Vasoactive intestinal peptide (VIP) acts as a vasodilator on coronary and gastrointestinal arteries. During coronary occlusion, the locally released VIP may exert a protective effect on the heart, but it may aggravate the shock state through its vasodilatory effect in the gastrointestinal tract.
After left thoracotomy, the left circumflex coronary artery (LCx) was prepared, and a pneumatic occluder was introduced around it. After 60 min of coronary occlusion, the LCx was reperfused in six dogs (reperfusion group), while in another six the occlusion was maintained for 6 h (occlusion group). Five dogs served as sham-operated controls. The plasma concentration of VIP was determined at baseline, after the 60 min occlusion and 10 min, 3 h and 6 h after reperfusion, or 3 h and 6 h after continuous occlusion in the coronary sinus and in the femoral and portal veins.
The plasma VIP concentrations in all three vessels were increased after 60 min of LCx occlusion. During the 6 h constant coronary occlusion, concentrations remained increased in both the coronary sinus and the portal vein, but not in the femoral vein. In the reperfusion group, 10 min after reperfusion, the plasma concentrations of VIP in all three vessels had decreased.
Coronary artery occlusion causes a long-term increase in plasma VIP concentrations that decreases after reperfusion, when measured in the portal vein and coronary sinus, but not in the femoral veins.
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