Persistent hypertension does not alter the cerebral blood flow and glucose utilization in young-adult Dahl salt-sensitive rats

2002 ◽  
Vol 197 (1-2) ◽  
pp. 19-26 ◽  
Author(s):  
Tetsujiro Yasuda ◽  
Junya Shigematsu ◽  
Shozo Tobimatsu ◽  
Shosuke Takahashi ◽  
Motohiro Kato
1992 ◽  
Vol 15 ◽  
pp. 258B
Author(s):  
K. Satoh ◽  
M. Narita ◽  
T. Someya ◽  
S. Takahashi ◽  
T. Suzuki ◽  
...  

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.


1988 ◽  
Vol 254 (2) ◽  
pp. H250-H257
Author(s):  
H. Schrock ◽  
W. Kuschinsky

Rats were kept on a low-K+ diet for 25 or 70 days. Local cerebral blood flow (LCBF) and local cerebral glucose utilization (LCGU) were measured in 31 different structures of the brain by means of the [14C]iodoantipyrine and [14C]2-deoxy-D-glucose method. After 25 and 70 days of K+ depletion LCBF was decreased significantly in 27 and 30 structures, respectively, the average decrease being 19 and 25%. In contrast, average LCGU was not changed. Cisternal cerebrospinal fluid (CSF) K+ concentration decreased significantly from 2.65 +/- 0.02 mM in controls to 2.55 +/- 0.02 mM and 2.47 +/- 0.02 mM in the two treated groups (P less than 0.01). CSF [HCO3-], pH, and PCO2 were increased in K+-depleted animals. These data show that K+ depletion induces an increase in CSF pH and a decrease in CSF K+ concentration, both of which cause a reduction in cerebral blood flow. The increased CSF PCO2 is secondary to the reduction of blood flow, since brain metabolism and arterial PCO2 remained constant.


1993 ◽  
Vol 265 (4) ◽  
pp. H1243-H1248 ◽  
Author(s):  
K. Waschke ◽  
H. Schrock ◽  
D. M. Albrecht ◽  
K. van Ackern ◽  
W. Kuschinsky

The effects of a blood exchange on cerebral blood flow and glucose utilization were studied. A near to total blood exchange (hematocrit < 3%) was achieved in conscious rats by isovolemic hemodilution. Ultrapurified, polymerized, bovine hemoglobin (UPBHB) served as a blood substitute. Local cerebral blood flow (LCBF) and local cerebral glucose utilization (LCGU) were measured in 34 brain structures of conscious rats by means of the ido[14C]antipyrine and the 2-[14C]-deoxy-D-glucose methods. A group of rats without blood exchange served as control. After blood exchange LCBF increased from 36 to 126% in the different brain structures resulting in a nearly doubled mean cerebral blood flow (+82%). LCGU increased only moderately by 0-24%. Significant increases in LCGU were observed in 16 brain structures. Mean cerebral glucose utilization slightly increased (+14%). The relationship between LCGU and LCBF was found to be tight both in the control group (r = 0.95) as well as after blood replacement (r = 0.94), although it was reset to a higher overall LCBF-to-LCGU ratio. The profound increases in LCBF observed after blood exchange, which were not paralleled by comparable increases in LCGU, might be explained by a reduction of blood viscosity after blood exchange. Additional effects of blood exchange observed in the present study were an increase of mean arterial blood pressure and a decline of heart rate. The results indicate that replacement of blood with the hemoglobin-based oxygen carrier UPBHB appears to meet the cerebral circulatory and metabolic demands of the brain tissue.


1972 ◽  
Vol 114 (3) ◽  
pp. 292-303 ◽  
Author(s):  
Edgar L. Makowski ◽  
Jack M. Schneider ◽  
Nicholas G. Tsoulos ◽  
James R. Colwill ◽  
Frederick C. Battaglia ◽  
...  

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