Regional cerebral blood flow of acute carbon monoxide poisoning in cats

1987 ◽  
Vol 72 (4) ◽  
pp. 389-393 ◽  
Author(s):  
R. Okeda ◽  
T. Matsuo ◽  
T. Kuroiwa ◽  
M. Nakai ◽  
T. Tajima ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Regional Cerebral Blood Flow ◽  
Carbon Monoxide Poisoning ◽  
Regional Cerebral Blood ◽  
Acute Carbon Monoxide Poisoning

Effect of hypoxia and hypercapnia on neurohypophyseal blood flow

1986 ◽  
Vol 250 (1) ◽  
pp. H7-H15
Author(s):  
D. F. Hanley ◽  
D. A. Wilson ◽  
R. J. Traystman
Keyword(s):  
Blood Pressure ◽  
Carbon Monoxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Regional Cerebral Blood Flow ◽  
Brain Regions ◽  
Regulatory Mechanisms ◽  
Similar Increase ◽  
Regional Cerebral Blood ◽  
Pressure Controlled

Neurohypophyseal blood flow responses to hypoxia and hypercapnia were studied in pentobarbital anesthetized, paralyzed dogs. Arterial O2 content was lowered from control (18 +/- 2 vol%) to 8 +/- 1 vol% by either decreasing O2 tension (hypoxic hypoxia, HH) or by increasing carboxyhemoglobin saturation (carbon monoxide hypoxia, COH) at normal O2 tension. In all animals HH and COH resulted in similar increases in total cerebral blood flow (239 and 300%, respectively). Regional cerebral blood flow showed a similar increase for all brain regions except the neurohypophysis (NH). The NH increased its blood flow with HH (approximately 320% of control) but was unchanged with COH (117% of control). The responsiveness of NH blood vessels was tested under conditions of hypercapnia (10% CO2) and HH with blood pressure controlled by concurrent hemorrhage. The response of NH vessels to altered arterial O2 tension occurs independently of blood pressure. Systemic [H+] or CO2 tension produce only small changes in NH blood flow. These data suggest that hypoxic and hypercapnic regulatory mechanisms for the NH are different from those of other brain regions. The precise mechanism by which the NH hypoxic response occurs remains unclear, but our data suggest an important role for systemic arterial O2 tension and chemoreceptors.

Regional Cerebral Blood Flow of the Rat in Acute Carbon Monoxide Intoxication

1975 ◽  
Vol 53 (4) ◽  
pp. 644-650 ◽  
Author(s):  
V. MacMillan
Keyword(s):  
Carbon Monoxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Regional Cerebral Blood Flow ◽  
Energy State ◽  
Principal Factor ◽  
Co Poisoning ◽  
Regional Cerebral Blood ◽  
Co Intoxication ◽  
Cortical Cerebral Blood Flow

The effect of carbon monoxide (CO) on the regional cerebral blood flow was studied by exposing lightly anesthetized rats for 30 min to 0.5, 1.0, 1.5, and 2.0% CO gas mixtures. Cortical cerebral blood flow (CBF) increases of near 200%, 300%, and 400% control were observed at 0.5, 1.0, and 1.5% CO, respectively; whereas at 2.0% CO a reversal of the CBF increase was observed with values declining to near 300% control. The CBF response of subcortical, cerebellar, and brain stem areas was quantitatively similar to that of cortex, indicating that the CBF changes in CO intoxication are general. The decrease in CBF at 2.0% CO was related to significant decreases in arterial CO2 tension. Comparison of the CBF data to previous metabolic results in CO poisoning suggests that the CBF increases are a principal factor in the maintenance of an intact energy state in CO poisoning.

Regional cerebral blood flow in schizophrenia while performing an attention task

2014 ◽  
Author(s):  
Scott Harcourt ◽  
Daniel G. Amen ◽  
Kristin C. Willeumier ◽  
Charles J. Golden
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Regional Cerebral Blood Flow ◽  
Regional Cerebral Blood ◽  
Attention Task
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