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CEREBRAL OXYGENATION DURING ACUTE NORMOVOLEMIC ANEMIA IN RATS.

Department of Anesthesia, University of Toronto, St. Michael's Hospital, 30 Bond Street, Toronto, Ontario M5B 1W8.

INTRODUCTION

Cerebral hypoxia may be responsible for the cognitive impairment observed with acute and chronic anemia in humans ^1–2. This study tests the hypothesis that severe acute normotensive normovolemic anemia causes cerebral hypoxia in vivo.

METHODS

Experiments were performed in concordance with the Animal Care and Use Committee. Anesthetized male Sprague Dawley rats (isoflurane 1-2%), were ventilated to maintain normoxia and normocapnia. Tail artery and jugular vein cannulae provided vascular access for hemodilution and measurement of mean arterial blood pressure (MAP). Bilateral burr holes were trephined at the level of the bregma, and brain temperature and oxygenation (P_BrO₂) probes (LICOX, GMS) were inserted 6-8 mm into the caudate nucleus using stereotaxic coordinates. A laser doppler flow probe (Transonic) measured contralateral cerebral blood flow (CBF). Hemoglobin concentrations were determined by co-oximetry (Radiometer). Anemia was induced by performing acute normovolemic hemodilution (ANH), simultaneously exchanging 30 ml.kg^-1 of blood with an equal volume of pentastarch (Dupont) over 10 minutes (n=7). Animals were monitored for another 40 minutes, prior to sacrifice by anaesthetic overdose. Controls did not undergo ANH (n=6). Comparisons between and within groups were performed using Wilcoxon rank sum and signed rank tests, respectively (mean ± SEM).

RESULTS

ANH reduced the hemoglobin concentration from 126.9 ± 7.2 to 51.0 ± 1.2 g.L^-1 (p<0.003). MAP did not change significantly from baseline (67.8 ± 2.6 mmHg), following ANH. Cerebral P_BrO₂ decreased from 17.3 ± 4.1 to a minimum of 14.4 ± 4.1 mmHg (p< 0.01), but returned to baseline 10 minutes after completion of ANH. The recovery of P_BrO₂ coincided with an increase in CBF from 39.5 ± 5.5 to 60.0 ± 7.0 ml.min^{- 1.}100 g^-1 after ANH (p< 0.001). No significant changes were observed in controls.

CONCLUSION

Induction of severe normotensive, normovolemic anemia caused a transient fall in cerebral oxygenation. Rapid return of P_BrO₂ to baseline was associated with a substantial increase in CBF, suggesting the existence of a highly efficient mechanism for protecting cerebral oxygen delivery. Preliminary RT-PCR data suggest that this increase in CBF may be mediated by neuronal nitric oxide synthase.

(Supported by the Canadian Anesthesiologists' Society, JP Bickell Foundation, PSI)

REFERENCES

1 Anesthesiology 92: 1646–52, 2000.[Medline]

2 Am J Kidney Dis 33:1122–30, 1999.[Medline]

This Article Full Text (PDF) Submit a scholarly reply Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Hare, G. M.T. Articles by Mazer, C. D. Search for Related Content PubMed Articles by Hare, G. M.T. Articles by Mazer, C. D.