High-resolution Myocardial Perfusion Imaging in Mice with High-frequency Echocardiographic Detection of a Depot Contrast Agent

Kaufmann, Beat A.; Lankford, M.F.; Behm, Carolyn Z.; French, Brent A.; Klibanov, Alexander L.; Xu, Yaqin; Lindner, Jonathan R.

doi:10.1016/j.echo.2006.08.008

Cited by 26 publications

(22 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…To determine whether Pdgfrb MerCre mice had a global decline in myocardial perfusion in response to TAC, we used a microbubble perfusion method, producing a contrast-enhanced ultrasound signal in the myocardium that is directly proportional to perfusion (34). Using this technique throughout all assessable portions of the heart (the anterior and lateral segments of the left ventricle), we observed a reduction in myocardial perfusion in Pdgfrb MerCre mice compared with Pdgfrb fl/fl controls ( Figure 5E).…”

Section: Angiogenic Gene Expression Profile Correlates With Defectivementioning

confidence: 98%

Cardiomyocyte PDGFR-β signaling is an essential component of the mouse cardiac response to load-induced stress

Chintalgattu¹,

Ai²,

Langley³

et al. 2010

J. Clin. Invest.

173

140

View full text Add to dashboard Cite

PDGFR is an important target for novel anticancer therapeutics because it is overexpressed in a wide variety of malignancies. Recently, however, several anticancer drugs that inhibit PDGFR signaling have been associated with clinical heart failure. Understanding this effect of PDGFR inhibitors has been difficult because the role of PDGFR signaling in the heart remains largely unexplored. As described herein, we have found that PDGFR-β expression and activation increase dramatically in the hearts of mice exposed to load-induced cardiac stress. In mice in which Pdgfrb was knocked out in the heart in development or in adulthood, exposure to loadinduced stress resulted in cardiac dysfunction and heart failure. Mechanistically, we showed that cardiomyocyte PDGFR-β signaling plays a vital role in stress-induced cardiac angiogenesis. Specifically, we demonstrated that cardiomyocyte PDGFR-β was an essential upstream regulator of the stress-induced paracrine angiogenic capacity (the angiogenic potential) of cardiomyocytes. These results demonstrate that cardiomyocyte PDGFR-β is a regulator of the compensatory cardiac response to pressure overload-induced stress. Furthermore, our findings may provide insights into the mechanism of cardiotoxicity due to anticancer PDGFR inhibitors.

show abstract

Section: Angiogenic Gene Expression Profile Correlates With Defectivementioning

confidence: 98%

Cardiomyocyte PDGFR-β signaling is an essential component of the mouse cardiac response to load-induced stress

Chintalgattu¹,

Ai²,

Langley³

et al. 2010

J. Clin. Invest.

173

140

View full text Add to dashboard Cite

show abstract

“…Separation of microbubbles into small size population was performed by flotation-centrifugation at 400g for 1 min and isolation of the turbid subnatant. 13 For confocal microscopy, lipid microbubble shells were fluorescently labeled by adding dioctadecylindocarbocyanine (DiI) to the suspension before sonication. Studies with albumin-shelled octofluoropropane microbubbles (MB-A) were performed with Optison (GE Healthcare, Princeton, NJ).…”

Section: Methodsmentioning

confidence: 99%

Renal Retention of Lipid Microbubbles: A Potential Mechanism for Flank Discomfort During Ultrasound Contrast Administration

Liu

Khangura

Xie

et al. 2013

Journal of the American Society of Echocardiography

Self Cite

View full text Add to dashboard Cite

Background The etiology for flank pain sometimes experienced during administration of ultrasound contrast agents is unknown. We investigated whether microbubble ultrasound contrast agents are retained within the renal microcirculation which could lead to either flow disturbance or local release of vasoactive and pain mediators downstream from complement activation. Methods Retention of lipid-shelled microbubbles in the renal microcirculation of mice was assessed by confocal fluorescent microscopy and contrast-enhanced ultrasound (CEU) imaging with dose-escalating intravenous injection. Studies were performed with size-segregated microbubbles to investigate physical entrapment, after glycocalyx degradation, and in wild-type and C3-deficient mice to investigate complement-mediated retention. Urinary bradykinin was measured before and after microbubbles. Renal CEU in human subjects (n=13) was performed 7–10 min after completion of lipid microbubble administration. Results In both mice and humans, microbubble retention was detected in the renal cortex by persistent CEU signal enhancement. Microbubble retention in mice was linearly related to dose and occurred almost exclusively in cortical glomerular microvessels. Microbubble retention did not affect microsphere-derived renal blood flow. Microbubble retention was not influenced by glycocalyx degradation nor by microbubble size, thereby excluding lodging, but was reduced by 90% (p<0.01) in C3-deficient mice. Urinary bradykinin increased by 65% five minutes after microbubble injection. Conclusion Lipid-shelled microbubbles are retained in the renal cortex due to complement-mediated interactions with glomerular microvascular endothelium. Microbubble retention does not adversely affect renal perfusion but does generate complement-related intermediates that are known to mediate nociception and could be responsible for flank pain.

show abstract

“…After day 15.5, the heart chambers begin to darken in the ultrasound image, and the ventricular wall, endocardium, and septum are easier to be discerned (Figure 10(e)). The improved contrast seen after day 15.5 means that ventricular chamber dimensions and wall thickness measurements become feasible [5, 58]. Fetal blood is echodense at UBM frequencies, due to nucleated erythroblasts, and this may facilitate assessment of major vascular development.…”

Section: Applicationsmentioning

confidence: 99%

Ultrasound Biomicroscopy in Small Animal Research: Applications in Molecular and Preclinical Imaging

Greco

Mancini

Gargiulo

et al. 2012

Journal of Biomedicine and Biotechnology

View full text Add to dashboard Cite

Ultrasound biomicroscopy (UBM) is a noninvasive multimodality technique that allows high-resolution imaging in mice. It is affordable, widely available, and portable. When it is coupled to Doppler ultrasound with color and power Doppler, it can be used to quantify blood flow and to image microcirculation as well as the response of tumor blood supply to cancer therapy. Target contrast ultrasound combines ultrasound with novel molecular targeted contrast agent to assess biological processes at molecular level. UBM is useful to investigate the growth and differentiation of tumors as well as to detect early molecular expression of cancer-related biomarkers in vivo and to monitor the effects of cancer therapies. It can be also used to visualize the embryological development of mice in uterus or to examine their cardiovascular development. The availability of real-time imaging of mice anatomy allows performing aspiration procedures under ultrasound guidance as well as the microinjection of cells, viruses, or other agents into precise locations. This paper will describe some basic principles of high-resolution imaging equipment, and the most important applications in molecular and preclinical imaging in small animal research.

show abstract

High-resolution Myocardial Perfusion Imaging in Mice with High-frequency Echocardiographic Detection of a Depot Contrast Agent

Cited by 26 publications

References 16 publications

Cardiomyocyte PDGFR-β signaling is an essential component of the mouse cardiac response to load-induced stress

Cardiomyocyte PDGFR-β signaling is an essential component of the mouse cardiac response to load-induced stress

Renal Retention of Lipid Microbubbles: A Potential Mechanism for Flank Discomfort During Ultrasound Contrast Administration

Ultrasound Biomicroscopy in Small Animal Research: Applications in Molecular and Preclinical Imaging

Contact Info

Product

Resources

About