scholarly journals THE EFFECTS OF ACTIVE AND PASSIVE HYPERVENTILATION ON CEREBRAL BLOOD FLOW, CEREBRAL OXYGEN CONSUMPTION, CARDIAC OUTPUT, AND BLOOD PRESSURE OF NORMAL YOUNG MEN 1

1946 ◽  
Vol 25 (1) ◽  
pp. 107-119 ◽  
Author(s):  
Seymour S. Kety ◽  
Carl F. Schmidt
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Cerebral Blood Flow ◽  
Oxygen Consumption ◽  
Young Men ◽  
Cerebral Oxygen ◽  
Men 1 ◽  
Cerebral Oxygen Consumption

Cerebral blood flow is reduced by N omega-nitro-L-arginine methyl ester during delayed hypoperfusion in cats

1994 ◽  
Vol 267 (1) ◽  
pp. H174-H181
Author(s):  
N. Clavier ◽  
J. R. Kirsch ◽  
P. D. Hurn ◽  
R. J. Traystman
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Oxygen Consumption ◽  
Methyl Ester ◽  
Cerebral Oxygen ◽  
Physiological Variables ◽  
Arterial Blood ◽  
Subclavian Artery Occlusion ◽  
Cerebral Oxygen Consumption

We tested the hypothesis that decreased tonic release of nitric oxide (NO) or a NO-containing compound, during postischemic delayed hypoperfusion, would result in an impaired response of cerebral blood flow (CBF) to NO synthase inhibition. We measured CBF (microspheres), cerebral oxygen consumption, and physiological variables in 30 halothane-anesthetized cats. In 12 animals, complete cerebral ischemia (verified by midischemic CBF measurement) was produced for 12 min by brachiocephalic and left subclavian artery occlusion with hemorrhagic hypotension (mean arterial blood pressure = 40 mmHg). Steady-state hypoperfusion was present by 120 min of reperfusion (30 +/- 4% of baseline). Nonischemic animals (n = 12) were submitted to the same surgical procedures and anesthetic duration. N omega-nitro-L-arginine methyl ester (L-NAME, 10 mg/kg iv) or saline was administered 160 min after baseline measurements, equivalent to 140 min of reperfusion for animals treated with ischemia (n = 6 in each group). Blood pressure was controlled (aortic ligature) so that there was no change following L-NAME administration both in the ischemic and nonischemic groups. L-NAME reduced CBF during reperfusion in ischemic animals (from 37 +/- 2 to 24 +/- 2 ml.min-1 x 100 g-1) and in nonischemic animals (from 122 +/- 15 to 68 +/- 8 ml.min-1 x 100 g-1) with no change in cerebral oxygen consumption. In six additional cats, administration of L-arginine (250 mg/kg iv) reversed the effect of L-NAME. We conclude that tonic NO-mediated cerebral vasodilation occurs following transient global ischemia despite delayed hypoperfusion.

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 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
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