Cyclic variations in coronary blood flow (CFVs) in dogs with experimental coronary artery stenosis and endothelial injury appear to result primarily from the aggregation of platelets at the site of stenosis followed by dislodgement and distal embolization. Using this canine model, we tested the hypotheses: (a) that thrombin is an important mediator of CFVs in dogs with coronary stenoses and endothelial injury; (b) that inhibition of thrombin with heparin, or MCI-9038, a selective thrombin inhibitor, abolishes CFVs in this model; and (c) that abolition of CFVs by thrombin inhibition is time dependent. CFVs, produced in open-chest dogs by placing a flow-reducing plastic constrictor around the left anterior coronary artery, were monitored for either 30 min (group I) or 3 h (group II) before treatment with either heparin or 4-methyl-14N'-+(3-methyl-1,2,3,4-tetrahydro-8-quinolinyl

Subclinical increases in serum creatinine that do not meet acute renal injury criteria are independently associated with 30-day all-cause mortality in patients with normal renal function or preoperative renal insufficiency undergoing coronary artery bypass grafting.

These results suggest that the potential for transfusion-mediated transmission of herpesviruses from healthy adult blood donors is high for EBV and HHV-7; moderately high for HHV-6; uncommon for CMV; and rare for HSV-1, HSV-2, VZV, and HHV-8. Perhaps the most remarkable finding in this study was the detection of a single donor sample with greater than 6.1 x 10(7) HHV-6 Type B genome equivalents per mL blood. Given that this extraordinarily high level of HHV-6 DNA was obtained from a healthy adult blood donor, this phenomenon is likely unrelated to active infection or immunodeficiency.