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Local cerebral blood flow in spontaneously breathing rats subjected to graded isobaric hypoxia
Author(s) -
Dahlgren N.
Publication year - 1990
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1111/j.1399-6576.1990.tb03124.x
Subject(s) - medicine , isobaric process , hypoxia (environmental) , cerebral blood flow , anesthesia , breathing , cardiology , oxygen , chemistry , physics , organic chemistry , thermodynamics
Local cerebral blood flow (1‐CBF) was measured with an autoradiographic technique in spontaneously breathing rats exposed to air or gas mixtures of O 2 and N 2 , giving inspired oxygen fractions (Fio 2 ) ranging from 0.21 to 0.07. The arterial O 2 tension (Pao 2 ) changed from 10.9 0.3 (Fio 2 0.21) to 3.9 kPa (Fio 2 0.07) (82 2 to 29 mmHg). Hypoxia caused hyperventilation, and the arterial CO 2 tension (Paco 2 ) fell from 5.21 0.05 kPa (Fio 2 0.21) to 3.27 kPa (Fio 2 0.07) (39.1 0.4 to 24.5 mmHg). The hyperventilatory response was markedly augmented when changing Fio 2 from 0.13 to 0.11, causing a fall in Paco 2 of 0.75 kPa and a shift in arterial pH from 7.45 0.01 (Fio 2 0.13) to 7.54 0.01 (Fio 2 0.11). The 1‐CBF response to hypoxia was found to be biphasic for all the observed regions. At Fio 2 0.13, 1‐CBF was measured about 75% above control but at Fio 2 0.11, only 30% above control. A further reduction in Fio 2 to 0.07 caused a marked increase in 1‐CBF, at least 240% of control; however, the applied CBF technique did not admit quantitation. These results suggest that the mechanisms controlling the cerebrovascular response to hypoxia and changes in arterial CO 2 tensions are different. The results also indicate that hyperventilation might be harmful to the patient suffering from acute hypoxia.