Abstract
BackgroundThe induction of the pneumoperitoneum increases intraabdominal pressure (IAP), causing splanchnic ischemia, whereas its deflation normalizes IAP and splanchnic blood flow. We investigated the oxidant-antioxidant status of dogs who underwent low pressure (7 mm Hg), standard pressure (12 mm Hg), and high pressure (15 mm Hg) pneumoperitoneum.ResultsTwenty-four beagle dogs (12 males and 12 females), 4–6 years old, weighing 8–11 kg were used. The animals were assigned to one of four groups (n = 6 dogs). Group 1 served as a control; these animals received only anaesthesia for 90 min. In groups 2, 3 and 4, intra-abdominal pressure was increased to 7, 12 and 15 mmHg, respectively, and maintained for 60 min. Total oxidant status (TOS) and total antioxidant status (TAS) were determined in venous blood samples. The percentage ratio of TOS to TAS provided an oxidative stress index (OSI).No significant difference in TOS levels was found among the groups. A significant decrease in TAS levels and an increase in OSI levels were observed at 90 min and 24 h of pneumoperitoneum deflation within group 4. No differences were found among the groups.ConclusionsA high pressure pneumoperitoneum induced significant changes in TAS and OSI. In addition, TOS and TAS levels are useful markers for evaluating changes in the oxidative status caused by a pneumoperitoneum during laparoscopy. Furthermore, a low-pressure pneumoperitoneum could attenuate oxidative stress induced by CO2 insufflation in dogs.
Highlights
The induction of the pneumoperitoneum increases intraabdominal pressure (IAP), causing splanchnic ischemia, whereas its deflation normalizes IAP and splanchnic blood flow
Experimental and clinical studies have shown that an increase in intra-abdominal pressure (IAP) associated with a pneumoperitoneum greater than normal physiological portal pressure (7–10 mm Hg) causes splanchnic ischemia [7], which leads to free radical production [8]
There were no significant worsening in heart rate, mean arterial pressure, rectal temperature, end-tidal carbon dioxide, peripheral oxygen saturation, and respiratory rates (Table 1)
Summary
The induction of the pneumoperitoneum increases intraabdominal pressure (IAP), causing splanchnic ischemia, whereas its deflation normalizes IAP and splanchnic blood flow. A pneumoperitoneum is generally established during a laparoscopy by continuous insufflation of carbon dioxide (CO2) into the peritoneal cavity to provide adequate visualization and exposure of structures. Experimental and clinical studies have shown that an increase in intra-abdominal pressure (IAP) associated with a pneumoperitoneum greater than normal physiological portal pressure (7–10 mm Hg) causes splanchnic ischemia [7], which leads to free radical production [8]. Abdominal deflation at the end of laparoscopic procedures reduces IAP and increases splanchnic perfusion, oxidative stress from the ischemic injury remains [9]. To minimize oxidative stress during a pneumoperitoneum, an IAP less than the portal pressure
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