Acutely sodded expanded polytetrafluoroethylene grafts produce only prostacyclin: a qualitative difference from saphenous veins.
Select subsets of patients require prosthetic graft material for revascularization. Although arterial prosthetic grafts of large caliber perform acceptably, grafts of <6 mm exhibit a high attrition rate. Microvessel endothelial sodding, a method resulting in the lining of prosthetic grafts with autologous endothelium, improves graft patency; however, aggressive antiplatelet therapy is still required, because terminating an antiplatelet regimen accelerates graft attrition. The present investigation was designed to address the acute production of vasoactive substances in microvessel endothelial cell sodded expanded polytetrafluoroethylene (ePTFE) grafts in an attempt to delineate a possible mechanism behind the continued requirement for antiplatelet therapy. Equal lengths of acutely sodded ePTFE grafts (canine falciform ligament source) and saphenous veins (SV) (canine source) were evaluated by superfusion bioassay. Basal secretion from ePTFE grafts relaxed the biodetector ring 1 +/- 3%, whereas SV relaxed the ring 10 +/- 3% (p < 0.05, ePTFE vs. SV). Relaxation with acetylcholine stimulation was 49 +/- 7% in grafts and 50 +/- 10% in veins (p = NS). Calcium ionophore stimulation produced relaxation of 37 +/- 9% from ePTFE grafts and 100 +/- 23% from SV (p < 0.05). Indomethacin added to perfusate reduced relaxations from sodded ePTFE grafts to 20.2 +/- 9.2% with acetylcholine stimulation and 12.5 +/- 4.3% with calcium ionophore (p < 0.05 vs. control); addition of N(G)-monomethyl-L-arginine (L-NMMA) had no effect on the release of vasoactive substances from ePTFE grafts. In contrast, relaxations of effluent from SV stimulated by acetylcholine and calcium ionophore were significantly attenuated with indomethacin and L-NMMA (p < 0.05 vs. control). Scanning electron microscopy demonstrated confluent endothelium in SV and a nonconfluent endothelial cell layer in grafts. Acutely sodded ePTFE grafts produce vasoactive substances that quantitatively and qualitatively differ from those produced by canine SV. The ePTFE grafts produce mainly prostanoids, whereas SV produce both nitric oxide and prostanoids. The endothelial cell isolation procedure and absence of immediate graft luminal confluence may contribute to the observed differences.
Desai
S B
SB
Section of Cardiovascular Surgery, Mayo Clinic and Mayo Foundation, Rochester, MN 55905, USA.
Cable
D G
DG
Phillips
M R
MR
Schaff
H V
HV
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology; D001681:Biological Assay; D001807:Blood Vessel Prosthesis; D000001:Calcimycin / Q000494:pharmacology; D002196:Capillaries / Q000166:cytology / Q000378:metabolism; D002470:Cell Survival / Q000187:drug effects; D004285:Dogs; D004730:Endothelium, Vascular / Q000378:metabolism / Q000637:transplantation* / Q000648:ultrastructure; D004791:Enzyme Inhibitors / Q000494:pharmacology; D011464:Epoprostenol / Q000378:metabolism*; D006085:Graft Survival / Q000187:drug effects; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology; D007476:Ionophores / Q000494:pharmacology; D008422:Materials Testing; D008855:Microscopy, Electron, Scanning; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology; D011138:Polytetrafluoroethylene; D012501:Saphenous Vein / Q000637:transplantation*; D019737:Transplants; D014665:Vasodilator Agents / Q000494:pharmacology; D019323:omega-N-Methylarginine / Q000494:pharmacology
D000894:Anti-Inflammatory Agents, Non-Steroidal; D004791:Enzyme Inhibitors; D007476:Ionophores; D010975:Platelet Aggregation Inhibitors; D014665:Vasodilator Agents; D019323:omega-N-Methylarginine; D000001:Calcimycin; D011138:Polytetrafluoroethylene; D011464:Epoprostenol; D000109:Acetylcholine; D007213:Indomethacin