Relationship between cerebral blood flow, metabolism and cerebrospinal fluid lactate in multi-infarct dementia.

Nosotchu ◽  
1994 ◽  
Vol 16 (1) ◽  
pp. 15-20 ◽  
Author(s):  
Katsumi Irie ◽  
Setsuro Ibayashi ◽  
Kenichiro Fujii ◽  
Seizo Sadoshima ◽  
Masatoshi Fujishima
1989 ◽  
Vol 11 (3) ◽  
pp. 150-151 ◽  
Author(s):  
A. Parma ◽  
R. Massei ◽  
A. Pesenti ◽  
C. Ferrari da Passano ◽  
G. Gran ◽  
...  

1976 ◽  
Vol 14 (5) ◽  
pp. 351-364 ◽  
Author(s):  
François Artru ◽  
Bernard Philippon ◽  
Françoise Gau ◽  
Michel Berger ◽  
Raymond Deleuze

1982 ◽  
Vol 243 (1) ◽  
pp. H33-H40 ◽  
Author(s):  
R. C. Koehler ◽  
R. J. Traystman

The relative importance of changes in extracellular fluid (ECF) pH in mediating increases in cerebral blood flow (CBF) during hypoxia and hypercapnia was assessed by varying [HCO(-3)]ECF in pentobarbital-anesthetized dogs. Blood flow to one caudate nucleus (CNBF) that was bathed by cerebrospinal fluid (CSF) of varied [HCO(-3)] was compared with CNBF (measured by radiolabeled microspheres) on the contralateral side, which received a normal-[HCO(-3)]CSF perfusate. Raising [HCO(-3)]CSF from 25 to 60 meq/l for 150 min lowered CNBF by 16% and suppressed the slope of cNBF response to hypercapnia by 61% but suppressed the slope of CNBF response to hypoxia significantly less (22%). Lowering [HCO(-3)]CSF to 8 meq/l increased CNBF by 71% and augmented the response to hypercapnia by 126% but did not alter the slope of the response to hypoxia. These data indicate that changes in [H+]ECF can account for the increased CBF during hypercapnia but not for the entire hypoxic response. The increase in lactic acid production that would be necessary to solely account for the increase in CBF during hypoxia is much greater than what has been reported in the literature.


1995 ◽  
Vol 82 (2) ◽  
pp. 512-520 ◽  
Author(s):  
Alan E. Feerick ◽  
William E. Johnston ◽  
Larry W. Jenkins ◽  
Cheng Y. Lin ◽  
Jonathan H. Mackay ◽  
...  

Background Hyperglycemia frequently occurs during cardiopulmonary bypass (CPB), although its direct effects on cerebral perfusion and metabolism are not known. Using a canine model of hypothermic CPB, we tested whether hyperglycemia alters cerebral blood flow and metabolism and cerebral energy charge. Methods Twenty anesthetized dogs were randomized into hyperglycemic (n = 10) and normoglycemic (n = 10) groups. The hyperglycemic group received an infusion of D50W, and the normoglycemic animals received an equal volume of 0.9% NaCl. Both groups underwent 120 min of hypothermic (28 degrees C) CPB using membrane oxygenators, followed by rewarming and termination of CPB. Cerebral blood flow (radioactive microspheres) and the cerebral metabolic rate for oxygen were measured intermittently during the experiment and brain tissue metabolites were obtained after bypass. Results Before CPB, the glucose-treated animals had higher serum glucose levels (534 +/- 12 mg/dL; mean +/- SE) than controls (103 +/- 4 mg/dL; P < 0.05), and this difference was maintained throughout the study. Cerebral blood flow and metabolism did not differ between groups at any time during the experiment. Sagittal sinus pressure was comparable between groups throughout CPB. Tissue high-energy phosphates and water contents were similar after CPB, although cerebral lactate levels were greater in hyperglycemic (37.2 +/- 5.7 mumol/g) than normoglycemic animals (19.7 +/- 3.7 mumol/g; P < 0.05). After CPB, pH values of cerebrospinal fluid for normoglycemic (7.33 +/- 0.01) and hyperglycemic (7.34 +/- 0.01) groups were similar. Conclusions Hyperglycemia during CPB significantly increases cerebral lactate levels without adversely affecting cerebral blood flow and metabolism, cerebrospinal fluid pH, or cerebral energy charge.


1995 ◽  
Vol 23 (Supplement) ◽  
pp. A73
Author(s):  
Robert Clark ◽  
Patrick Kochanek ◽  
Hector R. Wong ◽  
Timothy Billiar ◽  
Mark Mistrik ◽  
...  

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