EFFECTS OF HYPERCAPNIA ON ECOG AND OXIDATIVE-METABOLISM IN NEONATAL DOG BRAIN

被引：5

作者：

YOSHIOKA, H ^{[1
]}

MIYAKE, H ^{[1
]}

SMITH, DS ^{[1
]}

CHANCE, B ^{[1
]}

SAWADA, T ^{[1
]}

NIOKA, S ^{[1
]}

机构：

[1] UNIV PENN,SCH MED,DEPT BIOCHEM BIOPHYS,PHILADELPHIA,PA 19104

来源：

JOURNAL OF APPLIED PHYSIOLOGY | 1995年 / 78卷 / 06期

关键词：

ACIDOSIS; MICHAELIS-MENTEN CONSTANT; MAXIMAL REACTION VELOCITY; P-31-MAGNETIC RESONANCE SPECTROSCOPY; PHOSPHORYLATION POTENTIAL; ELECTROCORTICOGRAM;

D O I：

10.1152/jappl.1995.78.6.2272

中图分类号：

Q4 [生理学];

学科分类号：

071003 ;

摘要：

The effects of hypercapnia on cerebral electrical activity and mitochondrial oxidative phosphorylation were studied in the anesthetized neonatal dog by using the electrocorticogram (ECoG) and P-31-magnetic resonance spectroscopy. Three levels of hypercapnia with arterial Pco(2) values of similar to 70, 100, and 140 Torr reduced the intracellular pH of the brain from 7.11 to 6.99, 6.87, and 6.76, respectively. These levels of hypercapnia also reduced ADP concentration ([ADP]) from 21.5 to 18.1, 14.8, and 12.9 mu M as well as the average ECoG power output by 20, 30, and 40%. A Michaelis-Menten relationship for the mitochondrial respiratory enzymes was fitted with [ADP] and the change in the average ECoG. The result suggests that mitochondrial respiration is regulated by [ADP] and that the in vivo Michaelis-Menten constant for ADP was 21 mu M, a value close to the in vitro value. The mitochondrial maximal reaction velocity was reduced by only 10% during hypercapnia and showed no relationship with the degree of acidosis, suggesting that mitochondrial respiratory enzymes are not responsible for the inhibition of the brain electrical activity.

引用

页码：2272 / 2278

页数：7