Acute Kidney Injury Induced by Various Pneumoperitoneum Pressures in a Rabbit Model of Mild and Severe Hydronephrosis

Li, Wei; Cao, Zhixiu; Meng, Qingtao; Ye, Weimin; Yao, Xiaolan

doi:10.1159/000362845

Cited by 11 publications

(6 citation statements)

References 29 publications

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“…As mentioned previously, certain patients undergoing surgery also present with a certain degree of kidney hydronephrosis. It has been reported that kidneys with hydronephrosis are more likely to suffer hypoxia problems (26,27). According to our previous study, rabbit kidneys with severe hydronephrosis suffered acute kidney injury more readily compared with those with mildly nephrotic kidneys when exposed to pneumoperitoneal pressure (28).…”

Section: Discussionmentioning

confidence: 77%

Oxidative damage and mitochondrial injuries differ following pneumoperitoneum pressure in rabbit models of varying degrees of hydronephrosis

Zhao

Rao

et al. 2018

Mol Med Report

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The influence of intraabdominal pressure which is necessary to maintain the operating area during the surgery cannot be ignored especially on the kidneys. Many articles have reported the effect of intraabdominal pressure on normal kidneys. However, the influence of intraabdominal pressure on hydronephrosis kidneys is rarely studied. The aim of the present study was to clarify whether intraabdominal pressure tolerance is modified in various degrees of kidney hydronephrosis by evaluating oxidative damage and mitochondrial injuries. A total of 72 rabbits were randomly divided into three groups (groups N, M and S, which represented rabbits with no, mild and severe hydronephrosis, respectively). Rabbits in groups M (n=24) and S (n=24) underwent a surgical procedure inducing mild or severe hydronephrosis, respectively. Subsequently, rabbits in all groups were allocated to 4 subgroups (N0‑N3, M0‑M3 and S0‑S3) consisting of 6 rabbits each. Groups 0 to 3 were, respectively, subjected to intraabdominal pressures of 0, 5, 10 and 15 mmHg. Oxidative damage was assessed by analyzing levels of reactive oxygen species (ROS), superoxide dismutase (SOD), malondialdehyde (MDA), glutathione peroxidase (GSH‑Px), catalase (CAT) and lactate (LD). Mitochondrial injuries were assessed based on mitochondrial membrane potential (MMP) alterations, mitochondrial structure and cytochrome c (cytc) protein expression, as measured by JC‑1 staining, electron microscopy and western blotting, respectively. Oxidative damage and mitochondrial injuries were noticeably exacerbated in group N and M with increased levels of ROS, MDA and LD, decreased levels of SOD, GSH‑Px, CAT and MMP, mitochondrial vacuolization and higher expression of cytc when the intraabdominal pressure reached 15 mmHg. In group S, these alterations occurred at pressures of 10 and 15 mmHg. Therefore, it was concluded that in rabbits exposed to pneumoperitoneal pressure, kidneys with severe hydronephrosis were more likely to suffer from oxidative damage and mitochondrial injuries compared with kidneys with mild hydronephrosis and normal kidneys.

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Section: Discussionmentioning

confidence: 77%

Oxidative damage and mitochondrial injuries differ following pneumoperitoneum pressure in rabbit models of varying degrees of hydronephrosis

Zhao

Rao

et al. 2018

Mol Med Report

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“…Nevertheless, the majority of studies associated with pneumoperitoneum pressure damage involve normal kidneys ( 14 ); however, a number of patients who undergo laparoscopic surgery also exhibit a degree of kidney obstruction. To date, only a limited number of studies have reported how pneumoperitoneum affects kidneys with hydronephrosis ( 15 ).…”

Section: Introductionmentioning

confidence: 99%

High-pressure carbon dioxide pneumoperitoneum induces oxidative stress and mitochondria-associated apoptotic pathway in rabbit kidneys with severe hydronephrosis

Zhao

Rao

et al. 2018

Int J Mol Med

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The primary aim of the present study was to investigate the potential effect of high-pressure carbon dioxide (CO2) pneumoperitoneum on kidneys with severe hydronephrosis and to investigate the possible underlying mechanism. A total of 18 rabbits underwent a surgical procedure inducing severe hydronephrosis. Rabbits were then divided at random into three groups (n=6 each) and subjected to intraabdominal pressure of 0, 8 or 18 mmHg, respectively. CO2 inflation lasted for 90 min in the pneumoperitoneum groups. Oxidative stress was assessed by measurements of reactive oxygen species (ROS). Activation of apoptosis was analyzed by western blot analysis of B-cell lymphoma 2 (Bcl-2), Bcl-2-associated x protein (Bax), cytochrome c (Cyt c), caspase-3 and caspase-9 levels. In addition, TUNEL assay, hematoxylin and eosin (H&E) staining, measurement of mitochondrial membrane potential (MMP) and detection of changes to kidney ultramicrostructure were performed. In the 0 and 8 mmHg groups, all results were normal and similar. However, in the 18 mmHg group, the kidneys suffered oxidative damage and mitochondrial injuries, and increased ROS levels, lower MMP and mitochondrial vacuolization were observed. Furthermore, the mitochondrial/caspase-dependent pathway of apoptosis was activated, as indicated by the apoptotic index, and the expression levels and translocation of Bax, Bcl-2, Cyt c, caspase-3 and caspase-9. Therefore, it is concluded that high-pressure CO2 pneumoperitoneum induces oxidative damage and apoptosis in rabbit kidneys with severe hydronephrosis, which is associated with the mitochondrial apoptotic pathway.

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“…The susceptibility to kidney damage due to hemodynamic or biological insults during “IAH exposure” might be theoretical detectable through the use of biomarkers of AKI (Li et al, 2014 ). Several biomarkers have been proposed to identify the kidney damage during clinical scenarios at risk for AKI, for example the perioperative urinary liver-type fatty-acid-binding protein during endovascular abdominal repair (Obata et al, 2016 ).…”

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confidence: 99%

The Pathophysiological Hypothesis of Kidney Damage during Intra-Abdominal Hypertension

et al. 2016

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Acute Kidney Injury Induced by Various Pneumoperitoneum Pressures in a Rabbit Model of Mild and Severe Hydronephrosis

Cited by 11 publications

References 29 publications

Oxidative damage and mitochondrial injuries differ following pneumoperitoneum pressure in rabbit models of varying degrees of hydronephrosis

Oxidative damage and mitochondrial injuries differ following pneumoperitoneum pressure in rabbit models of varying degrees of hydronephrosis

High-pressure carbon dioxide pneumoperitoneum induces oxidative stress and mitochondria-associated apoptotic pathway in rabbit kidneys with severe hydronephrosis

The Pathophysiological Hypothesis of Kidney Damage during Intra-Abdominal Hypertension

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