Submitted on September 22, 2004
Accepted on December 1, 2004
Regional myocardial perfusion under exchange transfusion with liposomal hemoglobin: in vivo and in vitro studies using rat hearts
T Matsumoto1*, A Takahisa2, K Mano3, H Tachibana2, M Todoh3, M Tanaka3, and F Kajiya4
1 Division of Bioengineering, Osaka University Graduate School of Engineering Science, Toyonaka, Osaka, Japan; Department of Medical Engineering and Systems Cardiology, Kawasaki Medical School, Kurashiki, Okayama, Japan
2 Department of Medical Engineering and Systems Cardiology, Kawasaki Medical School, Kurashiki, Okayama, Japan
3 Division of Bioengineering, Osaka University Graduate School of Engineering Science, Toyonaka, Osaka, Japan
4 Department of Medical Engineering and Systems Cardiology, Kawasaki Medical School, Kurashiki, Okayama, Japan; Department of Cardiovascular Physiology, Okayama University Graduate School of Medicine and Dentistry, Okayama, Okayama, Japan
* To whom correspondence should be addressed. E-mail: matsu{at}me.es.osaka-u.ac.jp.
The purpose of this study was to test the hypothesis that exchange transfusion with liposomal hemoglobin (LH) reduces the microheterogeneity of regional myocardial
flows while sustaining cardiac function. Neo Red Cell mixed with albumin was used as LH solution, in which LH volume fraction was 17~18% and hemoglobin density was
nearly two-thirds smaller than in rat blood. Regional myocardial flows in left ventricular
free walls were measured by tracer digitalradiography (100-µm resolution) in anesthetized rats with or without 50% blood-LH exchange transfusion. Within-layer
flow distributions showed lower heterogeneity with (n=8) than without (n=8) LH transfusion. No extravasation of hemoglobin was confirmed by 3,3-diaminobenzidin
staining (n=2). Carotid flow increased by 68% due to LH transfusion while arterial pressure and heart rate remained unchanged. On the other hand, cross-circulated rat
hearts (n=7) were used to evaluate the effects of 50% blood-LH exchange on coronary flow and tone preservation under 300-bpm pacing and 100-mmHg perfusion pressure.
Blood-LH exchange caused 71% increase of coronary flow and 10% decrease of percent flow increase during hyperemia following 30-sec flow interruption. Myocardial O2 supply and consumption increased by 9 and 10%, respectively, while myocardial O2 extraction remained unchanged. The large increases of in vivo carotid flow and coronary flow in cross-circulated hearts due to LH coperfusion could be explained by the reduction of apparent flow viscosity. These results suggest that under LH coperfusion, the microheterogeneity of myocardial flows decreases with increased coronary flow while fairly preserving coronary tone and cardiac function.
