Critical oxygen tension in rat brain:: a combined 31P-NMR and EPR oximetry study

被引:69
作者
Rolett, EL
Azzawi, A
Liu, KJ
Yongbi, MN
Swartz, HM
Dunn, JF
机构
[1] Dartmouth Hitchcock Med Ctr, Nucl Magnet Resonance Res Ctr, Dept Med, Hanover, NH 03755 USA
[2] Dartmouth Hitchcock Med Ctr, Electron Paramagnet Resonance Res Ctr, Dept Med, Hanover, NH 03755 USA
[3] Dartmouth Hitchcock Med Ctr, Nucl Magnet Resonance Res Ctr, Dept Radiol, Hanover, NH 03755 USA
[4] Dartmouth Hitchcock Med Ctr, Electron Paramagnet Resonance Res Ctr, Dept Radiol, Hanover, NH 03755 USA
关键词
hypoxia; electron paramagnetic resonance; nuclear magnetic resonance spectroscopy; energy metabolism; pH;
D O I
10.1152/ajpregu.2000.279.1.R9
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
The relationship between cerebral interstitial oxygen tension (Pt-O2) and cellular energetics was investigated in mechanically ventilated, anesthetized rats during progressive acute hypoxia to determine whether there is a "critical" brain Pt-O2 for maintaining steady-state aerobic metabolism. Cerebral Pt-O2, measured by electron paramagnetic resonance oximetry, decreased proportionately to inspired oxygen fraction. P-31-nuclear magnetic resonance measurements revealed no changes in P-i, phosphocreatine (PCr)/P-i ratio, or intracellular pH when arterial blood oxygen tension (Pa-O2) was reduced from 145.1 +/- 11.7 to 56.5 +/- 4.4 mmHg (means +/- SE). Intracellular acidosis, a sharp rise in P-i, and a decline in the PCr/P-i ratio developed when Pa-O2 was reduced further to 40.7 +/- 2.3 mmHg. The corresponding Pt-O2 values were 15.1 +/- 1.8, 8.8 +/- 0.4, and 6.8 +/- 0.3 mmHg. We conclude that over a range of decreasing oxygen tensions, cerebral oxidative metabolism is not sensitive to oxygen concentration. Oxygen becomes a regulatory substrate, however, when Pt-O2 is decreased to a critical level.
引用
收藏
页码:R9 / R16
页数:8
相关论文
共 50 条
[1]   AMELIORATION OF HYPOXIA-INDUCED LACTIC-ACIDOSIS BY SUPERIMPOSED HYPERCAPNIA OR HYDROCHLORIC-ACID INFUSION [J].
ABUROMEH, S ;
TANNEN, RL .
AMERICAN JOURNAL OF PHYSIOLOGY, 1986, 250 (04) :F702-F709
[2]   MAPPING OF METABOLITES IN WHOLE ANIMALS BY P-31 NMR USING SURFACE COILS [J].
ACKERMAN, JJH ;
GROVE, TH ;
WONG, GG ;
GADIAN, DG ;
RADDA, GK .
NATURE, 1980, 283 (5743) :167-170
[3]   CEREBRAL PHARMACODYNAMICS OF ANESTHETIC AND SUBANAESTHETIC DOSES OF KETAMINE IN THE NORMOVENTILATED PIG [J].
AKESON, J ;
BJORKMAN, S ;
MESSETER, K ;
ROSEN, I ;
HELFER, M .
ACTA ANAESTHESIOLOGICA SCANDINAVICA, 1993, 37 (02) :211-218
[4]   BRAIN METABOLISM AND BLOOD-FLOW IN ACUTE CEREBRAL HYPOXIA STUDIED BY NMR-SPECTROSCOPY AND HYDROGEN CLEARANCE [J].
ALLEN, K ;
BUSZA, AL ;
CROCKARD, HA ;
GADIAN, DG .
NMR IN BIOMEDICINE, 1992, 5 (01) :48-52
[5]  
ANDERSON M L, 1990, Neurological Research, V12, P195
[6]   EFFECT OF CHEMODENERVATION ON THE CEREBRAL VASCULAR AND MICROVASCULAR RESPONSE TO HYPOXIA [J].
ANWAR, M ;
KISSEN, I ;
WEISS, HR .
CIRCULATION RESEARCH, 1990, 67 (06) :1365-1373
[7]   MECHANISMS ACTIVATING GLYCOLYSIS IN BRAIN IN ARTERIAL HYPOXIA [J].
BACHELARD, HS ;
LEWIS, LD ;
PONTEN, U ;
SIESJO, BK .
JOURNAL OF NEUROCHEMISTRY, 1974, 22 (03) :395-401
[8]   IMPROVED RENAL CORTICAL TUBULE SUSPENSION - SPECTROPHOTOMETRIC STUDY OF O2 DELIVERY [J].
BALABAN, RS ;
SOLTOFF, SP ;
STOREY, JM ;
MANDEL, LJ .
AMERICAN JOURNAL OF PHYSIOLOGY, 1980, 238 (01) :F50-F59
[9]   GLYCEROL 3-PHOSPHATE AND LACTATE AS INDICATORS OF THE CEREBRAL CYTOPLASMIC REDOX STATE IN SEVERE AND MILD HYPOXIA RESPECTIVELY - A C-13-NMR AND P-31-NMR STUDY [J].
BENYOSEPH, O ;
BADARGOFFER, RS ;
MORRIS, PG ;
BACHELARD, HS .
BIOCHEMICAL JOURNAL, 1993, 291 :915-919
[10]   HYPOXIA INCREASES VELOCITY OF BLOOD-FLOW THROUGH PARENCHYMAL MICROVASCULAR SYSTEMS IN RAT-BRAIN [J].
BERECZKI, D ;
WEI, L ;
OTSUKA, T ;
ACUFF, V ;
PETTIGREW, K ;
PATLAK, C ;
FENSTERMACHER, J .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1993, 13 (03) :475-486