The Acute Phase of Experimental Subarachnoid Hemorrhage: Intracranial Pressure Dynamics and Their Effect on Cerebral Blood Flow and Autoregulation

2018 ◽  
Vol 10 (5) ◽  
pp. 566-582 ◽  
Author(s):  
Catharina Conzen ◽  
Katrin Becker ◽  
Walid Albanna ◽  
Miriam Weiss ◽  
Annika Bach ◽  
...  
2009 ◽  
Vol 111 (5) ◽  
pp. 978-987 ◽  
Author(s):  
Saema Ansar ◽  
Lars Edvinsson

Object Cerebral ischemia remains the key cause of disability and death in the late phase after subarachnoid hemorrhage (SAH), and its pathogenesis is still poorly understood. The purpose of this study was to examine whether the change in intracranial pressure or the extravasated blood causes the late cerebral ischemia and the upregulation of receptors or the cerebral vasoconstriction observed following SAH. Methods Rats were allocated to 1 of 3 experimental conditions: 1) cisternal injection of 250 μl blood (SAH Group), 2) cisternal injection of 250 μl NaCl (Saline Group), or 3) the same procedure but without fluid injection (Sham Group). Two days after the procedure, the basilar and middle cerebral arteries were harvested, and contractile responses to endothelin (ET)–1 and 5-carboxamidotryptamine (5-CT) were investigated by means of myography. In addition, real-time polymerase chain reaction was used to determine the mRNA levels for ETA, ETB, and 5-HT1 receptors. Regional and global cerebral blood flow (CBF) were quantified by means of an autoradiographic technique. Results Compared with the sham condition, both SAH and saline injection resulted in significantly enhanced contraction of cerebral arteries in response to ET-1 and 5-CT. Regional and global CBF were reduced both in the Saline and SAH groups compared with the Sham Group. The mRNA levels for ETB and 5-HT1B receptors were upregulated after SAH and saline injection compared with the sham procedure. The effects in all parameters were more pronounced for SAH than for saline injection. Conclusions This study revealed that both the elevation of intracranial pressure and subarachnoid blood per se contribute approximately equally to the late CBF reductions and receptor upregulation following SAH.


Stroke ◽  
1985 ◽  
Vol 16 (1) ◽  
pp. 58-64 ◽  
Author(s):  
R A Solomon ◽  
J L Antunes ◽  
R Y Chen ◽  
L Bland ◽  
S Chien

1997 ◽  
Vol 87 (6) ◽  
pp. 1486-1493 ◽  
Author(s):  
Daniel J. Cole ◽  
Jeffrey C. Nary ◽  
Lowell W. Reynolds ◽  
Piyush M. Patel ◽  
John C. Drummond

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.


1981 ◽  
Vol 21 (4) ◽  
pp. 379-388 ◽  
Author(s):  
MINORU HAYASHI ◽  
HIDENORI KOBAYASHI ◽  
SHIGERU MUNEMOTO ◽  
SOTARO HIGASHI ◽  
JUN-ICHI NOZAKI ◽  
...  

2017 ◽  
Vol 8 ◽  
Author(s):  
Elham Rostami ◽  
Henrik Engquist ◽  
Timothy Howells ◽  
Elisabeth Ronne-Engström ◽  
Pelle Nilsson ◽  
...  

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