Low flow enhances platelet activation after acute experimental arterial injury

Abstract

Purpose: Vascular smooth muscle cell (VSMC) proliferation and migration to the subintima or intimal hyperplasia (IH) occur after arterial injury and are thought to be induced by mitogenic factors released from activated platelets. Because low flow (LF) and shear have been attributed to the localization and progression of IH, we postulated that hemodynamic factors may regulate the degree of platelet activation, as measured by plasma thromboxane B 2 (TXB 2) and platelet-derived growth factor-AB (PDGF-AB) release at regions of experimental arterial injury. Methods: The right common carotid artery (CCA) was subjected to balloon injury in 18 New Zealand White male rabbits. Flow in the injured CCA was reduced by out-flow ligation (LF group, n = 6) or increased by ligation of the left CCA (high flow [HF] group, n = 6). In six other animals, flow was preserved (normal flow [NF] group). Mean blood flow and pressure in the right CCA were measured thereafter at 10 and 30 minutes. Plasma TXB 2 and PDGF-AB levels were determined with the enzyme-linked immunosorbent assay method in each animal with blood samples taken systematically before injury (baseline) and in the distal CCA at similar 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 group 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. TXB 2 levels were more than fourfold greater in the LF group than in the HF and NF 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 LF group compared with baseline levels ( p < 0.05). Conclusion: Platelet activation at regions of acute vascular injury was determined to be flow dependent. Upregulated platelet activity in low flow conditions may be due to increased platelet exposure time to subendothelial collagen and is greatly attenuated if normal or increased flow is present.(J Vasc Surg 1998;27:910-8.)