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A New Model of Hemorrhagic Shock‐Induced Acute Kidney Injury
Author(s) -
Wang Lei,
Qu Phillip,
Lu Yan,
Wei Jin,
Wang Shaohui,
Zhang Jie,
Yip K.P.,
Liu Ruisheng
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.807.4
Subject(s) - medicine , acute kidney injury , hemorrhagic shock , shock (circulatory) , creatinine , renal blood flow , anesthesia , kidney , cardiology , urology
Acute kidney injury (AKI) is a major kidney disease associated with high mortality and morbidity rates. Hemorrhagic shock is a prevalent cause of AKI. However there is no animal model that mimics the clinic scenario for hemorrhagic shock‐induced AKI. We sought to develop a model of AKI induced by hemorrhagic shock to simulate the clinical conditions. The C57BL/6J mice (26‐28 g) were anesthetized with 50mg/kg I.P. pentobarbital. Basal MAP was 77 + 4 mmHg and RBF was 0.8 + 0.3 ml/min. Hemorrhagic shock was induced by withdrawing 0.4 ml blood through the right common carotid artery within 2 min to decrease MAP to below 40 mmHg. Thirty minutes later, bilateral pedicels were clamped for 18 min with the body temperature at 37 0 C. Then the clips were released to initiate the reperfusion for 24 hours. The renal blood flow decreased to 0.44 + 0.09 ml/min. Serum creatinine increased from 0.08 + 0.04 to 2.03 + 0.12 mg/dl. Serum N‐GAL increased to 127 + 13 ng/ml after 24 hours of ischemia reperfusion injury. This new AKI model is a well‐controlled, easily‐reproducible and reliable animal model induced by hemorrhagic shock, which will enable investigators to further understand the mechanism and identify novel targets for prevention and treatment of hemorrhagic shock‐induced AKI.