Cerebral Circulation Time and Cerebral Blood Flow

To determine 1) the effect of arterial CO2 change on the neonatal cerebral circulation and 2) whether 100% O2 would produce significant decrease in cerebral blood flow (CBF), we studied 24 preterm infants to explain the late (5 min) hyperventilation observed in them during hyperoxia. Of these, 12 were studied before and during inhalation of 2-3% CO2 and 12 before and during the inhalation of 100% O2. We measured CBF by a modification of the venous occlusion plethysmography technique and found that CBF increased 7.8% per Torr alveolar carbon dioxide pressure change and that it decreased 15% with 100% O2. These findings suggest that 1) CO2 is an important regulator of CBF in the perterm infant, 2) CBF-CO2 sensitivity in these infants may be greater than in adult subjects, 3) 100% O2 reduced CBF significantly, and 4) a decrease in CBF during administration of 100% O2 may be at least partially responsible for the increase in ventilation with hyperoxia.

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Prolonged Cerebral Circulation Time Is the Best Parameter for Predicting Vasospasm during Initial CT Perfusion in Subarachnoid Hemorrhagic Patients

PLoS ONE ◽

10.1371/journal.pone.0151772 ◽

2016 ◽

Vol 11 (3) ◽

pp. e0151772 ◽

Cited By ~ 9

Author(s):

Chun Fu Lin ◽

Sanford P. C. Hsu ◽

Chung Jung Lin ◽

Wan Yuo Guo ◽

Chih Hsiang Liao ◽

...

Keyword(s):

Cerebral Circulation ◽

Ct Perfusion ◽

Circulation Time ◽

Best Parameter ◽

Cerebral Circulation Time

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Influence of endogenous norepinephrine on cerebral blood flow and metabolism

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1976.231.2.489 ◽

1976 ◽

Vol 231 (2) ◽

pp. 489-494 ◽

Cited By ~ 112

Author(s):

ET MacKenzie ◽

J McCulloch ◽

AM Harper

Keyword(s):

Blood Flow ◽

Cerebral Blood Flow ◽

Oxygen Consumption ◽

Glucose Uptake ◽

Cerebral Circulation ◽

Brain Metabolism ◽

Cerebral Metabolism ◽

Cerebral Oxygen ◽

Brain Norepinephrine ◽

Cerebral Oxygen Consumption

The influence of brain norepinephrine on cerebral metabolism and blood flow was examined because exogenous norepinephrine, administered in a way that the blood-brain barrier is bypassed, has been shown to effect pronounced changes in the cerebral circulation. Reserpine (40 mug/kg, by intracarotid infusion) was administered in order to release brain norepinephrine in five anesthetized baboons. Reserpine significantly increased cerebral oxygen consumption (23%) and cerebral blood flow (50%). This response lasted for approximately 60 min. In a further five animals, effects of central beta-adrenoreceptor blockade were studied. Pro pranolol (12 mug/kg-min) produced an immediate, significant reduction in both cerebral oxygen consumption (40%) and cerebral glucose uptake (39%). Cerebral blood flow was reduced minimally. However, the responsiveness of the cerebral circulation to induced hypercapnia was severely attenuated from a gradient of 3.22 before, to 1,11 after, administration. These experiments suggest that central norepinephrine can influence the cerebral circulation primarily through noradrenergic effects on brain metabolism.

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