Effect of adrenalin and noradrenalin on volume velocity of the cerebral blood flow and oxygen tension in brain tissue

1971 ◽  
Vol 72 (3) ◽  
pp. 1034-1036
Author(s):  
M. D. Gaevyi
2009 ◽  
Vol 107 (6) ◽  
pp. 1799-1805 ◽  
Author(s):  
Peter Rasmussen ◽  
Camilla A. Madsen ◽  
Henning B. Nielsen ◽  
Morten Zaar ◽  
Albert Gjedde ◽  
...  

Activation-induced increase in cerebral blood flow is coupled to enhanced metabolic activity, maybe with brain tissue redox state and oxygen tension as key modulators. To evaluate this hypothesis at the onset of exercise in humans, blood was sampled at 0.1 to 0.2 Hz from the radial artery and right internal jugular vein, while middle cerebral artery mean flow velocity (MCA Vmean) was recorded. Both the arterial and venous lactate-to-pyruvate ratio increased after 10 s ( P < 0.05), and the arterial ratio remained slightly higher than the venous ( P < 0.05). The calculated average cerebral capillary oxygen tension decreased by 2.7 mmHg after 5 s ( P < 0.05), while MCA Vmean increased only after 30 s. Furthermore, there was an unaccounted cerebral carbohydrate uptake relative to the uptake of oxygen that became significant 50 s after the onset of exercise. These findings support brain tissue redox state and oxygenation as potential modulators of an increase in cerebral blood flow at the onset of exercise.


1982 ◽  
Vol 2 (1) ◽  
pp. 25-32 ◽  
Author(s):  
K.-A. Hossmann ◽  
I. Niebuhr ◽  
M. Tamura

Experimental brain tumors were produced in rats by intracerebral implantation of a neoplastic glial cell clone. Within 2–6 weeks, spherical brain tumors developed at the implantation site with a mean diameter of 6 mm. Local blood flow and local glucose utilization were measured under light barbiturate anesthesia by quantitative autoradiography in the tumor and peritumoral brain tissue. In solid parts of the tumor, blood flow was 57.8 ± 2.0 ml/100 g/min (mean ± SE), and glucose utilization was 87.2 ± 5.8 μmol/100 g/min, respectively. In necrotic regions, flow and glucose utilization were zero. In peritumoral brain tissue of the ipsilateral hemisphere blood flow was reduced by 13–23%, as compared to homologous regions of the opposite side, the greatest decrease being recorded in the ipsilateral thalamus. Flow in the opposite hemisphere was of the same order of magnitude as in normal control rats. Glucose consumption, in contrast, was distinctly reduced in both hemispheres: in the cortex and putamen, it was 40–50% lower than in normal controls. The following conclusions are drawn: (1) during tumor development the high glucose consumption in the tumor tissue is not coupled to an equal increase in blood flow; (2) peritumoral cerebral blood flow decreases on the ipsilateral but not on the contralateral side, and (3) the metabolic rate of glucose is distinctly inhibited in both hemispheres of tumor-bearing animals. The dissociation between blood flow and metabolism suggests that metabolic inhibition is not the consequence of a diaschitic depression of functional activity.


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