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J Physiol Volume 538, Number 3, 975-983, February 1, 2002 DOI: 10.1113/jphysiol.2001.013230
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Journal of Physiology (2002), 538.3, pp. 975-983
© Copyright 2002 The Physiological Society
DOI: 10.1113/jphysiol.2001.013230

Regional brain blood flow and cerebral hemispheric oxygen consumption during acute hypoxaemia in the llama fetus

Aníbal J. Llanos *†, Raquel A. Riquelme ‡, Emilia M. Sanhueza *, Emilio Herrera *, Gertrudis Cabello §, Dino A. Giussani || and Julian T. Parer ¶

* Laboratorio de Fisiología y Fisiopatología del Desarrollo, Programa de Fisiopatología, Instituto de Ciencias Biomédicas (ICBM), Facultad de Medicina, Universidad de Chile, Santiago, Chile, † Centro Internacional de Estudios Andinos (INCAS), Universidad de Chile, Santiago, Chile, ‡ Departamento de Bioquímica y Biología Molecular, Facultad de Ciencias Químicas y Farmacéuticas, Universidad de Chile, Santiago, Chile, § Departamento de Biología y Salud, Facultad de Ciencias, Unive rsidad de Tarapacá, Arica, Chile, || Department of Physiology, University of Cambridge, Cambridge CB2 3EG, UK and Department of Obstetrics, Gynaecology and Reproductive Sciences and Cardiovascular Research Institute, University of California, San Francisco, USA

Unlike fetal animals of lowland species, the llama fetus does not increase its cerebral blood flow during an episode of acute hypoxaemia. This study tested the hypothesis that the fetal llama brain maintains cerebral hemispheric O2 consumption by increasing cerebral O2 extraction rather than decreasing cerebral oxygen utilisation during acute hypoxaemia. Six llama fetuses were surgically instrumented under general anaesthesia at 217 days of gestation (term ca 350 days) with vascular and amniotic catheters in order to carry out cardiorespiratory studies. Following a control period of 1 h, the llama fetuses underwent 3 times 20 min episodes of progressive hypoxaemia, induced by maternal inhalational hypoxia. During basal conditions and during each of the 20 min of hypoxaemia, fetal cerebral blood flow was measured with radioactive microspheres, cerebral oxygen extraction was calculated, and fetal cerebral hemispheric O2 consumption was determined by the modified Fick principle. During hypoxaemia, fetal arterial O2 tension and fetal pH decreased progressively from 24 ± 1 to 20 ± 1 Torr and from 7.36 ± 0.01 to 7.33 ± 0.01, respectively, during the first 20 min episode, to 16 ± 1 Torr and 7.25 ± 0.05 during the second 20 min episode and to 14 ± 1 Torr and 7.21 ± 0.04 during the final 20 min episode. Fetal arterial partial pressure of CO2 (Pa,CO2, 42 ± 2 Torr) remained unaltered from baseline throughout the experiment. Fetal cerebral hemispheric blood flow and cerebral hemispheric oxygen extraction were unaltered from baseline during progressive hypoxaemia. In contrast, a progressive fall in fetal cerebral hemispheric oxygen consumption occurred during the hypoxaemic challenge. In conclusion, these data do not support the hypothesis that the fetal llama brain maintains cerebral hemispheric O2 consumption by increasing cerebral hemispheric O2 extraction. Rather, the data show that in the llama fetus, a reduction in cerebral hemispheric metabolism occurs during acute hypoxaemia.



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