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Updated: Aug 7, 2026
Microfluidic Flow Chambers Using Reconstituted Blood to Model Hemostasis and Platelet Transfusion In Vitro
Published on: March 19, 2016
A new method for quantitation of platelet microthrombi and microemboli from cardiopulmonary bypass in organs using
M K Dewanjee1, P Zhai, L C Hsu
1Department of Veterinary Biosciences, University of Illinois at Champaign-Urbana 61802, USA.
Abstract:
During cardiopulmonary bypass (CPB), showers of microemboli (ME) distribute among the organs and connective tissues according to regional blood flow. Post CPB, ME were quantified by subtracting residual platelets (RP) in the organs of a group of unoperated control Yorkshire pigs (n = 6) from those of operated pigs. The RP level was minimized by heparinization (300 IU/kg) before death and exsanguination. The number of adherent microthrombi (MT) and ME from the oxygenator (OX), arterial filter (AF), and thoracotomy site were determined using 111In labeled autologous platelets (INPLT) (525-585 microCi administered 24 hr before CPB) in two CPB groups (ACT > 400 sec) of 12 pigs (30-35 kg). CPB was carried out at a flow of 2.5-3.5 L/min at 28 degrees C with a roller or a centrifugal pump, OX (Bentley Univox 1.8 m2), AF (0.25 m2), and cardiotomy reservoir (CR) (Bentley BR: 3,500), for 90 (n = 6) and 180 (CPB 180, n = 6) min. Six pigs underwent thoracotomy without CPB. L-Arginine was infused at a dose of 2 mg/ kg/min during CPB (n = 6). Flow cytometry was used to estimate the circulating ME in blood. MT and organ trapped ME were imaged with a gamma camera and measured with an ion chamber and a gamma counter. ME values (percent of injected INPLT dose) in six organs and four connective tissues were calculated for all five groups. INPLT distribution indicated a uniform distribution of low level platelet MT in the CR and AF. Circulating ME amounted to 2.5% of total platelets. In the CPB circuit, ME generation in AF was the rate-limiting step (n = 4 x 10(5)). Similar studies in organs and tissues suggested the presence of a uniform distribution of the total events of ME (n = 500 x 10(6)). ME increase in brain, lung, liver, and skeletal muscle following thoracotomy and CPB was significant. The low level of ME in ischemia sensitive organs also indicated the presence of a thrombolytic threshold for cumulative ME. ME disaggregation was activated at an early stage to prevent ischemic damage, specifically in the brain. Measurement of trapped ME provided a novel, reliable, and one step method of evaluation of thrombogenicity of a CPB device and drugs.
Insights
Microemboli (ME) generated during cardiopulmonary bypass (CPB) distribute throughout organs. This study quantifies ME and demonstrates a thrombolytic threshold, suggesting early activation prevents ischemic damage, particularly in the brain.
Area of Science:
- Cardiovascular Surgery
- Biomedical Engineering
- Hematology
Background:
- Cardiopulmonary bypass (CPB) procedures can generate microemboli (ME) that distribute to organs.
- Understanding ME generation and distribution is crucial for mitigating CPB-related complications.
- Quantifying ME and assessing thrombogenicity of CPB devices and drugs requires reliable methods.
Purpose of the Study:
- To quantify microemboli (ME) generated during cardiopulmonary bypass (CPB) and their distribution in organs and tissues.
- To evaluate the thrombogenicity of CPB circuits and the potential protective effects of L-Arginine.
- To establish a novel method for evaluating the thrombogenicity of CPB devices and drugs.
Main Methods:
- Used 111In-labeled autologous platelets (INPLT) to track microthrombi (MT) and ME in Yorkshire pigs undergoing CPB.
- Quantified ME in organs and tissues by subtracting residual platelets from operated and control groups.
- Employed flow cytometry for circulating ME, gamma camera imaging, ion chamber, and gamma counter for trapped ME.
Main Results:
- Microemboli (ME) distribution was uniform across organs, with the arterial filter (AF) being the primary generation site.
- Significant ME increase observed in brain, lung, liver, and skeletal muscle post-CPB.
- A thrombolytic threshold was indicated by low ME levels in ischemia-sensitive organs, suggesting early ME disaggregation.
Conclusions:
- The arterial filter is a critical source of ME during CPB.
- Early activation of ME disaggregation mechanisms protects against ischemic damage, especially in the brain.
- Measuring trapped ME offers a novel, reliable method for assessing CPB device and drug thrombogenicity.
