Chronic cerebral intracellular alkalosis following forebrain ischemic insult in rats. | Zendy

Michael Chopp | Zendy; Annika Linde | Zendy; H Chen | Zendy; Robert A. Knight | Zendy; J.A. Helpern | Zendy; K.M.A. Welch | Zendy

AI Assistant Blog Pricing

Home ZAIA Blog

Open Access

Chronic cerebral intracellular alkalosis following forebrain ischemic insult in rats.

Author(s) -

Michael Chopp,

Annika Linde,

H Chen,

Robert A. Knight,

J.A. Helpern,

K.M.A. Welch

Publication year - 1990

Publication title -

stroke

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.397

H-Index - 319

eISSN - 1524-4628

pISSN - 0039-2499

DOI - 10.1161/01.str.21.3.463

Subject(s) - medicine , alkalosis , ischemia , forebrain , intracellular ph , anesthesia , in vivo , endocrinology , intracellular , cardiology , acidosis , central nervous system , biochemistry , biology , microbiology and biotechnology

We measured cerebral intracellular pH using in vivo phosphorus-31 nuclear magnetic resonance spectroscopy during 1 week after forebrain ischemia or sham operation in eight and seven rats, respectively. Mean maximum pH was significantly higher (p less than 0.003) in the ischemic group than in the sham-operated group (7.34 +/- 0.03 and 7.19 +/- 0.02, respectively). The difference between mean maximum pH and baseline pH (7.08 +/- 0.01 in each group) was significantly greater (p less than 0.02) in the ischemic group than in the sham-operated group. In the ischemic group, alkalosis occurred primarily after 48-72 hours of recirculation. We speculate that brain tissue alkalosis occurring chronically after ischemia is associated with delayed ischemic neuronal death.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.

Having issues? You can contact us here

Accelerating Research