title: Arterial bypass graft spasm: an examination of the role of high flow demands and endothelial function in the porcine GEA.
abstract: This study examined why an artery becomes vulnerable to spasm when used as a bypass graft. We hypothesized that high flow demands would decrease pressure distally in the conduit (afterload), thus increasing the sensitivity to vasoconstrictors. Furthermore, perioperative endothelial dysfunction would additionally sensitize the artery to constrictors. Six gastroepiploic arteries (GEA, 1.0-1.5 mm diameter, 11 cm length) were harvested from adult pigs (110-125 kg) and mounted on a computer-controlled perfusion system. The inflow pressure was set at 80 mmHg and outflow resistance was adjusted to simulate normal (in situ) or high (coronary bypass graft) flow demands. Gastroepiploic flow and distal pressures were measured at baseline [B] and after adding norepinephrine (NE, 10(-9) M to 10(-5) M). Under normal flow demand, a minimal pressure drop existed across the GEA and flow decreased only at high NE concentrations. High flow demand decreased distal GEA pressure and increased the sensitivity to NE. To block endothelial function N-Monomethyl-L-Arginine, Monoacetate (L-NMMA, 10(-5) M) was then added. Under high flow demand, blocking endothelial function resulted in an additional fivefold increase in sensitivity to NE (ED50 from 9.75 10(-8) M to 2.11 10(-8) M, P < 0.05). It was shown that in long narrow arterial grafts, high flow demands cause cumulative pressure losses. Even with normal endothelial function, these pressure losses render the artery responsive to vasoconstrictors. Endothelial dysfunction additionally increases the sensitivity of the artery. Anastomosis of a small arterial graft to a large myocardial perfusion bed may result in reduced distal conduit pressure and may predispose to the development of myocardial ischemia even when low doses of vasoconstrictors are used. Perioperative endothelial dysfunction may exacerbate this effect.
authors.affiliation: Division of Thoracic and Cardiovascular Surgery, University of Louisville, Kentucky 40292, USA.
authors.forename: W D
authors.initials: WD
authors.lastname: Montgomery
authors.forename: P A
authors.initials: PA
authors.lastname: Spence
authors.forename: S B
authors.initials: SB
authors.lastname: Hansen
authors.forename: F
authors.initials: F
authors.lastname: Randsbaek
authors.forename: W P
authors.initials: WP
authors.lastname: Santamore
mesh_terms: D000009:Abdominal Muscles / Q000098:blood supply*; D000818:Animals; D001158:Arteries / Q000637:transplantation*; D004730:Endothelium, Vascular / Q000502:physiology*; D009131:Muscle, Smooth, Vascular / Q000502:physiology*; D012039:Regional Blood Flow; D013035:Spasm; D013552:Swine