ARTERIAL BYPASS GRAFT SPASM - AN EXAMINATION OF THE ROLE OF HIGH-FLOWDEMANDS AND ENDOTHELIAL FUNCTION IN THE PORCINE GEA

Citation
Wd. Montgomery et al., ARTERIAL BYPASS GRAFT SPASM - AN EXAMINATION OF THE ROLE OF HIGH-FLOWDEMANDS AND ENDOTHELIAL FUNCTION IN THE PORCINE GEA, European journal of cardio-thoracic surgery, 10(1), 1996, pp. 12-19
Citations number
38
Categorie Soggetti
Cardiac & Cardiovascular System
ISSN journal
10107940
Volume
10
Issue
1
Year of publication
1996
Pages
12 - 19
Database
ISI
SICI code
1010-7940(1996)10:1<12:ABGS-A>2.0.ZU;2-F
Abstract
This study examined why an artery becomes vulnerable to spasm when use d as a bypass graft. We hypothesized that high flow demands would decr ease pressure distally in the conduit (afterload), thus increasing the sensitivity to vasoconstrictors. Furthermore, perioperative endotheli al 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 a nd outflow resistance was adjusted to simulate normal (in situ) or hig h (coronary bypass graft) flow demands. Gastroepiploic flow and distal pressures were measured at baseline [B] and after adding norepinephri ne (NE, 10(-9) M to 10(-5) M). Under normal flow demand, a minimal pre ssure drop existed across the GEA and flow decreased only at high NE c oncentrations. High flow demand decreased distal GEA pressure and incr eased the sensitivity to NE. To block endothelial function N-Monomethy l-L-Arginine, Monoacetate (L-NMMA, 10(-5) M) was then added. Under hig h flow demand, blocking endothelial function resulted in an additional fivefold increase in sensitivity to NE (ED(50) from 9.75 10(-8) M to 2.11 10(-8) M, P<0.05). It was shown that in long narrow arterial graf ts, high flow demands cause cumulative pressure losses. Even with norm al endothelial function, these pressure losses render the artery respo nsive to vasoconstrictors. Endothelial dysfunction additionally increa ses the sensitivity of the artery. Anastomosis of a small arterial gra ft to a large myocardial perfusion bed may result in reduced distal co nduit pressure and may predispose to the development of myocardial isc hemia even when low doses of vasoconstrictors are used. Perioperative endothelial dysfunction may exacerbate this effect.