scholarly journals Chronic cerebral blood flow changes following experimental subarachnoid hemorrhage in rats.

Stroke ◽  
1990 ◽  
Vol 21 (4) ◽  
pp. 577-581 ◽  
Author(s):  
A Kader ◽  
W E Krauss ◽  
S T Onesti ◽  
J P Elliott ◽  
R A Solomon
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Experimental Subarachnoid Hemorrhage ◽  
Flow Changes

scholarly journals Decrease in cerebral blood flow in rats after experimental subarachnoid hemorrhage: a new animal model.

Stroke ◽  
1985 ◽  
Vol 16 (1) ◽  
pp. 58-64 ◽  
Author(s):  
R A Solomon ◽  
J L Antunes ◽  
R Y Chen ◽  
L Bland ◽  
S Chien
Keyword(s):  
Animal Model ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Experimental Subarachnoid Hemorrhage

Experimental Subarachnoid Hemorrhage in Rats 

1997 ◽  
Vol 87 (6) ◽  
pp. 1486-1493 ◽  
Author(s):  
Daniel J. Cole ◽  
Jeffrey C. Nary ◽  
Lowell W. Reynolds ◽  
Piyush M. Patel ◽  
John C. Drummond
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Neuronal Death ◽  
Autologous Blood ◽  
The Other ◽  
Cerebral Hypoperfusion ◽  
Control Group ◽  
Experimental Subarachnoid Hemorrhage ◽  
Hematoxylin And Eosin

Background Hemodilution with diaspirin crosslinked hemoglobin (DCLHb) ameliorates occlusive cerebral ischemia. However, subarachnoid hemoglobin has been implicated as a cause of cerebral hypoperfusion. The effect of intravenous DCLHb on cerebral perfusion and neuronal death after experimental subarachnoid hemorrhage was evaluated. Methods Rats (n = 48) were anesthetized with isoflurane and subarachnoid hemorrhage was induced by injecting 0.3 ml of autologous blood into the cistema magna. Each animal received one of the following regimens: Control, no hematocrit manipulation; DCLHb, hematocrit concentration decreased to 30% with DCLHb; or Alb, hematocrit concentration decreased to 30% with human serum albumin. The experiments had two parts, A and B. In part A, after 20 min, cerebral blood flow (CBF) was assessed with 14C-iodoantipyrine autoradiography. In part B, after 96 h, in separate animals, the number of dead neurons was determined in predetermined coronal sections by hematoxylin and eosin staining. Results Cerebral blood flow was greater for the DCLHb group than for the control group; and CBF was greater for the Alb group than the other two groups (P < 0.05). In one section, CBF was 45.5 +/- 10.9 ml x 100 g(-1) x min(-1) (mean +/- SD) for the control group, 95.3 +/- 16.6 ml x 100 g(-1) x min(-1) for the DCLHb group, and 138.1 +/- 18.7 ml x 100 g(-1) x min(-1) for the Alb group. The number of dead neurons was less in the Alb group (611 +/- 84) than in the control group (1,097 +/- 211), and was less in the DCLHb group (305 +/- 38) than in the other two groups (P < 0.05). Conclusions These data support a hypothesis that hemodilution decreases hypoperfusion and neuronal death after subarachnoid hemorrhage. The data do not support the notion that intravascular molecular hemoglobin has an adverse effect on brain injury after subarachnoid hemorrhage.

Cerebral blood flow following induced subarachnoid hemorrhage in the monkey

1972 ◽  
Vol 37 (3) ◽  
pp. 316-324 ◽  
Author(s):  
K. C. Petruk ◽  
G. R. West ◽  
M. R. Marriott ◽  
J. W. McIntyre ◽  
T. R. Overtone ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Perfusion ◽  
Neurological Status ◽  
Neurological Deficits ◽  
Content Type ◽  
Arterial Vasospasm ◽  
Experimental Subarachnoid Hemorrhage ◽  
Angiographic Demonstration

✓ The acute effects of experimental subarachnoid hemorrhage on cerebral blood flow were investigated in 14 adult rhesus monkeys injected with fresh autogenous blood through a needle positioned within the subfrontal subarachnoid space. Cerebral blood flow was measured by the xenon133 tissue clearance method before hemorrhage, and afterward at 30-minute intervals for a 3-hour period. Post-anesthetic neurological status was graded according to Botterell's classification. Twelve monkeys showed a significant decrease in cerebral perfusion, eight displayed focal neurological deficits, and four were moribund. There was a correlation between the degree of impaired circulation and the severity of neurological deficit. Four additional monkeys subjected to subarachnoid acidic saline injection showed no reduction in cerebral blood flow. In three animals cerebral perfusion was increased during the first hour after injection. It is suggested that measurement of cerebral blood flow may be a more valuable prognostic indication of cerebral function and survival than the angiographic demonstration of arterial vasospasm.

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