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.

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.

scholarly journals Cerebral Blood Flow and Metabolism in Pernicious Anemia

Blood ◽  
1951 ◽  
Vol 6 (3) ◽  
pp. 213-227 ◽  
Author(s):  
PERITZ SCHEINBERG
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Oxygen Consumption ◽  
Pernicious Anemia ◽  
Vascular Resistance ◽  
Cerebral Metabolism ◽  
Glucose Consumption ◽  
Moderate Increase ◽  
Cerebral Oxygen ◽  
Cerebral Oxygen Consumption

Abstract 1. Cerebral blood flow and metabolism were measured in 16 patients with pernicious anemia. Seven of the patients were restudied in various stages of therapy. 2. The patients fell into two equal groups, those with severe anemia and those with moderate or no anemia. In the first group, cerebral blood flow was increased and cerebral vascular resistance decreased; in the second group, cerebal blood flow was decreased and vascular resistance increased. In both groups, cerebral oxygen and glucose consumption was decreased, as was cerebral venous oxygen tension . 3. There was a good correlation between the mental status defects and cerebral oxygen consumption and between severity of neurologic involvement and cerebral oxygen consumption. There was no correlation between cerebro-vascular resistance and cerebral oxygen consumption, nor between degree of anemia and cerebral oxygen consumption. 4. Specific therapy resulted in a moderate increase in cerebral oxygen consumption and cerebro-vascular resistance. In no instance did cerebral oxygen consumption become normal. 5. The disparity between the functional ability of the patients and the low values for cerebral metabolism is discussed. 6. It is concluded that pernicious anemia results in specific nervous system involvement not related to the anemia, and that this damage is at least partially irreversible in many patients.

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 Effects of Indomethacin on Cerebral Blood Flow and Oxygen Consumption in Barbiturate-Anesthetized Normocapnic and Hypercapnic Rats

1981 ◽  
Vol 1 (1) ◽  
pp. 109-115 ◽  
Author(s):  
Nils Dahlgren ◽  
Bo K. Siesjö
Keyword(s):  
Blood Flow ◽  
Nitrous Oxide ◽  
Cerebral Blood Flow ◽  
Oxygen Consumption ◽  
Fatty Acid ◽  
Cerebral Oxygen ◽  
Similar Technique ◽  
Cerebral Oxygen Consumption

Although results obtained in baboons and rats have demonstrated that the fatty acid cyclo-oxygenase inhibitor indomethacin reduces cerebral blood flow (CBF) under control conditions and markedly attenuates the CBF response to hypercapnia, nonconfirmatory results have been obtained in rabbits and cats. Since these latter studies were carried out under barbiturate anesthesia, we tested the effect of indomethacin (10 mg kg−1) on CBF and cerebral oxygen consumption in rats anesthetized with 150 mg kg−1 of phenobarbital. At normocapnia the barbiturate reduced CBF, measured with a 133Xe modification of the Kety-Schmidt technique, to about 50% of nitrous oxide control values as previously determined with a similar technique. At this CBF level, indomethacin induced a small, albeit highly significant decrease in CBF. We suggest that a reduction of this magnitude will escape detection with some CBF techniques in current use. Indomethacin induced a highly significant decrease in CBF during hypercapnia, demonstrating that the barbiturate does not eliminate the effect of indomethacin on CO2 responsiveness. The magnitude of the reduction in CO2 response was so large that it should be detected with most methods for measuring CBF. A comparison with previous data on animals under 70% N2O demonstrated that phenobarbital reduced the CO2 responsiveness, defined as the ratio ΔCBF/ΔPco2, to 39% of that observed under nitrous oxide analgesia. With both types of anesthesia, indomethacin curtailed the CO2 responsiveness 4- to 5-fold.

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