Effect of CO2 pneumoperitoneum on the systemic and peritoneal cytokine response in a LPS-induced sepsis model.

We studied the effect of carbon dioxide (CO2) pneumoperitoneum on the systemic and peritoneal cytokine response in a rat model of intraperitoneal sepsis. After intraperitoneal injection of bacterial lipopolysaccharide (LPS, 10 mg/kg), rats were divided into 3 groups (n = 49 in each group): control (abdominal puncture); CO2 pneumoperitoneum, and laparotomy. Blood and peritoneal lavage fluid (PLF) were sampled at 0, 1, 2, 3, 4, 6, and 8 h after LPS challenge. Blood cell counts, plasma endotoxin level, and the levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), and interleukin-6 (IL-6) in the plasma and PLF were measured. Blood cell counts did not differ between the 3 groups. Plasma endotoxin levels in the pneumoperitoneum group were significantly increased immediately after the procedure (p < 0.05). Although peak plasma TNF-alpha levels in the pneumoperitoneum group were seen immediately after the procedure, other changes in plasma cytokine levels did not differ significantly between the 3 groups. PLF TNF-alpha and IL-1beta levels in the pneumoperitoneum group were significantly lower than levels in the control and laparotomy groups soon after the procedure (p < 0.05). PLF IL-6 levels in the pneumoperitoneum group tended to be lower than those in the laparotomy group. In conclusion, CO2 pneumoperitoneum might induce different responses between systemic and peritoneal cytokines soon after the procedure in a rat model of intraperitoneal sepsis.

The effect of gases in the intraperitoneal space on cytokine response and bacterial translocation in a rat model.

BACKGROUND: The aim of this study was to examine cytokine response and bacterial translocation after exposure of the intraperitoneal space to carbon dioxide (CO2), helium (He), and air (Air) in a rat model. METHODS: For this study, 120 Sprague-Dawley rats underwent anesthesia only (Control), 10 mmHg pneumoperitoneum (PP), or abdominal wall lift (AWL). The rats were divided into five groups according to experimental procedure: Control, PP-CO2, AWL-CO2, AWL-He, and AWL-Air. At 0, 3, 6, and 24 h after the procedures, the levels of interleukin 1beta (IL-1beta) and interleukin 6 (IL-6) in both plasma and peritoneal lavage fluid (PLF) were measured, and the translocation of bacteria to the mesenteric lymph nodes was evaluated. RESULTS: The plasma IL-1beta and IL-6 levels in the PP-CO2, AWL-CO2, and AWL-He groups were significantly lower than those in AWL-Air group at 6 h (p < 0.05). The PLF IL-1beta (at 3, 6, and 24 h) and IL-6 (at 6 h) levels in the AWL-CO2 group were significantly lower than those in the AWL-Air group (p < 0.05). There were no significant differences in IL-1beta and IL-6 responses among the PP-CO2, AWL-CO2, and AWL-He groups. The AWL-CO2 and PP-CO2 groups had lower incidences of bacterial translocation than did the AWL-Air group (p < 0.05). CONCLUSIONS: The results from this study suggest that the gas in the intraperitoneal space, but not the increased intraabdominal pressure, causes the alterations in host cytokine response and bacterial translocation. Carbon dioxide may play a primary role in the reduced immune response associated with laparoscopic surgery.

Does portal hypertension contribute to the pathogenesis of gastric ulcer associated with liver cirrhosis?

The prevalence of gastric ulcers in patients with liver cirrhosis is increased compared with that in the general population, and portal hypertension may contribute to the increased risk of gastric ulcer in cirrhosis patients. Aggressive factors involved in the pathogenesis of gastric ulcer are diminished in association with portal hypertension. In contrast, most of the important gastric mucosal defense mechanisms are shown to be impaired in portal hypertension; many of these mechanisms are also found to be altered in patients with liver cirrhosis. Portal hypotensive treatment with propranolol reduces ethanol-induced gastric mucosal damage in portal hypertensive rats and improves endoscopic signs of portal hypertensive gastropathy in cirrhosis patients. Together, these findings suggest portal hypertension-induced impairment of the gastric mucosal defenses to be an important factor in the pathogenesis of gastric ulcer in patients with liver cirrhosis. Prospective studies of portal pressure-reducing procedures, such as pharmacotherapy with propranolol, and their effect on the incidence of gastric ulcer in cirrhosis patients are needed to confirm this suggestion.

Vasopressin antagonist improves renal function in a rat model of pneumoperitoneum.

Pneumoperitoneum (PP) is associated with oliguria and increased plasma arginine vasopressin (AVP) levels. This study investigated the role of AVP in the pathogenesis of oliguria due to PP. Anesthetized and ventilated rats (n = 12) were subjected for 1 h to carbon dioxide PP with an intra-abdominal pressure of 8 mmHg or, as control, at 0 mmHg, before the determination of plasma AVP level. Another group of rats (n = 48) subjected to PP or control conditions was pretreated with the AVP V2 receptor antagonist, OPC-31260 (5 mg/kg), or vehicle, and their renal parameters were measured. Glomerular filtration rate (GFR) was determined by inulin clearance in an additional group of rats (n = 12) subjected to PP with or without pretreatment with OPC-31260. Rats subjected to PP had higher plasma AVP levels than did controls (17.3 +/- 8.1 pg/ml vs 1.5 +/- 0. 6 pg/ml, P < 0.05). In rats pretreated with vehicle, PP decreased urine output, excretion of water, and urea nitrogen, leading to reduced serum osmolality and serum sodium levels as well as elevated blood urea nitrogen levels. OPC-31260 pretreatment improved urine output, excretion of water, and urea nitrogen, thereby preventing changes in serum osmolality, serum sodium levels, and blood urea nitrogen levels. OPC-31260 pretreatment did not affect GFR. Results suggest that plasma AVP contributes to the oliguria due to PP. OPC-31260 may be useful in treating the water retention associated with PP.