Blood-Brain Barrier Damage during the Acute Stage of Subarachnoid Hemorrhage, as Exemplified by a New Animal Model

Abstract

Models have been devised and characterized in the laboratory rat for studying the neuropathology of subarachnoid hemorrhage. Several ways of injecting blood via different routes have been tried; cortical subarachnoid administration is the most reproducible suitable model. The location of injected blood was detected in histological sections. In this rat model for subarachnoid hemorrhage, the arterial blood pressure and the intracranial pressure did not elevate significantly, and the influence of major ischemic components in the development of brain edema could also be ruled out. Measurements performed on the water, electrolyte, and albumin contents of brain tissue have clearly indicated that the brain edema developing in the acute stage of rat experimental subarachnoid hemorrhage could be classified as having a primarily vasogenic component as well. These findings may have implications in the treatment of subarachnoid hemorrhage.

Serum and cerebrospinal fluid C-reactive protein levels as predictors of vasospasm in aneurysmal subarachnoid hemorrhage

“…33,54,57 It is well known that leukocyte trafficking increases in SAH due to a breakdown of the blood-brain barrier. 5,[8][9][10][11]14,23,52,66 Increased levels of various soluble adhesion molecules (such as E-selectin, intercellular adhesion molecule-1, and vascular adhesion molecule-1) and cytokines (such as IL-6 and IL-1) have been noted in the plasma and CSF of patients with SAH.…”

NMDA Receptor Antagonist Felbamate Reduces Behavioral Deficits and Blood–Brain Barrier Permeability Changes after Experimental Subarachnoid Hemorrhage in the Rat

“…These impairments have been ascribed mainly to ischemic brain injury occurring either during the initial bleeding episode or as a consequence of macro-and microvascular dysfunction and delayed ischemic deterioration (d'Avella et al, , 1996Delgado et al, 1985Delgado et al, , 1986Doczi, 1985;Doczi et al, 1986;Germanò et al, 1992Germanò et al, , 2000Jackowski et al, 1990;Johshita et al, 1990;Sasaki et al, 1985Sasaki et al, , 1986Siesjo, 1992a,b;Zuccarello, 1989). Detailed knowledge about the pathological ischemic mechanisms in patients with SAH is critical to develop more efficient treatments.…”

The Effect of Blood Glutamate Scavengers Oxaloacetate and Pyruvate on Neurological Outcome in a Rat Model of Subarachnoid Hemorrhage

“…An increase in the permeability of the BBB has been shown to follow SAH in both human [66] and experimental settings [67][68][69][70], and it correlates with a worsened neurological outcome [48,[67][68][69][70]. The BBB breakdown develops even in the acute stage of SAH [66,67], and the indicator has been shown to be independent of influences, such as increased intracranial pressure or brain edema that may disrupt the BBB itself [48]. On the contrary, histological examination, including neuronal count, is usually used in models of SAH, which was induced by endovascular perforation of the internal carotid artery and is very rarely used in a model of SAH induced by the injection of blood into the cisterna magna [46].…”