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Articles in PresS, published online ahead of print May 7, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00080.2002
Submitted on January 30, 2002
Accepted on May 6, 2002
1 Department of Polymer Chemistry, ARISE, Waseda University, Tokyo, Japan
2 Department of Bioengineering, University of California, San Diego, La Jolla, California, USA
* To whom correspondence should be addressed. E-mail: eishun{at}mn.waseda.ac.jp.
A phospholipid vesicle encapsulating hemoglobin (Hb-vesicle, HbV) has been developed to provide O2 carrying capacity to plasma expanders. Its ability to restore systemic and microcirculatory condition after hemorrhagic shock was evaluated in conscious hamsters dorsal skinfold window preparation. The HbV was suspended in 8% HSA at Hb concentrations of 3.8 g/dl (HbV(3.8)/HSA) and 7.6 g/dl (HbV(7.6)/HSA). Shock was induced by 50% blood withdrawal and mean arterial pressure (MAP) at 40 mmHg was maintained for 1 hr by the additional blood withdrawal. The hamsters receiving either HbV(3.8)/HSA or HbV(7.6)/HSA suspensions restored MAP to 93 ± 14 and 93 ± 10 mmHg, respectively, similar with those receiving the shed blood (98 ± 13 mmHg), which were significantly higher by comparison with resuscitation with HSA alone (62 ± 12 mmHg). Only the HSA group tended to maintain hyperventilation and negative base excess after the resuscitation. Subcutaneous microvascular blood flow reduced to about 10 - 20% of baseline during shock, and re-infusion of shed blood restored blood flow to about 60 - 80%, of baseline, an effect primarily due to the sustained constriction of small arteries A0 (diameter 143 ± 29 µm). The HbV(3.8)/HSA group had significantly better microvascular blood flow recovery and non-significantly better tissue oxygenation than the HSA group. The recovery of base excess and improved tissue oxygenation appears to be primarily due to the increased oxygen carrying capacity of HbV fluid resuscitation.
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