cerebral tissue and the intravascular space. However, since cerebral blood volume is minimal (on the order of 2-4% of total volume) (52)(53)(54), the contribution of blood glucose to the measurement of brain glucose is small and without effect on the calculation of glucose transport kinetics across the blood-brain barrier. At a plasma concentration of 15 mmol/l, the contribution of blood to the glucose concentration measured in gray matter would be ϳ0.6 mmol/l or ϳ10% of the total glucose concentration measured in a volume of cerebral tissue.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Insulin on In Vivo Cerebral Glucose Concentrations and Rates of Glucose Transport/Metabolism in Humans

et al. 2001

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The continuous delivery of glucose to the brain is critically important to the maintenance of normal metabolic function. However, elucidation of the hormonal regulation of in vivo cerebral glucose metabolism in humans has been limited by the lack of direct, noninvasive methods with which to measure brain glucose. In this study, we sought to directly examine the effect of insulin on glucose concentrations and rates of glucose transport/metabolism in human brain using 1 H-magnetic resonance spectroscopy at 4 Tesla. Seven subjects participated in paired hyperglycemic (16.3 ؎ 0.3 mmol/l) clamp studies performed with and without insulin. Brain glucose remained constant throughout (5.3 ؎ 0.3 mol/g wet wt when serum insulin ‫؍‬ 16 ؎ 7 pmol/l vs. 5.5 ؎ 0.3 mol/g wet wt when serum insulin ‫؍‬ 668 ؎ 81 pmol/l, P ‫؍‬ NS). Glucose concentrations in gray matter-rich occipital cortex and white matter-rich periventricular tissue were then simultaneously measured in clamps, where plasma glucose ranged from 4.4 to 24.5 mmol/l and insulin was infused at 0.5 mU ⅐ kg -1 ⅐ min -1 . The relationship between plasma and brain glucose was linear in both regions. Reversible Michaelis-Menten kinetics fit these data best, and no differences were found in the kinetic constants calculated for each region. These data support the hypothesis that the majority of cerebral glucose uptake/metabolism is an insulin-independent process in humans. Diabetes 50: [2203][2204][2205][2206][2207][2208][2209] 2001 T he brain relies on the continuous delivery of glucose via the blood to maintain normal metabolic function. How glucose delivery into the central nervous system is regulated and how that delivery is altered by different metabolic conditions in the living human have been difficult to ascertain. In particular, the role of insulin in the regulation of cerebral glucose metabolism has been difficult to directly assess. Although evidence acquired using both in vitro and in vivo approaches support and refute the hypothesis that insulin regulates the entry of glucose into brain tissue (1-9), studies performed in living animals have been limited by their inability to directly measure cerebral glucose concentrations.The brain is composed of both gray and white matter. Both rely on glucose for the maintenance of normal function, but the rates at which they metabolize glucose have been found to be different (9,10). Whether these differences in glucose metabolism equate to differences in cerebral glucose concentrations and whether insulin differentially regulates regional cerebral glucose metabolism have not been directly examined in humans because, until recently, direct methods to measure brain glucose concentrations in healthy subjects have not been feasible. Invasive methods to measure intracerebral glucose concentrations, such as the use of an implanted equilibrium dialysis probe, have been reported in abstract form (11), but such a technique is not acceptable in the study of normal human physiology. Indirect methods to quantitate brain glucose concent...

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“…We conclude that CBF remains related to Ca O 2 during hypoxemia when hematocrit is reduced with and without proportional reductions in O 2 -carrying capacity. Thus O 2 transport to the brain is well regulated at a constant level independently of alterations in hematocrit, hemoglobin concentration, and O 2 saturation.anemia; blood; cats; oxygen transport BOTH EXPERIMENTAL (1,6,26,36) and clinical (2,14,15,30,40) anemia result in an increase in cerebral blood flow (CBF) that is inversely related to arterial O 2 content (Ca O 2 ). Because the increase in CBF does not require dilation of large cerebral arteries and pial arterioles (16,19,27,28,41), the passive decrease in viscosity is presumed to be sufficient for adequately decreasing cerebrovascular resistance.…”

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confidence: 99%

Cerebral blood flow during hypoxic hypoxia with plasma-based hemoglobin at reduced hematocrit

Ulatowski

Bucci

Razynska

et al. 1998

American Journal of Physiology-Heart and Circulatory Physiology

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. Cerebral blood flow during hypoxic hypoxia with plasma-based hemoglobin at reduced hematocrit. Am. J. Physiol. 274 (Heart Circ. Physiol. 43): H1933-H1942, 1998.-We determined whether cerebral blood flow (CBF) remained related to arterial O 2 content (Ca O 2 ) during hypoxic hypoxia when hematocrit and hemoglobin concentration were independently varied with cell-free, tetramerically stabilized hemoglobin transfusion. Three groups of pentobarbital sodium-anesthetized cats were studied with graded reductions in arterial O 2 saturation to 50%: 1) a control group with a hematocrit of 31 Ϯ 1% (mean Ϯ SE; n ϭ 7); 2) an anemia group with a hematocrit of 21 Ϯ 1% that underwent an isovolumic exchange transfusion with an albumin solution (n ϭ 8); and 3) a group transfused with an intramolecularly cross-linked hemoglobin solution to decrease hematocrit to 21 Ϯ 1% (n ϭ 10). Total arterial hemoglobin concentration (g/dl) after hemoglobin transfusion (8.8 Ϯ 0.2) was intermediate between that of the control (10.3 Ϯ 0.3) and albumin (7.2 Ϯ 0.4) groups. Forebrain CBF increased after albumin and hemoglobin transfusion at normoxic O 2 tensions to levels attained at equivalent reductions in Ca O 2 in the control group during graded hypoxia. Over a wide range of arterial O 2 saturation and sagittal sinus PO 2 , CBF remained greater in the albumin group. When CBF was plotted against Ca O 2 for all three groups, a single relationship was formed. Cerebral O 2 transport, O 2 consumption, and fractional O 2 extraction were constant during hypoxia and equivalent among groups. We conclude that CBF remains related to Ca O 2 during hypoxemia when hematocrit is reduced with and without proportional reductions in O 2 -carrying capacity. Thus O 2 transport to the brain is well regulated at a constant level independently of alterations in hematocrit, hemoglobin concentration, and O 2 saturation.anemia; blood; cats; oxygen transport BOTH EXPERIMENTAL (1,6,26,36) and clinical (2,14,15,30,40) anemia result in an increase in cerebral blood flow (CBF) that is inversely related to arterial O 2 content (Ca O 2 ). Because the increase in CBF does not require dilation of large cerebral arteries and pial arterioles (16,19,27,28,41), the passive decrease in viscosity is presumed to be sufficient for adequately decreasing cerebrovascular resistance. Interestingly, the increase in CBF during anemia is approximately the same as the increase in CBF during hypoxic hypoxia at equivalent reductions in Ca O 2 (20). With hypoxic hypoxia, the increase in CBF compensates for the decrease in Ca O 2 , thereby maintaining cerebral O 2 transport (CBF ϫ Ca O 2 ) to the cerebral microcirculation (20, 22, 42). With anemia, cerebral O 2 transport generally is well preserved (1, 16, 20), although small decreases have also been reported (6, 37). Whether preservation of O 2 transport during anemia is the result of active microcirculatory regulation by an O 2 -sensitive mechanism or simply a fortuitous passive effect of decreased hematocrit is unclear.Increases in CBF with meth...

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Effect of hemodilution on cerebral hemodynamics and oxygen metabolism.

Cited by 76 publications

References 24 publications

A theoretical model of selective cooling using intracarotid cold saline infusion in the human brain

A theoretical model of selective cooling using intracarotid cold saline infusion in the human brain

The Effect of Insulin on In Vivo Cerebral Glucose Concentrations and Rates of Glucose Transport/Metabolism in Humans

Cerebral blood flow during hypoxic hypoxia with plasma-based hemoglobin at reduced hematocrit

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