A Useful Device to Measure Kinetics of Platelet Contraction

Abstract

Platelet contraction provides a minimally invasive source for physiologic information. In this article, we describe a device that directly measures the kinetics of platelet contraction. Whole blood is injected between acrylic plates and an adherent clot forms. The bottom plate is fixed, and the top plate is attached to a wire cantilever. Platelet contraction drives deflection of the wire cantilever which is captured by a camera. Force generated by the clot with time is derived using beam equations. Force derivations were verified using a microelectromechanical (MEMS) force sensor. Kinetics of clot contraction were defined, including maximum contraction force (FMAX), lift-off time (TLIFTOFF), and contraction rate (CR). Metrics were compared with optical aggregometry and thromboelastography. FMAX correlates with optical aggregometry maximal amplitude with a Spearman's rho of 0.7904 and p = 0.0195 and thromboelastography maximal amplitude with a Spearman's rho of 0.8857 and p = 0.0188. Lift-off time correlates with optical aggregometry lag time with a Spearman's rho of 0.9048 and p = 0.002. This preliminary study demonstrates the repeatability of a useful platelet contraction device and its correlation with thromboelastography and optical aggregometry, the gold standard platelet function test.

Artificial neural networks accurately predict intra‐abdominal infection in moderately severe and severe acute pancreatitis

“…The LRM showed that HCT, TT, FIB, D‐dimer, MA and SIRS were independent predictors of intra‐abdominal infection. Moreover, ANN model showed the top five important parameters with high normalized importance, including D‐dimer, MA, INR, IL‐6 and PT, indicating the amount and function of platelets were the common factor in both models. As there was no statistical difference in the amount of platelet counts between patients with and without intra‐abdominal infection, platelet functions, including their capacity of adhesion, aggregation, deformation and release, may be the predictive factors with greater relevance to intra‐abdominal infection, which coincides with the results of previous studies demonstrating that platelet function was altered during AP .…”

Blood clot contraction: Mechanisms, pathophysiology, and disease

“…The same principle has been reproduced in a parallel plate rheometer, where a platelet-containing clot fills the gap between 2 horizontal plates and the contractile stress is measured as the negative normal (perpendicular) force pulling on the upper plate [ 6 , 18 ]. Devices to measure contractile forces, in the same manner, have been developed [ 27 , 28 ]. Importantly, almost all bulk clot methods measure isometric or constrained contraction, i.e., platelet-generated stress without volumetric clot shrinkage, which limits the utility of these assays for the assessment of averaged platelet functionality.…”

Microelectromechanical System Measurement of Platelet Contraction: Direct Interrogation of Myosin Light Chain Phosphorylation

“…Platelet Stimulation or Inhibition: Certain commercially available reagents cause either increased or decreased levels of pMLC through inhibition or activation of the regulatory pathways governing MLCK and MLCP ( Figure 4 ). Sildenafil citrate is an inhibitor of phosphodiesterase-5 (PDE-5), which is an upstream inhibitor of the cyclic GMP governing activation of MLCP [ 33 ]. CPD7a is a quinolone derivative and similarly to sildenafil inhibits PDE-5 [ 34 ].…”