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Background: Only two aortic stent grafts (Ancure-Guidant, Menlo Park, CA, and AneuRx-Medtronic, Sunnyvale, CA) have been FDA-approved for endovascular aortic aneurysm repair (EndoAAA). These grafts differ significantly in construction and clinical advantage, and combining components of these grafts (hybrid graft) is occasionally necessary. The role and outcome of hybrid aortic stent grafts is unknown., Methods: All EndoAAA procedures during an 18-month period (10/99-4/01) were reviewed using the hospital record and a computer registry. Endografts were classified as hybrid if components from more than one type of stent graft were used or standard if constructed from only one stent graft type. Hybrid grafts were further classified as "anticipated" or "unanticpated." Outcomes were compared between hybrid and standard grafts using Fisher's exact test., Results: One hundred forty-five EndoAAA repairs were performed (AneuRx, 67; Ancure, 70; and custom-made, 8) of which 14 (9.6%) were hybrid grafts. The majority of hybrid grafts (11) were constructed by adding AneuRx aortic or iliac cuffs to Ancure grafts. In most cases, the need for a hybrid graft was unanticipated (10) and related to an intraoperative proximal type I endoleak (7). Conversion to open operation was avoided in six patients by constructing hybrid grafts. When anticipated (4), hybrid grafts were constructed to treat complex iliac aneurysms. Outcomes in all categories were similar (P > 0.05) for hybrid vs standard grafts: technical success (93 vs 99%), conversion toopen AAA (7.1 vs 2.3%), vascular complications (7.1 vs 7.6%), systemic complications (21 vs 11%), endoleak (15 vs 14%), and rupture (0 vs 0%)., Conclusions: The short-term safety and effectiveness of hybrid grafts are similar to those of standard grafts. Combining graft components to create hybrid grafts may increase the ability to treat complex iliac aneurysmal disease and may reduce conversions to open AAA repair. Thus, access to multiple graft types may be an important factor in the success and safety of EndoAAA repair.

We hypothesized that the disrupted gastrointestinal transit that occurs during endotoxemia is mediated by nitric oxide (NO) and that the inhibition of NO synthesis will normalize intestinal transit and gastric emptying. To determine the effects of endotoxin and steroids on the activity of gastrointestinal smooth muscle NO synthase, rats underwent placement of an intravenous (iv) line and then were given Escherichia coli lipopolysaccharide (LPS) 10 mg/kg/iv; LPS, 10 mg/kg/iv + dexamethasone, 3 mg/kg/iv; or saline. The activity of nitric oxide synthase in the stomach, small intestine, and colon were determined by measuring the conversion of L-[3H]arginine to L-[3H]citrulline. To determine intestinal transit and gastric emptying, gavage feedings of nonabsorbable liquid markers were given and rats divided into eight groups: 0.9% NaCl, 1 ml/hr x 5 hr (control); LPS, 10 mg/kg/iv; LPS + N-omega-nitro-L-arginine methyl ester (L-NAME), 10 mg/kg/hr x 5 hr; LPS + N-omega-nitro-D-arginine methyl ester (D-NAME), 10 mg/kg/hr x 5 hr; LPS + L-arginine, 100 mg/kg/hr x 5 hr; LPS + L+NAME + L-arginine; LPS + N-omega-nitro-L-arginine (L-NNA) 10 mg/kg/hr; or LPS + L-NNA + L-arginine. LPS increased the enzymatic activity of both the constitutive and the inducible forms of NO synthase in the small intestine and fundus of the stomach. The acceleration of intestinal transit produced by endotoxemia was reversed with both L-NAME and L-NNA but not with D-NAME. Endotoxemia slowed gastric emptying but this effect was not reversed with either L-NAME or L-NNA. We conclude that NO plays a major role in mediating the rapid intestinal transit during endotoxemia.

Prostanoid activity was correlated with the hemodynamic effects of protamine sulfate reversal of heparin in 24 dogs undergoing three different pretreatment regimens: Group I (n = 8) received saline, Group II (n = 8) received the thromboxane synthetase inhibitor U63,557A (30 mg/kg), and Group III (n = 8) received indomethacin (10 mg/kg). Pretreatment substances were administered as 5-min intravenous infusions 20 min before anticoagulation with intravenous heparin (150 IU/kg). Protamine sulfate (1.5 mg/kg) was subsequently given as a 10-sec intravenous infusion 30 min after heparin had been administered. Hemodynamic data, as well as prostacyclin (PGI2) and thromboxane (TxA2) activity in aortic, venous, and pulmonary artery blood samples, were assessed over a 30-min time period following protamine administration. Group III indomethacin pretreatment provided the most protection from declines in blood pressure, heart rate, cardiac output, venous oxygen saturation, oxygen consumption, and elevations in pulmonary pressures and was accompanied with actual declines in PGI2. Group II U63,557A pretreatment was associated with the most severe hemodynamic changes and the greatest increase in PGI2 (+576%). Elevated PGI2 correlated with hypotension at 1 and 3 min (P less than 0.01), as well as pulmonary artery pressure declines at all times following protamine reversal. TxA2 changes did not correlate with hemodynamic changes. Protamine's adverse hemodynamic responses were attenuated with cyclooxygenase blockade by indomethacin, but were worsened with selective TxA2 blockade with U63,557A. Excess arachadonic acid precursors in the latter setting may increase PGI2 production. This study, for the first time, raises the possibility that PGI2 contributes to the adverse effects accompanying protamine reversal of heparin anticoagulation.