gms | German Medical Science

128. Kongress der Deutschen Gesellschaft für Chirurgie

Deutsche Gesellschaft für Chirurgie

03.05. - 06.05.2011, München

Progenitor cell homing in the postischemic myocardium: just an unmotivated pitstop in the microcirculation?

Meeting Abstract

  • Rene Schramm - Ludwig-Maximilians-Universität, Herzchirurgische Klinik und Poliklinik, München
  • Fabio Tuche - State University of Rio de Janeiro, Laboratory for Research in Microcirculation, Rio de Janero
  • Christina Körbel - Universität des Saarlandes, Institut für Klinisch-Experimentelle Chirurgie, Homburg/Saar
  • Eliete Bouskela - State University of Rio de Janeiro, Laboratory for Research in Microcirculation, Rio de Janero
  • Michael D. Menger - Universität des Saarlandes, Institut für Klinisch-Experimentelle Chirurgie, Homburg/Saar

Deutsche Gesellschaft für Chirurgie. 128. Kongress der Deutschen Gesellschaft für Chirurgie. München, 03.-06.05.2011. Düsseldorf: German Medical Science GMS Publishing House; 2011. Doc11dgch438

DOI: 10.3205/11dgch438, URN: urn:nbn:de:0183-11dgch4380

Veröffentlicht: 20. Mai 2011

© 2011 Schramm et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Introduction: We developed a new model for the direct assessment of bone marrow-derived progenitor cell (BMC) sequestration in the postischemic murine myocardium.

Materials and methods: Syngeneic heterotopic heart transplantation was used in C57/BL6 and atherosclerotic ApoE-/- mice. After short-term cold ischemia during transplantation, a 60min equilibration period was allowed before induction of 60 min warm ischemia. BMCs were harvested from the syngeneic heart donor and fluorescently labeled before intracoronary injection after additional 60 min of reperfusion.

Results: Intravital fluorescence microscopy (IVM) allowed detailed visualization of the subepicardial coronary microcirculation, including feeding arterioles, nutritive capillaries and postcapillary venules. Warm ischemia induced reperfusion failure in the myocardial microvasculature in C57/BL6 and atherosclerotic ApoE-/- mice, indicated by a reduced functional capillary density (FCD) (P<0.05 vs. non-warm ischemic C57/BL6 controls). We found that intracoronary BMC injection did not further impair the FCDs in both hearts exposed to warm ischemia and non-warm ischemic controls. Intracoronarily injected BMCs were found to sequester exclusively in myocardial capillaries. In contrast, blood-borne leukocytes were recruited in postcapillary coronary venules. Virtually no BMC-endothelial cell adhesive interactions were observed in coronary arterioles and venules, i.e. BMCs passed these segments of the coronary microcirculation within the free blood flow. The numbers of sequestered BMCs were comparable in warm ischemic C57/BL6 and atherosclerotic ApoE-/- mice as well as non-warm ischemic controls. Moreover, Comparable numbers of BMCs sequestered in syngeneically transplanted CD31-/- and LFA-1-/- hearts.

Conclusion: This is the first study allowing direct assessment of intracoronarily injected BMCs homing to postischemic myocardium in vivo. Our novel data demonstrate that intracoronarily injected BMCs sequester in the postischemic myocardium exclusively by plugging in nutritive myocardial capillaries rather than by active recruitment via the endothelial lining of coronary arterioles or postcapillary venules.