Effects of profound anemia on brain tissue oxygen tension, carbon dioxide tension, and pH in rabbits

Citation
Y. Morimoto et al., Effects of profound anemia on brain tissue oxygen tension, carbon dioxide tension, and pH in rabbits, J NEUROS AN, 13(1), 2001, pp. 33-39
Citations number
17
Categorie Soggetti
Aneshtesia & Intensive Care
Journal title
JOURNAL OF NEUROSURGICAL ANESTHESIOLOGY
ISSN journal
08984921 → ACNP
Volume
13
Issue
1
Year of publication
2001
Pages
33 - 39
Database
ISI
SICI code
0898-4921(200101)13:1<33:EOPAOB>2.0.ZU;2-C
Abstract
This study sought to determine the maximum tolerable limit of anemia for th e brain during halothane anesthesia. Using a multiparameter sensor, we cont inuously monitored brain tissue oxygen tension (PO2), carbon dioxide tensio n (PCO2), and pH during profound hemodilution and subsequent transfusion. T welve New Zealand White rabbits were anesthetized, intubated, and mechanica lly ventilated at a fraction of inspired oxygen (FiO(2)) of 21% to produce an arterial carbon dioxide tension (PaCO2) of 35 to 40 mm Hg. The femoral a rtery was cannulated to continuously monitor arterial blood pressure and to intermittently measure arterial blood gases. The electroencephalogram (EEG ) was recorded throughout the course of the study. A fiberoptic sensor was inserted into the brain for the continuous measurement of brain PO2, PCO2, pH, and temperature. Cerebral blood flow (CBF) was measured by the hydrogen clearance method. Severe anemia was induced by repeatedly withdrawing 50-m L aliquots of blood and infusing an equal volume of 6% hetastarch. This pro cedure was performed four times for each rabbit. After the forth blood draw and fluid infusion, a total of 60 ml, of packed red blood cells were trans fused. Upon completion of the hemodilution, the hemoglobin concentration wa s 2.4 +/- 0.3 g/dL (mean +/- SEM). Brain tissue PO2 decreased from 27 +/- 3 mm Hg to a minimum of 12 +/- 2 mm Hg. Brain tissue pH also decreased from 7.22 +/- 0.03 to 7.12 +/- 0.05 and returned to the baseline value with tran sfusion. Brain PCO2 did not change significantly during the experiment. Cer ebral blood flow increased from 37 +/- 3 to 66 +/- 15 mt x 100(-1) x min(-1 ) during hemodilution and returned to baseline after infusion of red blood cells. There was some loss of EEC amplitude and the calculated cerebral met abolic rate (CMRO2) decreased from 4.3 +/- 0.6 to 1.9 +/- 0.3 mt x 100g(-1) x min(-1) at the most profound level of anemia. This is the first report o f which the authors are aware of continuous monitoring of brain tissue pH, PCO2, and PO2 during profound hemodilution and transfusion. Hemodilution re sults in a decrease in brain tissue PO2. Increases in CBF and oxygen extrac tion can only partially compensate for the decreased oxygen carrying capaci ty of the blood. Decreases in brain tissue PO2, pH, CMRO2, and a loss of EE G amplitude suggest that the maximum tolerable limit of hemodilution was ac hieved in this study.