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不同中心静脉压水平在脓毒症相关性急性肾损伤中的作用

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目的 探讨中心静脉压(central venous pressure,CVP)水平在脓毒症相关性急性肾损伤(sepsis-associated acute kidney injury,SA-AKI)发生和发展过程中的作用.方法 应用盲肠结扎穿孔(cecal ligation and puncture,CLP)法诱导雄性SD大鼠脓毒症模型24h,以假手术组作为对照,给予两组大鼠静脉注射乳酸钠林格注射液诱导CVP升高至10、15和20mmHg,动态监测大鼠平均动脉压(mean arterial pressure,MAP)、心率(heart rate,HR)和动脉血乳酸(lactate,Lac),应用测流暗场成像(side stream darkfield imaging,SDF)技术检测大鼠肾脏皮质微循环灌注血管密度(perfused small vessel density,PVD)和微血管流动指数(microvascular flow index,MFI),并检测血肌酐(creatinine,CRE)、尿中性粒细胞明胶酶相关脂质运载蛋白(neutrophil gelatinase as-sociated lipocalin,NGAL)和肾组织白细胞介素6(interleukin-6,IL-6)水平和肾脏病理变化.结果 与假手术组比较,CLP大鼠的MAP显著下降、HR和Lac显著升高(P<0.05);肾脏PVD和MFI显著下降(P<0.05),血 CRE、尿NGAL和肾脏IL-6显著升高(P<0.05).与CVP 10mmHg比较,CLP大鼠在CVP 20mmHg时的PVD和MFI显著降低(P<0.05);假手术组大鼠在CVP 15mmHg 和 20mmHg 时的 PVD 和 MFI 显著低于 CVP 10mmHg(P<0.05).CLP 大鼠在 CVP 15mmHg 时的 IL-6 显著高于 CVP 10mmHg(P<0.05),CVP 20mmHg时的IL-6显著高于CVP 15mmHg(P<0.05).CLP大鼠随CVP逐渐升高而表现为皮质和髓质水肿,肾小管上皮细胞空泡变性、刷状缘脱落、肾小管阻塞、Bowman囊间隙消失,且髓质水肿较皮质明显.假手术组大鼠在CVP达20mmHg时,肾小球、肾小管肿胀,Bowman囊间隙变窄.结论 过高的CVP水平可以降低CLP大鼠肾脏皮质微循环灌注、促进局部炎性细胞因子活化和肾组织水肿,在SA-AKI过程中发挥损伤作用.
Role of Different Central Venous Pressure Levels in Septic-associated Acute Kidney Injury
Objective To explore the role of different CVP levels in the occurence and development of sepsis-associated acute kid-ney injury(SA-AKI).Methods Sepsis model was induced using the cecal ligation and puncture(CLP)method for 24h in male SD rats,with a sham group as the control.The rats in two groups were intravenously infused with Ringer's solution to induce an increase in CVP to 10,15 and 20mmHg,respectively.The hemodynamic parameters including mean arterial pressure(MAP),heart rate(HR),and arterial blood lactate(Lac)were dynamically monitored in rats.And side stream darkfield imaging(SDF)technique was used to de-tect the renal cortex microcirculation perfusion parameters including perfused small vessel density(PVD)and microvascular flow index(MFI).Renal injury markers including serum creatinine(CRE),urine neutrophil gelatinase associated lipocalin(NGAL),renal inflam-matory factor interleukin-6(IL-6)levels and renal histopathological changes were also detected.Results Compared with the sham group,the MAP of CLP rats significantly decreased,while HR and Lac significantly increased(P<0.05).The renal PVD and MFI were significantly decreased(P<0.05),while serum CRE,urine NGAL,and renal IL-6 were significantly increased(P<0.05).Com-pared with CVP 10mmHg,the PVD and MFI of CLP rats were significantly decreased at CVP 20mmHg(P<0.05);The PVD and MFI of sham group at CVP 15mmHg and 20mmHg were significantly lower than those of the CVP at CVP 10mmHg(P<0.05).The IL-6 of CLP rats at CVP 15mmHg was significantly higher than that at CVP 10mmHg(P<0.05),and the IL-6 levels at CVP 20mmHg were significantly higher than at CVP 15mmHg(P<0.05).In CLP rats,increasing CVP led to cortical and medullary edema,vacuolar degen-eration of renal tubular epithelial cells,loss of brush borders,tubular obstruction,and disappearance of Bowman's space;medullary ede-ma was more pronounced than in the cortex.In the sham group,glomerular and tubular swelling occurred at CVP 20mmHg,and Bowman's space became narrower.Conclusion Excessive CVP levels can decrease renal cortical microcirculation perfusion and promote the acti-vation of local inflammation and renal tissue edema in CLP rats,which exerting a detrimental effect during the process of S-AKI.

SepsisAcute kidney injuryCentral venous pressureRenal cortical microcirculation

刘景峰、李甜、白国强、赵梦雅、段美丽

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100050 首都医科大学附属北京友谊医院重症医学科

脓毒症 急性肾损伤 中心静脉压 肾脏皮质微循环

北京市自然科学基金资助项目北京市教育委员会科技计划重点项目

KZ201910025032

2024

医学研究杂志
中国医学科学院

医学研究杂志

CSTPCD
影响因子:0.702
ISSN:1673-548X
年,卷(期):2024.53(9)
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