The effect of peritoneal contamination on wound strength of small bowel and colonic anastomoses.

Primary bowel repair in the face of peritoneal soilage is still a controversial area. Previous studies using the rat model have demonstrated a difference in new collagen synthesis after 24 hours of peritoneal contamination. Currently, the effect of short-term fecal contamination of the peritoneal cavity on anastomotic healing and strength is not known. This study was designed to evaluate anastomotic wound strength in the face of fecal contamination during this time period. Twenty Sprague Dawley rats were randomized into two groups: twelve-hour control (n = 10) and 12-hour cecal ligation and puncture (CLP; n = 10). Both groups underwent laparotomy with either CLP (12-hour) or cecal manipulation (12-hour control). Animals were allowed to recover for 12 hours, according to their assigned groups. A second laparotomy was subsequently performed in which the CLP groups had partial cecectomy to remove the source of contamination, followed by mid-jejunal and colonic division with associated primary anastomosis. Control groups had a similar procedure without partial cecectomy. All abdomens were irrigated, and all animals received immediate postoperative antibiotics and an initial fluid bolus. Animals were recovered and received 3 days of postoperative antibiotics. On postoperative day 4, animals were sacrificed and anastomotic sites were resected. Specimens were then placed in a tensiometer and disrupted under dynamic stress. Peak load was recorded for each, and maximum standard load was calculated. Hydroxyproline content of each segment was also determined after disruption. CLP values were compared with control values using unpaired Student's t test. Statistical significance threshold was P < 0.5. There was no significant difference in maximum anastomotic wound strength or hydroxyproline content between 12-hour CLP and 12-hour control group for both small bowel and colon anastomoses. Short-term peritoneal soilage (12-hour) does not significantly effect the maximum tensile strength or hydroxyproline content of primary small bowel or colonic anastomoses in this model. This study suggests that short-term fecal contamination of the peritoneal cavity may not be a contraindication to primary bowel anastomosis.

Evidence for morphine downregulating immunocytes during cardiopulmonary bypass in a porcine model.

Cardiopulmonary bypass is associated with both cellular immunosuppression and an inflammatory response. Previous studies have demonstrated that morphine, a naturally occurring substance, can downregulate granulocyte, monocyte and endothelial activity. It can even prevent the activation caused by exposing these cells to plasma obtained from patients undergoing cardiopulmonary bypass. The present study demonstrates that preadministering a high dose of morphine (3.3 mg/kg) to pigs prior to cardiopulmonary bypass also diminishes the activation levels of these cells. In animals not given morphine, monocyte activation levels were 45% compared to 14% exposed to the opiate. Granulocytes also exhibited the same statistically significant (P < 0.05) drop in cellular activation. Activation is determined by computer-assisted microscopic image analysis whereby cellular shape is indicative of the cells activity. Additionally, in animals pretreated with morphine, a twofold increase in the number of cells was obtained, indicating that the endothelium also was downregulated.

Resuscitation with lactated Ringer's solution after hemorrhage: lack of cardiac toxicity.

The toxicity of D-lactate has been recognized for almost 30 years. This compound is found in the racemic mixture of lactated Ringer's solutions routinely used for peritoneal dialysis and the resuscitation of trauma victims. The current study was designed to investigate whether toxicity occurred at the D-lactate concentrations achieved during hemorrhage resuscitation with racemic lactated Ringer's solution. Conscious unrestrained male Sprague-Dawley rats (n = 24) were monitored for electrocardiographic abnormalities while undergoing hemorrhage and subsequent resuscitation with either L-lactated, D-lactated, or racemic lactated Ringer's solution. The rats infused with D-lactate showed significant toxicity as evidenced by bradycardia, premature ventricular contractions, and ventricular fibrillation. No such alterations were observed in the animals resuscitated with L-lactate or racemic solutions. Resuscitation with the racemic lactate mixture increased the D-lactate concentrations in the blood, but was not associated with overt changes in cardiac rhythm. The infusion of the different resuscitation fluids produced few significant differences in acid-base status of hemorrhaged rats. These findings indicate that although toxicity may be achieved with a Ringer's solution containing only D-lactate, resuscitation using the racemic mixture does not achieve D-lactate concentrations high enough to be detrimental to the animal.

Endogenous opiates do not modulate LPS-induced alterations in carbohydrate metabolism.

This study aimed to determine the contribution of endogenous opiates to the hormonal and glucose metabolic response to lipopolysaccharide (LPS). Rats were infused with naloxone (NAL) (32 micrograms/h) for 2 h prior to the injection of LPS (100 micrograms/100 g body weight) and hemodynamic, hormonal, and metabolic parameters were determined. NAL produced no detectable alterations in any of the parameters assessed. LPS transiently decreases (26%) mean arterial blood pressure (MABP) and increased plasma glucose concentration (100-130%), glucose rate of appearance (50-100%), and glucose rate of disappearance (50-100%). NAL did not alter the LPS-induced drop in mean arterial blood pressure or the glucose response to LPS. LPS reduced plasma insulin (54%), and increased glucagon (270%), corticosterone (180%), and tumor necrosis factor concentrations in plasma (peak 3200-4600 pg/mL at 90 min), with no modification by NAL pretreatment. These results suggest a lack of involvement of endogenous opiate pathways in the glucose metabolic and hormonal responses to LPS.