TY - JOUR
T1 - Regional response of cerebral blood volume to graded hypoxic hypoxia in rat brain
AU - Julien-Dolbec, C.
AU - Tropres, I.
AU - Montigon, O.
AU - Reutenauer, H.
AU - Ziegler, A.
AU - Decorps, M.
AU - Payen, J. F.
N1 - Funding Information:
This study was supported by a grant from the the DAAD/HSP II program, RhoÃnes-Alpes Region and the Ligue Nationale contre le Cancer. AMI-227 was kindly provided by Guerbet Laboratories. The authors thank Jonathan Coles and Raymond Koehler for helpful comments on the manuscript.
PY - 2002
Y1 - 2002
N2 - Background. The response of cerebral blood flow to hypoxic hypoxia is usually effected by dilation of cerebral arterioles. However, the resulting changes in cerebral blood volume (CBV) have received little attention. We have determined, using susceptibility contrast magnetic resonance imaging (MRI), changes in regional CBV induced by graded hypoxic hypoxia. Methods. Six anaesthetized rats were subjected to incremental reduction in the fraction of inspired oxygen: 0.35, 0.25, 0.15, and 0.12. At each episode, CBV was determined in five regions of each hemisphere after injection of a contrast agent: superficial and deep neocortex, striatum, corpus callosum and cerebellum. A control group (n=6 rats) was studied with the same protocol without contrast agent, to determine blood oxygenation level dependent (BOLD) contribution to the MRI changes. Results. Each brain region exhibited a significant graded increase in CBV during the two hypoxic episodes: 10-27% of control values at 70% SaO2, and 26-38% at 55% SaO2. There was no difference between regions in their response to hypoxia. The mean CBV of all regions increased from 3.6 (SD 0.6) to 4.1 (0.6) ml (100 g)-1 and to 4.7 (0.7) ml (100 g)-1 during the two hypoxic episodes, respectively (Scheffé F-test; P<0.01). Over this range, CBV was inversely proportional to SaO2 (r2=0.80). In the absence of the contrast agent, changes due to the BOLD effect were negligible. Conclusions. These findings imply that hypoxic hypoxia significantly raises CBV in different brain areas, in proportion to the severity of the insult. These results support the notion that the vasodilatory effect of hypoxia is deleterious in patients with reduced intracranial compliance.
AB - Background. The response of cerebral blood flow to hypoxic hypoxia is usually effected by dilation of cerebral arterioles. However, the resulting changes in cerebral blood volume (CBV) have received little attention. We have determined, using susceptibility contrast magnetic resonance imaging (MRI), changes in regional CBV induced by graded hypoxic hypoxia. Methods. Six anaesthetized rats were subjected to incremental reduction in the fraction of inspired oxygen: 0.35, 0.25, 0.15, and 0.12. At each episode, CBV was determined in five regions of each hemisphere after injection of a contrast agent: superficial and deep neocortex, striatum, corpus callosum and cerebellum. A control group (n=6 rats) was studied with the same protocol without contrast agent, to determine blood oxygenation level dependent (BOLD) contribution to the MRI changes. Results. Each brain region exhibited a significant graded increase in CBV during the two hypoxic episodes: 10-27% of control values at 70% SaO2, and 26-38% at 55% SaO2. There was no difference between regions in their response to hypoxia. The mean CBV of all regions increased from 3.6 (SD 0.6) to 4.1 (0.6) ml (100 g)-1 and to 4.7 (0.7) ml (100 g)-1 during the two hypoxic episodes, respectively (Scheffé F-test; P<0.01). Over this range, CBV was inversely proportional to SaO2 (r2=0.80). In the absence of the contrast agent, changes due to the BOLD effect were negligible. Conclusions. These findings imply that hypoxic hypoxia significantly raises CBV in different brain areas, in proportion to the severity of the insult. These results support the notion that the vasodilatory effect of hypoxia is deleterious in patients with reduced intracranial compliance.
KW - Blood, volume, cerebral
KW - Brain, magnetic resonance imaging
KW - Complications, hypoxia
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U2 - 10.1093/bja/aef182
DO - 10.1093/bja/aef182
M3 - Article
C2 - 12378669
AN - SCOPUS:0035993509
SN - 0007-0912
VL - 89
SP - 287
EP - 293
JO - British Journal of Anaesthesia
JF - British Journal of Anaesthesia
IS - 2
ER -