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

Abstract

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.

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

“…Severe hydronephrosis leads to prolonged operating time in laparoscopic surgery, which may consequently lead to increased oxidative stress ( 38 ). Based on these facts and the observations of our previous study ( 16 ), it can be inferred that high-pressure CO 2 pneumoperitoneum may cause severe oxidative stress, mitochondrial injuries and even cell apoptosis in rabbit kidneys with severe hydronephrosis. Therefore, the present study examined the effects of high-pressure CO 2 pneumoperitoneum on kidneys with severe hydronephrosis and investigated the possible underlying mechanism.…”

“…In our previous study, the effect of pneumoperitoneum pressure on rabbit kidneys with no hydronephrosis, and with mild or severe hydronephrosis was investigated ( 16 ). The results indicated that severely obstructed kidneys have reduced cell tolerance to intraabdominal pressure, and that they are more likely to suffer oxidative damage and mitochondrial injuries when they were exposed to pneumoperitoneal pressure.…”

The effect of shear on the cytoskeleton remodeling and physiological performance of myocardium cells through Tmod1

“…ROS, MDA and T-SOD are important indexes for detecting oxidative damage and antioxidative damage in cells. 8 Compared with control group, ROS uorescence intensity and mitochondrial calcium uorescence intensity signicantly enhanced in si-Tmod1 group. Compared with si -Tmod1 group, shear group can signicantly reduce the increasement of ROS levels and calcium content produced by Tmod1 restrain (P < 0.05).…”

Damage-associated molecular patterns in trauma

“…CytC which is also released from dying cells during cellular trauma can act as a danger signal in the extracellular space. In experiments on rabbits, oxidative injury to mitochondria has been demonstrated to be associated with high mitochondrial expression of CytC [352]. In studies on a burn model in mice, circulating CytC levels were found to be elevated eightfold within 3 h post-injury and remained elevated at 24 h [353].…”