Kidney Injury in a Hemodilution Model of Hemorrhagic Shock and Fluid Resuscitation

Abstract

Background: Fluid therapy is indispensable in treating patients with hemorrhagic shock. However, fluid overload correlates with kidney injury in patients with hemorrhagic shock. We hypothesized that hemodilution after fluid treatment contributes to the kidney injury.

Methods: An animal model was established to mimic different severity of hemodilution, through resuscitating hemorrhagic shock with mixture of blood and lactated Ringer's solution (LR) in different ratios. A total of 20 rats were divided into the following four groups, the Sham group, Mild group, Moderate group, and Severe group. In the Sham group, rats were anesthetized and catheterized only. In the other three groups, shock was induced by extracting 40% of the estimated circulating blood. One hour later, rats were resuscitated with a mixture of blood and LR with ratio 1:0 in the Mild group, 0.5:0.5 in the Moderate group, and 0:1 in the Severe group. The histology of the kidneys was observed with hematoxylin and eosin (HE) staining. The mitochondria membrane potential ψ and adenosine triphosphate (ATP) production of the kidneys were measured. The serum creatinine (SCr) and blood urine nitrogen (BUN) were measured.

Results: Renal tubular lumina dilation and mild interstitial edema occurred in the Mild group with HE staining. Proximal convoluted tubule damage, including tubular casts, narrow renal tubular lumina, and interstitial edema occurred in the Moderate group and Severe group. Mitochondrial JC-1 and ATP production decreased as hemodilution progressed. SCr and BUN increased in the Moderate group and Severe group.

Conclusions: The hemodilution post hemorrhagic shock and fluid resuscitation led to kidney injury.

Keywords: Fluid resuscitation: Hemodilution; Kidney injury; Mitochondria damage.