Fall in nitric oxide (no) and increase in platelet activation in coronary sinus blood following angioplasty

Up to forty percent of angioplasty cases are followed by restenosis within six months. Enhanced mitosis and migration of vascular smooth muscle cells (VSMC) from the media to the intima are important in this process. Since nitric oxide is a known antimitogen for both VSMC and the endothelial cells we have now measured the metabolites of NO, nitrite and nitrate, in the coronary sinus blood, prior to, during and after angioplasty. In addition, we assayed soluble P-selectin as a reflection of platelet activity in these samples. There was a consistent fall on NO2/NO, the major metabolites of NO following angioplasty, in each of the sequence of samples tested (<0.0l). There was also an increase in plasma sP-selectin concentrations in 7 out of 12 sequences tested. There was an inverse relationship between sP-selectin concentrations and platelet aggregability. We conclude that angioplasty results in a dramatic fall in NO output probably due to ischemia damage to the endothelium at the site of angioplasty and distally. This fall in NO may contribute to post angioplasty coronary vasoconstriction and activation of platelets enough to cause increased expression of sP-selectin but not gross platelet aggregation. Fall in NO may also contribute to the 'stunning' of the coronary arteries and trigger VSMC mitogenesis which may contribute to coronary restenosis.