Low-dose ketamine pretreatment reduces oxidative damage and inflammatory response following CO2 pneumoperitoneum in...

The duration of pneumoperitoneum during laparoscopic procedures may contribute to post-surgical oxidative stress. Previous studies have shown that low-dose ketamine, an anesthetic with anti-inflammatory properties, protects various organs from ischemia-reperfusion injury. This study investigated the effects of low-dose ketamine on the overproduction of oxidants and the tissue damage caused by intra-abdominal pressure during CO2 pneumoperitoneum.

Male Sprague Dawley rats received a CO2 pneumoperitoneum of 15 mmHg and preceded by either low-dose ketamine (KP1, 5 mg/kg; KP2, 10 mg/kg) or 0.9% saline (PR, 3 ml). General anethesia was provided by pentobarbital and sevoflurane. The control group (CR) received an intraperitoneal saline injection and sham surgery. Three hours after pneumoperitoneum, serum concentrations of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), malondialdehyde (MDA), superoxide dismutase (SOD) and intestinal fatty acid binding protein (iFABP) were measured and liver, kidney, lung, and intestine were evaluated for tissue damage.

The highest plasma MDA, TNF-α, IL-6 and iFABP values were observed at T1 (after 3 hours of pneumoperitoneum) in the PR group, followed by the KP1, KP2, and CR groups (P < 0.01). SOD concentrations showed an opposite trend and were highest in the CR group, followed by the KP2, KP1, and PR groups (P < 0.01). TNF-α concentration was significantly lower in the KP2 than the KP1 group (P < 0.05). Histopathologic scoring of organ sections demonstrated the lowest scores in the KP2 group, followed by the KP1 and PR groups, in an increasing order (P < 0.05).

Pretreatment with low-dose ketamine before general anaesthesia protects against potential oxidative damage and inflammatory response caused by CO2 pneumoperitoneum.