LOW-FLOW ENHANCES PLATELET ACTIVATION AFTER ACUTE EXPERIMENTAL ARTERIAL INJURY

Purpose: Vascular smooth muscle cell (VSMC) proliferation and migratio n to the subintima or intimal hyperplasia (IH) occur after arterial in jury and are thought to be induced by mitogenic factors released from activated platelets. Because low flow (LF) and shear have I-teen attri buted to the localization and progression of IH, we postulated that he modynamic factors may regulate the degree of platelet activation, as m easured by plasma thromboxane B-2 (TXB2) and platelet-derived growth f actor-AB (PDGF-AB) release at regions of experimental arterial injury. Methods: The right common carotid artery (CCA) was subjected to ballo on injury in 18 New Zealand White male rabbits. Flout in the injured C CA was reduced by out-flow ligation (LF group, n = 6) or increased by ligation of the left CCA (high flow [HP] group, n = 6). In six other a nimals, flow was preserved (normal flow [NF] group). Mean blood flow a nd pressure in the right CCA were measured thereafter at 10 and 30 min utes. Plasma TXB2 and PDGF-AB levels were determined with the enzyme-l inked immunosorbent assay method in each animal with blood samples tak en systematically before injury (baseline) and in the distal CCA at si milar time points. Results: At 10 minutes, mean blood flow was reduced from 20 +/- 2 ml/min in the NF group to 7 +/- 1 ml/min in the LF grou p animals (p < 0.01) and increased to 32 +/- 2 ml/min in the HF group animals (p < 0.05). Mean arterial blood pressure did not differ among the groups, Hemodynamic parameters were similar at 10 and 30 minutes. TXB2 levels were more than fourfold greater in the LF group than in th e HF and NP groups at both time points (p < 0.05), In addition, there was a twofold increase in plasma PDGF-AB level at 10 minutes in the LP group compared with baseline levels (p < 0.05). Conclusion: Platelet activation at regions of acute vascular injury was determined to be fl ow dependent. Upregulated platelet activity in low non conditions may be due to increased platelet exposure time to subendothelial collagen and is greatly attenuated if normal or increased flow is present.