TY - JOUR
T1 - Blood flow and ionic responses in the awake brain due to carbon monoxide
AU - Mendelman, Avivit
AU - Zarchin, Nili
AU - Meilin, Sigal
AU - Guggenheimer-Furman, Esther
AU - Thom, S. R.
AU - Mayevsky, Avraham
PY - 2002/12
Y1 - 2002/12
N2 - This study examined the effect of 2000 ppm CO on the brain of an awake rat. Measurements of regional perfusion as well as metabolic, ionic and electrical activities were used to examine whether mechanisms responsible for changes in brain perfusion were separable from those attributable to compromises in neuronal metabolism. Exposure to 2000 ppm CO resulted in elevation of cerebral blood flow. The stability of mitochondrial NADH redox level during CO exposure indicated that tissue hypoxia did not develop. The elevation in blood flow was inhibited by L-nitroarginine methyl ester, indicating that nitric oxide was responsible for the CO-induced elevation in blood flow. Exposure to 2000 ppm CO also triggered a significant decrease in pH and rise in extracellular potassium ion, possibly due to ion-pump inhibition. The amplitude of the electrocorticogram wave activity decreased, indicative of a compromise to physiological activity. These changes were not observed in rats anesthetized with pentobarbital during CO exposure, although anesthesia had no effect on the CO-induced elevation in blood flow and there was still no change in mitochondrial NADH redox level. We concluded that CO acts by separate mechanisms to alter cerebral vasoactivity and neuronal metabolic responses and that both processes are independent of hypoxic stress.
AB - This study examined the effect of 2000 ppm CO on the brain of an awake rat. Measurements of regional perfusion as well as metabolic, ionic and electrical activities were used to examine whether mechanisms responsible for changes in brain perfusion were separable from those attributable to compromises in neuronal metabolism. Exposure to 2000 ppm CO resulted in elevation of cerebral blood flow. The stability of mitochondrial NADH redox level during CO exposure indicated that tissue hypoxia did not develop. The elevation in blood flow was inhibited by L-nitroarginine methyl ester, indicating that nitric oxide was responsible for the CO-induced elevation in blood flow. Exposure to 2000 ppm CO also triggered a significant decrease in pH and rise in extracellular potassium ion, possibly due to ion-pump inhibition. The amplitude of the electrocorticogram wave activity decreased, indicative of a compromise to physiological activity. These changes were not observed in rats anesthetized with pentobarbital during CO exposure, although anesthesia had no effect on the CO-induced elevation in blood flow and there was still no change in mitochondrial NADH redox level. We concluded that CO acts by separate mechanisms to alter cerebral vasoactivity and neuronal metabolic responses and that both processes are independent of hypoxic stress.
KW - Brain electrical activity
KW - Carbon monoxide
KW - Cerebral blood flow
KW - Extracellular ions
KW - Mitochondrial redox state
UR - http://www.scopus.com/inward/record.url?scp=0036897611&partnerID=8YFLogxK
U2 - 10.1179/016164102101200861
DO - 10.1179/016164102101200861
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C2 - 12500698
AN - SCOPUS:0036897611
SN - 0161-6412
VL - 24
SP - 765
EP - 772
JO - Neurological Research
JF - Neurological Research
IS - 8
ER -