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Influence of severe hemodilution on brain function and brain oxidative metabolism in the cat
R Bauer1, T Iijima, K A Hossmann
1Max-Planck Institute for Neurological Research, Department of Experimental Neurology, Koln, Germany.
Insights
Healthy mammals tolerate significant hemodilution without brain impairment. Previously observed issues during bypass perfusion likely stem from flow regulation problems, not reduced oxygen-carrying capacity.
Area of Science:
- Physiology
- Neuroscience
- Hematology
Background:
- Brain metabolism declines with falling hematocrit during bypass perfusion.
- The cause of this deterioration (flow regulation vs. oxygen-carrying capacity) remains unclear.
Purpose of the Study:
- To determine the brain's functional and biochemical impairment threshold during severe hemodilution.
- To differentiate between flow regulation and oxygen-carrying capacity effects on brain metabolism.
Main Methods:
- Adult cats underwent gradual isovolemic hemodilution using Ringer lactate/dextran.
- Blood was exchanged to achieve final hematocrit levels between 6.1% and 11%.
Main Results:
- Cerebral blood flow increased significantly below 10% hematocrit.
- Brain oxygen delivery remained stable; electrocorticography and evoked potentials were unaffected.
- Brain ATP and phosphocreatine levels were maintained, with elevated lactate.
Conclusions:
- Healthy mammals can withstand substantial hemodilution without major brain dysfunction.
- Deterioration during bypass perfusion is likely due to flow regulation issues, not solely hematocrit decline.
Objective:
It has been established that during constant pressure arterio-venous bypass perfusion, brain metabolism gradually deteriorates in parallel with the declining hematocrit. However, whether this is due to a disturbance of flow regulation or to the decline in the oxygen-carrying capacity of the blood has not been documented. Therefore, intact animals were submitted to severe hemodilution to determine the threshold for the beginning of functional and biochemical impairment of the brain.
Methods:
Six anesthetized and paralyzed adult mongrel cats were submitted to gradual isovolemic hemodilution by stepwise exchange of blood with Ringer lactate/dextran (1 : 1) solution. Exchange of 80 ml/kg body weight resulted in a final hematocrit level ranging from 6.1% to 11%.
Results:
Cerebral blood flow gradually increased during hemodilution, with a sharp rise to eight times the prehemodilution value when the hematocrit fell below 10%. The calculated oxygen delivery to the brain remained relatively unchanged. Hemodilution did not cause suppression of spontaneous ECoG or somatically evoked primary cortical potentials, even at the lowest hematocrit value of 6.1%. Brain tissue ATP and phosphocreatine content were largely maintained, although tissue lactate content was elevated (9.54 +/- 5.99 micromol/g).
Conclusions:
The hemodynamically unimpaired healthy mammal is able to support a substantial degree of hemodilution without major functional or biochemical disturbance to the brain. The previously observed disturbances during prolonged bypass perfusion are, therefore, most probably due to the associated abnormalities of flow regulation.