Effect of cAMP on endothelial cell function and fibromuscular proliferation in an injured swine carotid and coronary artery

Introduction and objective. Reendothelization of damaged blood vessels prot ects against the vascular injury response. We evaluated in vivo whether a s ystemic increase in cAMP accelerates reendothelization and attenuates intim al hyperplasia in injured swine carotid and coronary arteries. Methods. Both carotid arteries of 10 swines were subjected to balloon injur y. Five animals had been treated with 2 ml (10 mg) of Forskolin, an activat or of the adenylate cyclase, and another 5 with 2 ml of saline solution. Th ese animals were sacrificed at day 8, and carotid artery reendothelization was evaluated. The descendent coronary (DC) artery of another 19 pigs was i njured by atherotome. Nine animals had been treated with 2 ml of Forskolin, and another 10 with 2 ml of saline solution. These animals were sacrified at day 28, with myointimal proliferation and arterial geometric remodelatio n being evaluated. Likewise, in these animals intracellular cAMP levels wer e measured at baseline and 28 and 60 minutes after saline solution or Forsk olin administration and 90 min after arterial injury. Results. Eight days after balloon injury, carotid artery reendothelization was greater in the Forskolin-treated group compared with the control group (p = 0.02), and the number of CD31 possitive cells was statistically increa sed in the treated group (38 +/- 11 cells) versus controls (11 +/- 9 cells) . Although the degree of vascular injury caused by atherotome was similar i n all of the arteries in the control group, restenosis was only observed in 40% of these animals. Correlation analysis demonstrated that intracellular cAMP may condition arterial geometric remodeling and the diameter of the l umen after vascular injury. Conclusion. Our results suggest that cAMP may promote reendothelization and attenuate fibromuscular proliferation.