Acutely increased intra-abdominal pressure (IAP) can lead to
multiple organ failure. As blood flow to intra-abdominal organs is reduced by high venous resistance,
ischemia-reperfusion (I/R) injury plays an important role in the pathogenesis of
abdominal compartment syndrome (ACS) following IAP.
Melatonin, a secretory product of the pineal gland, is known to have
free radical scavenging and antioxidative properties in several oxidative processes. The objective of this study was to examine the potential protective properties of
melatonin on the oxidative organ damage in a rat model of ACS. Under
ketamine anesthesia, an arterial
catheter was inserted intraperioneally (i.p.) and using an aneroid manometer connected to the
catheter, IAP was kept at 20 mmHg (
ischemia group; I) for 1 hr. In the
ischemia/reperfusion (I/R) group, pressure applied for an hour was decompressed and a 1-hr reperfusion period was allowed. In another IR group,
melatonin was administered (10 mg/kg, i.p.) immediately before the
decompression of IAP. The results demonstrate that tissue levels of
malondialdehyde (MDA) and
myeloperoxidase activity (MPO; index of tissue neutrophil infiltration) were elevated, while
glutathione (GSH; a key to
antioxidant) levels were reduced in both I and I/R groups (P < 0.05-0.001).
Melatonin treatment in I/R rats reversed these changes (P < 0.01-0.001). Moreover,
melatonin given to the I/R group reduced the elevations in serum
aspartate aminotransferase,
alanine aminotransferase and blood
urea nitrogen levels and abolished the increase in serum
creatinine levels. Our results indicate that
melatonin, because of
antioxidant and
free radical scavenging properties, ameliorates reperfusion-induced oxidative organ damage. In conclusion, the results of the present study suggest that the therapeutic value of
melatonin as a '
reperfusion injury-limiting' agent must be considered in ACS.