Absence of intestinal bile promotes bacterial translocation.

Previously, the authors documented that extrahepatic biliary obstruction promotes the systemic translocation of bacteria from the intestine to visceral tissues. The current experiments were performed to determine whether it was the absence of intestinal bile or the presence of biliary obstruction that promoted bacterial translocation. Four groups of rats were studied: 1) nonoperated controls (n = 20), sham common bile duct-ligated (n = 22), common bile duct-ligated (n = 25), and common bile duct-diverted (choledochovesical bypass) (n = 23). The sham-ligated group underwent laparotomy and manipulation of the portal region; whereas the ligated group had their common bile ducts ligated, while the choledochovesical group had a silastic tube placed from the common bile duct to the bladder. Seven days later, at death, the incidence of bacterial translocation was higher in the groups of rats subjected to common bile duct ligation (41%) or diversion (32%) than in the control (3%) or sham-ligated (5%) groups (P less than 0.05). Histologic sections of ileums of ligated and diverted animals both showed subepithelial edema. These findings suggest that it is primarily the absence of bile in the intestine that promotes mucosal injury and bacterial translocation and not biliary obstruction.

Early mucosal and microvascular changes in feline intestinal transplants.

BACKGROUND: Bowel transplantation in humans is being performed with increasing success, but little is known about the early physiological alterations occurring in the graft. The objectives of this study were to characterize the mucosal and microvascular alterations that occur in the early stages of reperfusion of small intestinal allografts after varying intervals of hypothermic preservation and to assess the role of reactive oxygen metabolites and leukocyte adhesion glycoproteins in mediating these alterations. METHODS: A feline model of small intestinal transplantation was developed in which ileal grafts underwent 0-24 hours of cold ischemia before reperfusion. Some allografts, which underwent 6 hours of cold ischemia, were treated with monoclonal antibodies directed against either leukocyte (CD11/CD18) or endothelial cell (ICAM-1 or P-selectin) adhesion molecules or with a combination of superoxide dismutase and catalase. RESULTS: Cold preservation for 6 hours resulted in significant increases in intestinal microvascular fluid and protein exchange, and mucosal function was compromised. These alterations were not affected by treatment with either superoxide dismutase and catalase or monoclonal antibodies against ICAM-1 or P-selectin; however, the microvascular dysfunction was largely prevented by immunoneutralization of CD11/CD18 on leukocytes. CONCLUSIONS: CD11/CD18 antibodies may be useful in preserving microvascular function in allografts after prolonged hypothermic ischemia.

Use of enoxaparin in patients with heparin-induced thrombocytopenia syndrome.

PURPOSE: To determine whether low molecular weight heparin (LMWH) can be an alternative to unfractionated heparin (UH) for patients with heparin-induced thrombocytopenia syndrome (HIT). METHODS: The diagnosis of HIT was established in 126 patients by platelet aggregometry with UH (1 U/ml). These plasma samples were also tested for the ability to aggregate platelets in the presence of the LMWH enoxaparin (1 U/ml). Two patients with the HIT syndrome, after negative platelet aggregometry testing with enoxaparin, were anticoagulated with enoxaparin. RESULTS: Fifteen plasma samples that tested negative to UH also tested negative to enoxaparin. Forty-three of 126 (34%) UH-positive plasma samples aggregated platelets in the presence of enoxaparin. Twenty-two of 102 (22%) plasma samples with limited positive aggregation responses (minimal or no change in optical density) aggregated platelets in the presence of enoxaparin. However, 21 of 24 (88%) strongly positive plasma samples (30% to 60% change in optical density at 3 to 27 minutes) also aggregated platelets in the presence of enoxaparin. Two patients with HIT who received enoxaparin after aggregation testing demonstrated no cross-reactivity to enoxaparin achieved adequate anticoagulation and did not develop HIT. CONCLUSIONS: Thirty-four percent of plasma samples from patients with HIT (88% of those strongly positive) aggregated platelets in the presence of enoxaparin. Patients with HIT may safely receive enoxaparin if their plasma does not aggregate platelets in the presence of enoxaparin.

Neodymium:yttrium-aluminum-garnet laser fusion of endarterectomy flaps.

PURPOSE: This study evaluated the efficacy of neodymium:yttrium-aluminum-garnet laser welding of flaps in canine arteries and in securing the distal flap during human carotid endarterectomy. METHODS: Endarterectomy flaps were created in both common carotid and both common femoral arteries in 12 dogs. The flaps were repaired with either the neodymium:yttrium-aluminum-garnet laser or with 6-0 polypropylene sutures. The arteries were removed after duplex scanning at either 7 or 28 days. Eighteen high carotid endarterectomy flaps in 16 patients have been subsequently secured with the laser welding technique. RESULTS: Laser repairs (125 +/- 19 joule) of the canine arteries were completed more quickly than suture repairs (mean 25 seconds vs 135 seconds, respectively; p < 0.04). Duplex ultrasonography revealed no discernable differences between the two groups of arteries. Arteries studied at 7 days revealed three microscopic flaps (two suture, one laser), more subintimal fibroblastic proliferation in suture than laser-repaired carotid arteries (3: 1, p = 0.0530), and similar amounts of inflammation in suture- and laser-repaired arteries. Arteries studied at 28 days revealed one microscopic intimal flap (suture-repaired); equal fibroblastic and inflammatory responses in suture- and laser-repaired vessels; and no evidence of laser thermal injury. Eighteen carotid endarterectomy flaps have been successfully fused with no immediate or long-term complications in 16 patients (follow-up of 0 to 24 months). CONCLUSION: Laser fusion appears to be a safe and effective method for securing distal carotid endarterectomy flaps.