Abstract
Background. Microvascular dysfunction and microthrombi formation are believed to contribute to development of early brain injury (EBI) after aneurysmal subarachnoid hemorrhage (SAH). Objective. This study aimed to determine (i) extent of microthrombus formation and neuronal apoptosis in the brain parenchyma using a blood shunt SAH model in rabbits; (ii) correlation of structural changes in microvessels with EBI characteristics. Methods. Acute SAH was induced using a rabbit shunt cisterna magna model. Extent of microthrombosis was detected 24 h post-SAH (n = 8) by fibrinogen immunostaining, compared to controls (n = 4). We assessed apoptosis by terminal deoxynucleotidyl transferase nick end labeling (TUNEL) in cortex and hippocampus. Results. Our results showed significantly more TUNEL-positive cells (SAH: 115 ± 13; controls: 58 ± 10; P = 0.016) and fibrinogen-positive microthromboemboli (SAH: 9 ± 2; controls: 2 ± 1; P = 0.03) in the hippocampus after aneurysmal SAH. Conclusions. We found clear evidence of early microclot formation in a rabbit model of acute SAH. The extent of microthrombosis did not correlate with early apoptosis or CPP depletion after SAH; however, the total number of TUNEL positive cells in the cortex and the hippocampus significantly correlated with mean CPP reduction during the phase of maximum depletion after SAH induction. Both microthrombosis and neuronal apoptosis may contribute to EBI and subsequent DCI.
Highlights
Aneurysmal subarachnoid hemorrhage (SAH) is a devastating cerebrovascular disease with high mortality and disability rates [1]
To model the physiological situation in humans with aneurysmal SAH [7], this study investigated the association between early injury after SAH, microclot formation, and apoptosis in an extra-ntracranial blood shunt model in the rabbit
Evidence has indicated that early brain injury (EBI) and delayed cerebral ischemia (DCI) largely contribute to the unfavorable outcome and mortality after aneurysmal SAH [1, 2]
Summary
Aneurysmal subarachnoid hemorrhage (SAH) is a devastating cerebrovascular disease with high mortality and disability rates [1]. Intensive research in recent years revealed many different causes of SAH, including cerebral vasospasm, early brain injury (EBI) mediated by impaired microcirculatory function, microthrombosis, cortical spreading depression, oxidative stress, inflammation, and apoptosis. The extent of microthrombosis did not correlate with early apoptosis or CPP depletion after SAH; the total number of TUNEL positive cells in the cortex and the hippocampus significantly correlated with mean CPP reduction during the phase of maximum depletion after SAH induction. Both microthrombosis and neuronal apoptosis may contribute to EBI and subsequent DCI
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