Lack of Dependence of Cerebral Blood Flow on Blood Viscosity after Blood Exchange with a Newtonian O₂ Carrier

Abstract

Whether the increase in cerebral blood flow measured after hemodilution is mediated by a decrease in blood viscosity or in oxygen delivery to the brain is debated. In the present study, blood was replaced by an oxygen-carrying blood substitute, ultrapurified, polymerized, bovine hemoglobin (UPBHB). In contrast to normal blood, UPBHB yields a constant and defined viscosity in the brain circulation, since its viscosity is not dependent on the shear rate. CBF was determined after blood exchange with UPBHB in one group of conscious rats (UPBHB group) and in another group of blood-exchanged conscious rats in which viscosity was increased fourfold by the addition of 2% polyvinylpyrrolidone (PVP), mw 750,000 (UPBHB-PVP group). Local CBF (LCBF) was measured in 34 brain structures by means of the quantitative iodo(14C)antipyrine method. After blood replacement, systemic parameters such as cardiac index, arterial blood pressure, blood gases, and acid-base status were not different between the UPBHB and the UPBHB-PVP groups. In particular, arterial oxygen content was similar in both groups. Compared with a control group without blood exchange, LCBF was increased after blood exchange in the different brain structures by 60-102% (UPBHB group) and by 33-101% (UPBHB-PVP group). Mean CBF was increased by 77% in the UPBHB group and by 69% in the UPBHB-PVP group. No significant differences were observed in the values of LCBF or mean CBF between the UPBHB group and the UPBHB-PVP group. The results show that a fourfold variation in the viscosity of a Newtonian blood substitute does not result in differences in CBF values.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of blood transfusion and haemodilution on cerebral oxygenation and haemodynamics in newborn infants investigated by near infrared spectrophotometry

“…Haemodilution will reduce the red cell mass resulting in improvement of microcirculation in many organs including the brain [1,22,30]. The increased CBF after haemodilution seems to be the result of the compensation for decreased arterial O 2 content and not to be related to decreased blood viscosity [7,31,39]. Therefore, determination of the blood viscosity in our patients was considered unnecessary.…”

Blood viscosity maintains microvascular conditions during normovolemic anemia independent of blood oxygen-carrying capacity

“…Our laboratory (6,39) showed that the reduction of FCD found after decreasing systemic Hct to 18% of baseline with low-viscosity plasma expanders was not decreased further by continuing hemodilution with high-viscosity plasma expanders. Waschke et al (43) found that cerebral perfusion was not changed when blood was replaced with fluids with the same oxygen-carrying capacity and viscosities varying from 1.4 to 7.7 cP. Krieter et al (21) increased plasma viscosity using dextran 500 kDa and found that medians in tissue PO 2 in skeletal muscle were maximal at 3 cP of plasma viscosity and that there were no changes in tissue oxygenation and organ perfusion when blood was he- Calculations of global oxygen transport are not directly measurable in our model.…”

Microcirculatory effects of intravenous fluids in critical illness: plasma expansion beyond crystalloids and colloids

“…Chen et al [21] elevated plasma viscosity four-fold (4 cP), finding vasodilation and reduction of vascular hindrance in several vital organs. Waschke et al [22] found unchanged cerebral perfusion when blood was replaced with fluids with the same oxygen-carrying capacity and viscosities varying from 1.4 to 7.7 cP. Krieter et al [23] infused dextran (500 kDa) and found maximal tissue p O 2 in skeletal muscle and liver at plasma viscosities of 3 and 2 cP, respectively.…”