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Updated: Jul 30, 2026

In vivo Measurement of the Mouse Pulmonary Endothelial Surface Layer
Published on: February 22, 2013
Albumin microbubble persistence during myocardial contrast echocardiography is associated with microvascular
J R Lindner1, S Ismail, W D Spotnitz
1Cardiovascular Division and the Division of Thoracic and Cardiovascular Surgery, University of Virginia School of Medicine, Charlottesville, VA, USA.
Background:
We hypothesized that the persistence of albumin microbubbles within the myocardium during crystalloid cardioplegia (CP) infusion and ischemia-reperfusion (I-R) occurs because of endothelial injury.
Methods And Results:
The myocardial transit rate of albumin microbubbles was measured in 18 dogs perfused with different CP solutions and in 12 dogs undergoing I-R. Electron microscopy with cationized ferritin labeling of the glycocalyx was performed in 9 additional dogs after CP perfusion and in 3 additional dogs undergoing I-R. Microbubble transit was markedly prolonged during crystalloid CP perfusion. The addition of whole blood to the CP solution accelerated the transit rate in a dose-dependent fashion (P<0.05), which was greater with venous than with arterial blood (P<0.05). The addition of plasma or red blood cells to CP solutions was less effective in improving transit rate than addition of whole blood (P<0.05). Microbubble transit rate was independent of the temperature, K+ content, pH, PO2, osmolality, viscosity, and flow rate of the perfusate. Similarly, a proportion of microbubbles persisted in the myocardium after I-R, which was related to the duration of ischemia (P<0.01) but not of reflow. Crystalloid CP perfusion and I-R resulted in extensive loss of the endothelial glycocalyx without other ultrastructural changes. This effect was partially reversed in the case of crystalloid CP when it was followed by blood CP.
Conclusions:
Sonicated albumin microbubbles persist within the myocardium in situations in which the endothelial glycocalyx is damaged. The measurement of the myocardial transit rate of albumin microbubbles may provide an in vivo assessment of endothelial glycocalyx damage.
Insights
Albumin microbubbles persist in the heart after cardioplegia and ischemia-reperfusion due to endothelial glycocalyx damage. Measuring microbubble transit may assess this endothelial injury in vivo.
Area of Science:
- Cardiovascular Research
- Cell Biology
- Surgical Innovation
Background:
- Endothelial injury during crystalloid cardioplegia (CP) and ischemia-reperfusion (I-R) may cause albumin microbubble persistence in the myocardium.
- Investigating the mechanisms behind microbubble retention is crucial for understanding myocardial protection strategies.
Purpose of the Study:
- To investigate the relationship between albumin microbubble persistence in the myocardium and endothelial injury during CP and I-R.
- To evaluate the impact of CP composition on microbubble transit and endothelial glycocalyx integrity.
- To determine if microbubble transit rate can serve as an in vivo marker for endothelial glycocalyx damage.
Main Methods:
- Myocardial transit rate of albumin microbubbles was measured in dogs undergoing CP and I-R.
- Electron microscopy with cationized ferritin labeling was used to assess the endothelial glycocalyx.
- CP solutions with varying additives (whole blood, plasma, red blood cells) were tested.
Main Results:
- Crystalloid CP markedly prolonged microbubble transit.
- Addition of whole blood to CP accelerated transit in a dose-dependent manner, more so with venous than arterial blood.
- Crystalloid CP and I-R caused significant loss of the endothelial glycocalyx.
- Microbubble persistence post-I-R correlated with ischemia duration.
- Blood CP partially reversed glycocalyx damage caused by crystalloid CP.
Conclusions:
- Sonicated albumin microbubbles persist in the myocardium when the endothelial glycocalyx is damaged.
- Myocardial transit rate of albumin microbubbles offers a potential in vivo method for assessing endothelial glycocalyx integrity.
- Optimizing CP solutions with blood components may mitigate endothelial glycocalyx damage.
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