4 +/- 0.2). Sections from group A animals revealed the mildest EC injury (1.3 +/- 0.3 vs. group D p < 0.01). No significant difference was detected between group A and B. EC injury grade in group C (2.7 +/- 0.6) was higher than that in group B (1.8 +/- 0.6) but did not reach statistical significance (p = 0.58).
Conclusion: When possible, vascular reconstruction following
use of shunts should include an interposition graft after debridement Ispinesib of the arterial edges having interfaced with the shunt. Finally, to minimize intimal injury to the native vessel, this model suggests that indwell times of shunts should be <9 hours.”
“OBJECTIVE: Glucose intolerance is frequently associated with an altered plasma lipid profile and increased cardiovascular Etomoxir disease risk. Nonetheless, lipid metabolism is scarcely studied in normolipidemic glucose-intolerant patients. The aim of this study
was to investigate whether important lipid metabolic parameters, such as the kinetics of LDL free and esterified cholesterol and the transfer of lipids to HDL, are altered in glucose-intolerant patients with normal plasma lipids.
METHODS: Fourteen glucose-intolerant patients and 15 control patients were studied; none of the patients had cardiovascular disease manifestations, and they were paired for age, sex, race and co-morbidities. A nanoemulsion resembling a LDL lipid composition (LDE) labeled with C-14-cholesteryl ester and H-3-free cholesterol was intravenously injected, and blood samples were collected over a 24-h period to determine the fractional clearance rate of the labels by compartmental analysis. The transfer of free and esterified cholesterol, triglycerides and phospholipids from the LDE to HDL was measured by the incubation of the LDE with plasma and radioactivity counting
of the supernatant after chemical precipitation of non-HDL fractions.
RESULTS: The levels of LDL, non-HDL and HDL cholesterol, triglycerides, ML323 apo A1 and apo B were equal in both groups. The 14 C-esterified cholesterol fractional clearance rate was not different between glucose-intolerant and control patients, but the H-3-free- cholesterol fractional clearance rate was greater in glucose-intolerant patients than in control patients. The lipid transfer to HDL was equal in both groups.
CONCLUSION: In these glucose-intolerant patients with normal plasma lipids, a faster removal of LDE free cholesterol was the only lipid metabolic alteration detected in our study. This finding suggests that the dissociation of free cholesterol from lipoprotein particles occurs in normolipidemic glucose intolerance and may participate in atherogenic signaling.”
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