To unequivocally show that cycling myocytes are normally perfused, we performed ex vivo retrograde perfusion of hearts (obtained from BrdU-pulsed bitransgenic mice) with a fluorescent dye (Celltracker RED), followed by enzymatic dissociation.
The perfusion of hearts with hypoxic buffer had no effect on cardiac GSH status in any group.
Perfusion of hearts with hypoxic buffer caused a significant increase in tracer retention to 45.6% ± 5.8% ID after 5 min and further still to 59.1% ± 6.3% ID after 25 min (Figure 6B).
Perfusion of hearts with fluorescently labeled lec-tin demonstrated that implanted tissues became vascularized and immunostaining verified the presence of proteins important in electromechanical integration of myogenic cells with surrounding re-cipient rat cardiomyocytes.
Following cannulation and subsequent perfusion of hearts, approximately 10% of preparations were discarded because of signs of ischaemia.
Perfusion of hearts with this TAT-HK2 peptide significantly decreased mitochondrial HK2 levels without affecting baseline cardiac function.
Ventricular cardiomyoblasts were isolated from male Wistar rats by perfusion of hearts with collagenase type II (300 U/mL) and cultured, as previously described [ 40].
Perfusion of hearts with labelled intralipid resulted in a 3-fold increase in labelled lipids deposited as cholesterol ester, comparing oleate and intralipid-perfused hearts (P < 0.05: Fig. 6).
Leak of cytochrome c was not prevented by 10 min of pre-ischaemic perfusion of hearts with 0.2 μM CsA, a treatment that we have shown previously inhibits mPTP opening both in situ and in subsequently isolated mitochondria [ 26].
In vitro studies performed in the late '90 s and based on rat or human hearts isolated with the Langendorff technique demonstrated a direct pathogenic role of antibodies from mothers of children with CHB, as perfusion of hearts with maternal IgG containing anti-Ro and anti-La antibodies induced bradycardia and complete AV block within 15 minutes [ 49, 50].
