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Reduced Nicotinamide Adenine Dinucleotide Fluorescence and Cortical Blood Flow in Ischemic and Nonischemic Squirrel Monkey Cortex. 2. Effects of Alterations in Arterial Carbon Dioxide Tension, Blood Pressure, and Blood Volume
Author(s) -
Thoralf M. Sundt,
Robert E. Anderson
Publication year - 1975
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.6.3.279
Subject(s) - hypercapnia , medicine , ischemia , cerebral blood flow , anesthesia , blood flow , nicotinamide adenine dinucleotide , blood pressure , cerebral cortex , cardiology , acidosis , nad+ kinase , biochemistry , chemistry , enzyme
The fluorescence of reduced nicotinamide adenine dinucleotide (NADH) from cerebral cortex was measured before, during, and after middle cerebral artery (MCA) occlusion and then at death of the animal. In normal cortex, NADH remained constant throughout a wide range of variations in blood pressure and Paco2. In ischemic cortex, NADH levels were higher in hypovolemic hypotensive animals than in normotensive normovolemic animals. Neither hypercapnia nor hypocapnia was effective in decreasing NADH in regions of ischemia, but the latter was associated with a degree of hypotension that interfered with interpretation of data. NADH returned to normal with restoration of flow, supporting the reversibility of this degree of ischemia. The high levels of NADH at death, compared to those during ischemia, are consistent with incomplete ischemia in this model of cerebral infarction.

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