Using a newly developed Doppler probe, we have found that a standard suture anastomosis in a rat femoral artery is accompanied by significant (30-60%) cross-sectional area stenosis, which dissipates to baseline levels within 24 hours. We hypothesized that spasm, deposition of coagulation products, or the suture technique itself was responsible. Topical vasodilators (papaverine, sodium nitroprusside, lidocaine) and intravenous thromboxane A2 synthetase inhibitor and receptor blocking agent (Ridogrel, 4 mg/ml), anticoagulants heparin and SC4992 (an experimental platelet inhibitor/arginine-glycine-aspartic acid analogue), were administered. No drug had any significant effect on preventing postoperative stenosis. Varied suture bites affected stenosis measurements. Scanning electron microscopy and light microscopy displayed "bunching" of vessel wall in the suture ties. This was confirmed with methyl methacrylate corrosion casts and microangiography. "Sham" anastomoses also produced stenosis, which was relieved when sutures were removed. We conclude that suture anastomosis of small vessels is accompanied by significant cross-sectional stenosis caused by the physical action of tensioned sutures. This effect dissipates over a 24-hour postoperative period. The mechanism behind these changes and the clinical importance of this effect are still under investigation.