摘要
Background： Majority of the research on cardiac arrest （CA） have focused on post-CA brain injury and myocardial dysfunction, the renal dysfunction and acute kidney injury （AKI） in other critical illnesses after CA have not been well described. This study was designed to assess AKI with renal Doppler and novel AK1 biomarkers in a swine model of ventricular fibrillation cardiac arrest （VFCA）. Methods： Thirty healthy piglets were divided into VFCA group （17 = 22） and Sham group （n = 8） in a blinded manner. Mean arterial pressure, heart rate. and cardiac output were recorded continuously. Cardiac arrest （CA） was induced by programmed electric stimulation in the VFCA group, and then cardiopulmonary resuscitation was performed. Twenty piglets returned of spontaneous circulation （ROSC） and received intensive care. Blood and urine samples were collected for AKI biomarkers testing, and Color Doppler flow imaging was performed at baseline, 6 h, 12 h, and 24 11. respectively after ROSC. At ROSC 24 h, the animals were sacrificed and a semi-quantitative evaluation of pathologic kidney injury was performed. Results： In the VFCA group, corrected resistive index （cRl） increased from 0.47 ± 0.03 to 0.64 ± 0.06, and pulsatility index （PI） decreased from 0.82 ± 0.03 to 0.68 ± 0.04 after ROSC. Cystatin C （CysC） in both serum and urine samples increased at ROSC 6 h, but neutrophil gelatinase-associated lipocalin （NGAL） in serum increased to 5.34 ± 1.68 ng/ml at ROSC 6 h, and then decreased to 3.16 ± 0.69 ng/ml at ROSC 24 h while CysC increasing constantly. According to the renal histopathology, 18 of 20 animals suffered from kidney injury. The grade of renal injury was highly correlated with RI, cRI, NGAL, and CysC. Linear regression equation was established： Grade of renal injury = 0.002× serum CysC ＋ 6.489 × PI ＋ 4.544 × cRI - 8.358 （r^2 = 0.698, F = 18.506, P 〈 0.001）. Conclusions： AKI is common in post-CA syndrome. Renal Doppler and novel AKI biomarkers in serum and urine are of significant importance as early predictors of post-CA AKI.
Background： Majority of the research on cardiac arrest （CA） have focused on post-CA brain injury and myocardial dysfunction, the renal dysfunction and acute kidney injury （AKI） in other critical illnesses after CA have not been well described. This study was designed to assess AKI with renal Doppler and novel AK1 biomarkers in a swine model of ventricular fibrillation cardiac arrest （VFCA）. Methods： Thirty healthy piglets were divided into VFCA group （17 = 22） and Sham group （n = 8） in a blinded manner. Mean arterial pressure, heart rate. and cardiac output were recorded continuously. Cardiac arrest （CA） was induced by programmed electric stimulation in the VFCA group, and then cardiopulmonary resuscitation was performed. Twenty piglets returned of spontaneous circulation （ROSC） and received intensive care. Blood and urine samples were collected for AKI biomarkers testing, and Color Doppler flow imaging was performed at baseline, 6 h, 12 h, and 24 11. respectively after ROSC. At ROSC 24 h, the animals were sacrificed and a semi-quantitative evaluation of pathologic kidney injury was performed. Results： In the VFCA group, corrected resistive index （cRl） increased from 0.47 ± 0.03 to 0.64 ± 0.06, and pulsatility index （PI） decreased from 0.82 ± 0.03 to 0.68 ± 0.04 after ROSC. Cystatin C （CysC） in both serum and urine samples increased at ROSC 6 h, but neutrophil gelatinase-associated lipocalin （NGAL） in serum increased to 5.34 ± 1.68 ng/ml at ROSC 6 h, and then decreased to 3.16 ± 0.69 ng/ml at ROSC 24 h while CysC increasing constantly. According to the renal histopathology, 18 of 20 animals suffered from kidney injury. The grade of renal injury was highly correlated with RI, cRI, NGAL, and CysC. Linear regression equation was established： Grade of renal injury = 0.002× serum CysC ＋ 6.489 × PI ＋ 4.544 × cRI - 8.358 （r^2 = 0.698, F = 18.506, P 〈 0.001）. Conclusions： AKI is common in post-CA syndrome. Renal Doppler and novel AKI biomarkers in serum and urine are of significant importance as early predictors of post-CA AKI.
基金
This research was supported by a grant from the Natural Science Foundation of China （No. 81372025）.
