Cerebral circulation and norepinephrine: relevance of the blood-brain barrier

1976 ◽  
Vol 231 (2) ◽  
pp. 483-488 ◽  
Author(s):  
ET MacKenzie ◽  
J McCulloch ◽  
M O'Kean ◽  
JD Pickard ◽  
AM Harper
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Oxygen Consumption ◽  
Glucose Uptake ◽  
Blood Brain Barrier ◽  
Cerebral Circulation ◽  
Brain Barrier ◽  
Cerebral Oxygen ◽  
Blood Brain ◽  
Cerebral Oxygen Consumption

The systemic administration of norepinephrine has minimal effects on the cerebral circulation, perhaps due to blood-brain barrier mechanisms. To test hypothesis, the cerebrovascular effects of norepinephrine beyond the blood-brain barrier were studied in anesthetized baboons, Intraventricular norepinephrine (40 mug/kg) resulted in significant increases in cerebral blood flow (40%), cerebral oxygen consumption (21%), and cerebral glucose uptake (153%). Intracarotid hypertonic urea opens the blood-brain barrier by osmotic disruption; Consequent to hypertonic urea, the intracarotid infusion of norepinephrine, 50 ng/kg-min, significantly increase cerebral blood flow (49%), cerebral oxygen consumption (21%), and cerebral glucose uptake (76%), It appears probable that the cerebrovascular responses to norepinephrine are dependent on the integrity of the blood-brain barrier; It is likely that the increase in cerebral blood flow, associated with norepinephrine when it bypasses the barrier, is secondary to an increase in cerebral metabolism.

Cerebral circulatory and metabolic effects of vasoactive intestinal polypeptide

1980 ◽  
Vol 238 (4) ◽  
pp. H449-H456 ◽  
Author(s):  
J. McCulloch ◽  
L. Edvinsson
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Oxygen Consumption ◽  
Blood Brain Barrier ◽  
Vasoactive Intestinal Polypeptide ◽  
Brain Barrier ◽  
Cerebral Oxygen ◽  
Blood Brain ◽  
Cerebral Oxygen Consumption ◽  
Intestinal Polypeptide

Two aspects of the action of vasoactive intestinal polypeptide (VIP) within the cerebral vascular bed have been examined. First, in anesthetized rats, the vasomotor responses of individual pial arterioles on the convexity of cerebral cortex to the perivascular microinjection of vasoactive intestinal polypeptide were examined and, second, in anesthetized baboons, the effects of VIP on cerebral blood flow, cerebral oxygen consumption, and the electroencephalogram (EEG) were investigated both prior to and following the osmotic opening of the blood-brain barrier. The perivascular microinjection of VIP resulted in statistically significant increase in arteriolar caliber in the concentration range 10(-9) to 10(-6) M. For example, arteriolar caliber was increased by 22 +/- 3% (mean +/- SE) following the injection of VIP (10(-8) M). In the second series, in baboons, the intracarotid infusion of vasoactive intestinal polypeptide (10(-11) mol/min) did not affect cerebral blood flow, cerebral oxygen consumption, or the EEG under normal circumstances. If the same concentration of vasoactive intestinal polypeptide was administered following hypertonic opening of the blood-brain barrier, cerebral blood flow and oxygen consumption were both elevated (by 37 +/- 7% and 28 +/- 10%, respectively), accompanied by increased EEG activity.

Influence of endogenous norepinephrine on cerebral blood flow and metabolism

1976 ◽  
Vol 231 (2) ◽  
pp. 489-494 ◽  
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.

Time courses of changes in cerebral blood flow and blood-brain barrier integrity by focal proton radiation in the rat

1996 ◽  
Vol 18 (1) ◽  
pp. 83-86 ◽  
Author(s):  
Hiroki Namba ◽  
Toshiaki Irie ◽  
Kiyoshi Fukushi ◽  
Masaomi lyo ◽  
Takahiro Hashimoto ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Proton Radiation ◽  
Barrier Integrity ◽  
Blood Brain ◽  
Time Courses ◽  
Blood Brain Barrier Integrity

Cerebral Blood Flow and Cerebral Oxygen Consumption during Nitroprusside-induced Hypotension to Less than 50 mmHg

1989 ◽  
Vol 70 (2) ◽  
pp. 255-260 ◽  
Author(s):  
Michel Pinaud ◽  
Réml Souron ◽  
Jean-Noël Lelausque ◽  
Marie-France Gazeau ◽  
Youenn Lajat ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Oxygen Consumption ◽  
Cerebral Oxygen ◽  
Induced Hypotension ◽  
Cerebral Oxygen Consumption

scholarly journals Effect of the Calcium Antagonist, Nimodipine, on Cerebral Blood Flow and Metabolism in the Primate

1981 ◽  
Vol 1 (3) ◽  
pp. 349-356 ◽  
Author(s):  
A. M. Harper ◽  
L. Craigen ◽  
S. Kazda
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Calcium Antagonist ◽  
Arterial Blood Pressure ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Arterial Blood ◽  
Blood Brain ◽  
Significant Change

The effect of the calcium antagonist nimodipine was tested in anaesthetised primates. A rapid intravenous injection of 3 or 10 μg kg−1 produced a transient rise in end-tidal Pco2 and a fall in arterial blood pressure, but 10 min after the injection there was no significant change in CBF. A continuous intravenous infusion of 2 μg kg−1 min−1 caused a modest fall in mean arterial blood pressure and an increase in cerebral blood flow (CBF), which gradually increased to 27% above control after 50 min infusion. There was no significant change in CMRO2. A continuous intracarotid infusion of 0.67 μg kg−1 min−1 caused an increase in CBF of between 46 and 57%. This was further increased to 87% above control after disruption of the blood-brain barrier with hyperosmolar urea. Thirty minutes after the urea, the CBF returned to 43% above control. Twenty minutes after the infusion of nimodipine had been stopped, the CBF had returned to control values. EEG studies in this group showed no obvious increase in electrocortical activity. This evidence suggests that nimodipine has no effect on cerebral metabolism but increases CBF, particularly after disruption of the blood-brain barrier.

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