The construction of an improved model of acute subdural hematoma in rats

Xian, Liang; Wang, Cheng; Wang, Wei; Wei, Liangfeng; Zhang, Yaying; Chen, Weiqiang; Wang, Shousen

doi:10.1016/j.jneumeth.2021.109075

Cited by 7 publications

(5 citation statements)

References 20 publications

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“…The ASDH model was created based on previous methods described by Xian and Zhang 27 , 58 . Briefly, the dura mater was cut at the right craniotomy hole, and an 8-G gavage needle with an external diameter of 1.4 mm was placed close to the craniotomy hole and the surrounding seal was maintained.…”

Section: Methodsmentioning

confidence: 99%

“…In the second part, all rats were performed by the ASHD model and DC model operation successively. Meanwhile, the rats in sham and vehicle group were injected with normal saline (20 ug/g) 30 min after model establishment, and the IFX group rats were administered an intraperitoneal injection of IFX (diluted with normal saline to 2.5 mg/ml, 20 ug/g, cilag Ag) 38 , 58 , 59 .…”

Section: Methodsmentioning

confidence: 99%

“…The dynamic blood perfusion rates of the observed vessels were quantified using the formula: , where V is equal to the blood flow velocity and D is equal to the vessel diameter. Subsequently, the dynamic Q values and baseline values were normalized to obtain the rBPR values 27 , 58 , 60 .…”

Section: Methodsmentioning

confidence: 99%

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Assessment of cerebrovascular alterations induced by inflammatory response and oxidative–nitrative stress after traumatic intracranial hypertension and a potential mitigation strategy

Zhang,

Chen,

Chen

et al. 2024

Sci Rep

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The rapid perfusion of cerebral arteries leads to a significant increase in intracranial blood volume, exposing patients with traumatic brain injury to the risk of diffuse brain swelling or malignant brain herniation during decompressive craniectomy. The microcirculation and venous system are also involved in this process, but the precise mechanisms remain unclear. A physiological model of extremely high intracranial pressure was created in rats. This development triggered the TNF-α/NF-κB/iNOS axis in microglia, and released many inflammatory factors and reactive oxygen species/reactive nitrogen species, generating an excessive amount of peroxynitrite. Subsequently, the capillary wall cells especially pericytes exhibited severe degeneration and injury, the blood–brain barrier was disrupted, and a large number of blood cells were deposited within the microcirculation, resulting in a significant delay in the recovery of the microcirculation and venous blood flow compared to arterial flow, and this still persisted after decompressive craniectomy. Infliximab is a monoclonal antibody bound to TNF-α that effectively reduces the activity of TNF-α/NF-κB/iNOS axis. Treatment with Infliximab resulted in downregulation of inflammatory and oxidative–nitrative stress related factors, attenuation of capillary wall cells injury, and relative reduction of capillary hemostasis. These improved the delay in recovery of microcirculation and venous blood flow.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Assessment of cerebrovascular alterations induced by inflammatory response and oxidative–nitrative stress after traumatic intracranial hypertension and a potential mitigation strategy

Zhang,

Chen,

Chen

et al. 2024

Sci Rep

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“…A 450-g copper weight was allowed to fall freely from a height of 2 m through a glass tube onto the centre of a 10-mm metal disc attached between the coronal and lambdoid sutures of the rat, and the rat was immediately removed upon impact to prevent a second impact. Subsequently, SDH was produced by injection in accordance with the method reported by Xian et al [ 10 ]. The dura mater was cut open at the injection site on the right side, and an 8G gavage needle with an external diameter of 1.4 mm was inserted into the cranial hole and under the dura mater.…”

Section: Methodsmentioning

confidence: 99%

Acute subdural haematoma exacerbates cerebral blood flow disorder and promotes the development of intraoperative brain bulge in patients with severe traumatic brain injury

et al. 2023

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Background Decompressive craniectomy (DC) is a routine procedure used for the treatment of severe traumatic brain injury (TBI) with concomitant acute subdural haematoma (SDH). However, certain patients are prone to developing malignant brain bulge during DC, which prolongs the operative time and worsens patient outcomes. Previous studies have shown that malignant intraoperative brain bulge (IOBB) may be associated with excessive arterial hyperaemia caused by cerebrovascular system disorders. Through a clinical retrospective analysis and prospective observations, we found that the cerebral blood flow of patients who possessed risk factors manifested high resistance and low flow velocity, which severely affected brain tissue perfusion and resulted in the occurrence of malignant IOBB. In the current literature, rat models of severe brain injury-associated brain bulge have rarely been reported. Methods To gain an in-depth understanding of cerebrovascular changes and the cascade of responses related to brain bulge, we introduced acute SDH into the Marmarou model for the preparation of a rat model of high intracranial pressure (ICP) to simulate the pathological conditions experienced by patients with severe brain injury. Results With the introduction of a 400-µL haematoma, significant dynamic changes occurred in ICP, mean arterial pressure, and relative blood perfusion rate of the cerebral cortical vessels. ICP increased to 56.9 ± 2.3 mmHg, mean arterial pressure showed reactive decrease, and the blood flow of cerebral cortical arteries and veins on the non-SDH-affected side decreased to < 10%. These changes could not fully recover even after DC. This resulted in generalised damage to the neurovascular unit and a lag effect to the venous blood reflux, which triggered malignant IOBB formation during DC. Conclusion An excessive increase in ICP causes cerebrovascular dysfunction and brings about a cascade of damage to brain tissue, which forms the basis for the development of diffuse brain swelling. The subsequent heterogeneous responses of the cerebral arteries and veins during craniotomy may be the main cause of primary IOBB. Clinicians should pay particular attention to the redistribution of CBF to various vessels when performing DC in patients with severe TBI.

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“…1b) between the coronal and lambdoid sutures of the rat, and the rat was immediately removed upon impact to prevent a second impact. Subsequently, SDH was produced by injection in accordance with the method reported by Xian et al [10]. The dura mater was cut open at the injection site on the right side, and an 8G gavage needle with an external diameter of 1.4 mm was inserted into the cranial hole and under the dura mater (Fig.…”

Section: Model Constructionmentioning

confidence: 99%

Acute subdural haematoma exacerbates cerebral blood flow disorder and promotes the development of intraoperative brain bulge in rats with severe traumatic brain injury

Zhang

Chen

Xian

et al. 2023

Preprint

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Background Intraoperative brain bulge (IOBB) is a malignant complication of decompressive craniectomy (DC) in patients with severe traumatic brain injury (TBI), which seriously worsens the prognosis of patients. Previous studies have shown that malignant intraoperative brain bulge (IOBB) may be associated with excessive arterial hyperaemia, but changes in cerebral vein have not been mentioned. In the current literature, rat models of severe brain injury-associated brain bulge have rarely been reported. Methods To gain an in-depth understanding of cerebrovascular changes and the cascade of responses related to brain bulge, we introduced acute SDH into the Marmarou model for the preparation of high intracranial pressure (ICP) to simulate the pathological conditions experienced by patients with severe brain injury. Results With the introduction of a 400 µL haematoma, ICP increased to 56.9 ± 2.3 mmHg, mean arterial pressure showed reactive decrease, and the blood flow of cerebral cortical arteries and veins on the non-SDH-affected side decreased to < 10%. These changes could not fully recover even after DC. This resulted in generalised damage to the neurovascular unit and a lag effect to the venous blood reflux, which triggered malignant IOBB formation during DC. Conclusion An excessive increase in ICP causes cerebrovascular dysfunction and brings about a cascade of damage to brain tissue, which forms the basis for the development of diffuse brain swelling. The subsequent heterogeneous responses of the cerebral arteries and veins during craniotomy may be the main cause of primary IOBB. Clinicians should pay particular attention to the redistribution of CBF to various vessels when performing DC in patients with severe TBI.

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The construction of an improved model of acute subdural hematoma in rats

Cited by 7 publications

References 20 publications

Assessment of cerebrovascular alterations induced by inflammatory response and oxidative–nitrative stress after traumatic intracranial hypertension and a potential mitigation strategy

Assessment of cerebrovascular alterations induced by inflammatory response and oxidative–nitrative stress after traumatic intracranial hypertension and a potential mitigation strategy

Acute subdural haematoma exacerbates cerebral blood flow disorder and promotes the development of intraoperative brain bulge in patients with severe traumatic brain injury

Acute subdural haematoma exacerbates cerebral blood flow disorder and promotes the development of intraoperative brain bulge in rats with severe traumatic brain injury

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