Regional cerebral blood flow of acute carbon monoxide poisoning in cats

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.

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Regional cerebral blood flow measurements with Xenon-CT in the prediction of delayed encephalopathy after carbon monoxide intoxication

Acta Neurologica Scandinavica ◽

10.1111/j.1600-0404.1996.tb00536.x ◽

1996 ◽

Vol 93 ◽

pp. 22-27 ◽

Cited By ~ 13

Author(s):

M. Sesay ◽

A. M. Bidabé ◽

M. Guyot ◽

R. Bédry ◽

J. M. Caillé ◽

...

Keyword(s):

Carbon Monoxide ◽

Blood Flow ◽

Cerebral Blood Flow ◽

Regional Cerebral Blood Flow ◽

Regional Cerebral Blood ◽

Flow Measurements ◽

Xenon Ct ◽

Carbon Monoxide Intoxication ◽

Blood Flow Measurements ◽

Delayed Encephalopathy

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Regional cerebral blood flow in patients with carbon monoxide intoxication

Annals of Nuclear Medicine ◽

10.1007/s12149-012-0638-8 ◽

2012 ◽

Vol 26 (10) ◽

pp. 771-776 ◽

Cited By ~ 3

Author(s):

Yu-Yu Lu ◽

Shih-Chuan Tsai ◽

Chia-Hung Kao ◽

Wan-Yu Lin

Keyword(s):

Carbon Monoxide ◽

Blood Flow ◽

Cerebral Blood Flow ◽

Regional Cerebral Blood Flow ◽

Regional Cerebral Blood ◽

Carbon Monoxide Intoxication

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

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y75-089 ◽

1975 ◽

Vol 53 (4) ◽

pp. 644-650 ◽

Cited By ~ 17

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.

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