Extracellular pH, Potassium, and Calcium Activities in Progressive Ischaemia of Rat Cortex
Author(s) -
Robert J. Harris,
L. Symon
Publication year - 1984
Publication title -
journal of cerebral blood flow and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.167
H-Index - 193
eISSN - 1559-7016
pISSN - 0271-678X
DOI - 10.1038/jcbfm.1984.26
Subject(s) - extracellular , calcium , occlusion , anesthesia , ischemia , potassium , chemistry , cerebral blood flow , medicine , halothane , extracellular fluid , endocrinology , acidosis , anatomy , biochemistry , organic chemistry
We measured the relationships between changes in extracellular pH (pH e ), potassium (K e ), and calcium (Ca e ) activities and DC potential (DC e ) in progressive ischaemia of rat cerebral cortex. pH e and K e , or Ca e and K e , were measured at the same point simultaneously, using triple-barrelled, double-ion-sensitive microelectrodes. Ischaemia was produced using bilateral carotid artery occlusion and hypotension in rats under 50% N 2 O-0.4% halothane anaesthesia. Unilateral carotid artery occlusion did not affect blood flow, but bilateral occlusion reduced flow to ∼40% of normal. Autoregulation of blood pressure (BP) changes was lost after bilateral occlusion, and so progressive hypotension produced a linear decrease in flow. pH e began to decrease at high levels of flow (30–35 ml 100 g −1 min −1 ) and showed stepwise acidotic shifs with reductions in BP. K e was affected at flows of ∼15 ml 100 g −1 min −1 , during which time it was critically dependent on BP. When K e reached 6 m M, it increased rapidly to 40 m M and was associated with a negative shift in DC e . When K e reached ∼10 m M, Ca e decreased rapidly to ∼0.1 m M. pH e had reached 6.87 when K e increased rapidly and showed a transient alkalotic shift of ∼0.14 units at that time. Possible mechanisms for the sequence of ion changes described are discussed.
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