doi: 10.1161/hs1201.099820
(Stroke. 2001;32:2932.)
© 2001 American Heart Association, Inc.
Original Contributions |
Mechanisms of Edema Formation After Intracerebral Hemorrhage
Effects of Extravasated Red Blood Cells on Blood Flow and Blood-Brain Barrier Integrity
From the Departments of Neurosurgery (all authors) and Physiology (R.F.K.), University of Michigan, Ann Arbor.
Reprint requests to Guohua Xi, MD, R5550 Kresge I, University of Michigan, Ann Arbor, Michigan 48109-0532. E-mail guohuaxi{at}umich.edu
Background and Purpose— Red blood cell (RBC) lysis contributes to brain edema formation after intracerebral hemorrhage (ICH), and RBC hemolysate (oxyhemoglobin) has been implicated to be a spasminogen in subarachnoid hemorrhage. Whether cerebral ischemia contributes to brain edema formation after ICH remains unclear, however. The aims of this study were to test whether extravasation of RBCs induces cerebral ischemia and/or blood-brain barrier disruption in a rat ICH model characterized by perihematomal brain edema.
Methods— In this study, 87 pentobarbital-anesthetized Sprague-Dawley rats were used. In each animal, saline, packed RBCs, or lysed RBCs were injected into the right caudate nucleus. Sham injections served as controls. Regional cerebral blood flow, brain water and ion contents, blood-brain barrier integrity, and plasma volume were measured.
Results— Intraparenchymal infusion of lysed RBCs caused severe brain edema by the first day but did not induce ischemic cerebral blood flows. In contrast, blood-brain barrier permeability increased during the first day after infusion of lysed RBCs (a 3-fold increase) and 3 days after infusion of packed RBCs (a 4-fold increase).
Conclusions— These results suggest that ischemia is not present at 24 or 72 hours after hematoma induction by injection of intact or lysed RBCs. RBC constituents that appear after delayed lysis, however, increase blood-brain barrier permeability, which contributes to edema formation.
Key Words: cerebral hemorrhage • brain edema • cerebral blood flow • blood-brain barrier permeability
This article has been cited by other articles:
 |
|
 |
|
  T.J. Yun, D.G. Na, B.J. Kwon, H.G. Rho, S.-H. Park, Y.-L. Suh, and K.-H. Chang A T1 Hyperintense Perilesional Signal Aids in the Differentiation of a Cavernous Angioma from Other Hemorrhagic Masses AJNR Am. J. Neuroradiol., March 1, 2008; 29(3): 494 - 500. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Hua, R. F. Keep, J. T. Hoff, and G. Xi Brain Injury After Intracerebral Hemorrhage: The Role of Thrombin and Iron Stroke, February 1, 2007; 38(2): 759 - 762. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
NINDS ICH Workshop Participants Priorities for Clinical Research in Intracerebral Hemorrhage: Report From a National Institute of Neurological Disorders and Stroke Workshop Stroke, March 1, 2005; 36(3): e23 - e41. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Silva, R. Leira, J. Tejada, J. M. Lainez, J. Castillo, A. Davalos, and by the Stroke Project, Cerebrovascular Diseases Gr Molecular Signatures of Vascular Injury Are Associated With Early Growth of Intracerebral Hemorrhage Stroke, January 1, 2005; 36(1): 86 - 91. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. D. Ardizzone, A. Lu, K. R. Wagner, Y. Tang, R. Ran, and F. R. Sharp Glutamate Receptor Blockade Attenuates Glucose Hypermetabolism in Perihematomal Brain After Experimental Intracerebral Hemorrhage in Rat Stroke, November 1, 2004; 35(11): 2587 - 2591. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. K. Kamal, J. P. Dyke, J. M. Katz, B. Liberato, C. G. Filippi, R. D. Zimmerman, and A. M. Ulug Temporal Evolution of Diffusion after Spontaneous Supratentorial Intracranial Hemorrhage AJNR Am. J. Neuroradiol., May 1, 2003; 24(5): 895 - 901. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Hua, T. Schallert, R. F. Keep, J. Wu, J. T. Hoff, and G. Xi Behavioral Tests After Intracerebral Hemorrhage in the Rat Stroke, October 1, 2002; 33(10): 2478 - 2484. [Abstract] [Full Text] [PDF]
|
|