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    Please use this identifier to cite or link to this item: http://ir.cnu.edu.tw/handle/310902800/31668

    標題: Combined Hemorrhagic Shock and Unilateral Common Carotid Occlusion Induces Neurological Injury in Adult Male Rats
    作者: Chio, Chung-Ching
    Hsu, Chien-Chin
    Tian, Yu-Feng
    Wang, Chung-Han
    Lin, Mao-Tsun
    Chang, Ching-Ping
    Lin, Hung-Jung
    貢獻者: Chi Mei Med Ctr, Dept Surg, Div Neurosurg
    Southern Taiwan Univ Sci & Technol, Dept Biotechnol
    Chi Mei Med Ctr, Dept Emergency Med
    Chi Mei Med Ctr, Dept Surg, Div Gen Surg
    Chia Nan Univ Pharm & Sci, Dept Hlth & Nutr
    Chi Mei Med Ctr, Dept Med Res
    Taipei Med Univ, PhD Program Neural Regenerat Med
    關鍵字: hemorrhagic shock
    multiple organ injuries
    ischemia/reperfusion injury
    cerebral blood flow
    日期: 2017
    上傳時間: 2018-11-30 15:52:13 (UTC+8)
    出版者: Ivyspring Int Publ
    摘要: Background: Clinical assessment reveals that patients after surgery of cardiopulmonary bypass or coronary bypass experience postoperative cognitive dysfunction. This study aimed to investigate whether resuscitation after a hemorrhagic shock (HS) and/or mild cerebral ischemia caused by a unilateral common carotid artery occlusion (UCCAO) can cause brain injury and concomitant neurological dysfunction, and explore the potential mechanisms. Methods: Blood withdrawal (6 mL/100 g body weight) for 60 min through the right jugular vein catheter-induced an HS. Immediately after the termination of HS, we reinfused the initially shed blood volumes to restore and maintain the mean arterial blood pressure (MABP) to the original value during the 30-min resuscitation. A cooling water blanket used to induce whole body cooling for 30 min after the end of resuscitation. Results: An UCCAO caused a slight cerebral ischemia (cerebral blood flow [CBF] 70%) without hypotension (MABP 85 mmHg), systemic inflammation, multiple organs injuries, or neurological injury. An HS caused a moderate cerebral ischemia (52% of the original CBF levels), a moderate hypotension (MABP downed to 22 mmHg), systemic inflammation, and peripheral organs injuries. However, combined an UCCAO and an HS caused a severe cerebral ischemia (18% of the original CBF levels), a moderate hypotension (MABP downed to 17 mmHg), systemic inflammation, peripheral organs damage, and neurological injury, which can be attenuated by whole body cooling. Conclusions: When combined with an HS, an UCCAO is associated with ischemic neuronal injury in the ipsilateral hemisphere of adult rat brain, which can be attenuated by therapeutic hypothermia. A resuscitation from an HS regards as a reperfusion insult which may induce neurological injury in patients with an UCCAO disease.
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