›› 2010, Vol. 30 ›› Issue (9): 1106-.doi: 10.3969/j.issn.1674-8115.2010.09.021

• Original article (Basic research) • Previous Articles     Next Articles

Miniature pig model of combined traumatic brain injury and acute intracranial hypertension with hemorrhagic shock

LUO Wei1, LI Xue-yuan2, LI Jia2, QU Xing-qian1, CHEN Li-jun1, SHEN Bo-xiong1, FENG Dong-fu2   

  1. 1.Department of Anesthesiology, 2.Department of Neurosurgery, Institute of Traumatic Medicine, The Third People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 201900, China
  • Online:2010-09-25 Published:2010-09-27
  • Supported by:

    Shanghai Science and Technology Committee Foundation, 064119639;Foundation of The Third People's Hospital, Shanghai Jiaotong University School of Medicine, syz09-12

Abstract:

Objective To establish the miniature pig model of combined traumatic brain injury and acute intracranial hypertension with superimposed hemorrhagic shock so as to simulate the human local traumatic brain injury and acute epidural hematoma and superimposed hemorrhagic shock, and analyse the morphological changes. Methods Unilateral brain frontal lobes were injured by simplified controlled cortical impact devices in 16 miniature pigs, epidural balloon method was adopted to induce acute intracranial hypertension, and modified Wigger shock model was employed to cause hemorrhagic shock. Mean arterial blood pressure (MAP), intracranial pressure (ICP) and cerebral perfusion pressure (CPP) were observed at the time points of before model preparation (T01), immediately after blood withdrawal (T0), and 15 min (T15), 30 min (T30) and 60 min (T60) after blood withdrawl. O2 suturation of jugular venous blood (SjvO2) was monitored at T01 and T60. Two miniature pigs were randomly selected, and cranial CT and MRI examinations at coronal plane were performed before model preparation and 6 h after model preparation. Two miniature pigs were randomly selected 6 h after model establishment for cranial gross pathological examination, observation with HE staining and ultramicrostructure observation. Results MAP and CPP were significantly lower and ICP was significantly higher at T0 than those at T01 (P<0.05). There was no significant difference between MAP, ICP and CCP of T15, T30 and T60 and those of T0 (P>0.05). SjvO2 at T60 was significantly lower than that at T01 (P<0.05). Imaging examinations revealed traumatic subdural hemorrhage, midline shift and contralateral cerebral ventricle dilation. It was observed by HE staining that there were significant edema in traumatic lesions and adjacent tissues, infiltration of inflammatory cells, pericapillary hemorrhage, petechial hemorrhages in the white matter and cortical laceration. Ultramicrostructure observation revealed a series of changes in the tissues of traumatic lesions, adjacent tissues and contralateral cerebral tissues, including necrosis and degeneration of neurons, myelinolysis of axons, mitochondrial swelling and distension of endothelia. Conclusion The miniature pig model of traumatic brain injury combined with acute intracranial hypertension and hemorrhagic shock, established successfully with controlled cortical impact, epidural balloon and blood withdrawal, can effectively simulate human local traumatic brain injury and acute epidural hematoma and superimposed hemorrhagic shock, and can monitor the cerebral perfusion and balance of supply and demand of cerebral oxygen.

Key words: traumatic brain injury, intracranial hypertension, hemorrhagic shock, O2 suturation of jugular venous blood, animal model, miniature pigs