Artificial Oxygen Carrier Improves Fatigue-Resistance in Slow-muscle but not in Fast-muscle in a Rat in situ Model.

Effects of liposome-encapsulated hemoglobin with high O₂ -affinity (h-LEH), an artificial O₂ carrier on skeletal muscle, were studied by in situ fatigue-resistance test in fast-type Plantaris (PLT) and slow-type Soleus (SOL) muscles with or without ischemia in the rat. The distal tendons of PLT and SOL muscles were isolated in situ and individually attached to the force-transducers to record developed tension in response to stimuli (80Hz tetanus train, 1.5 min) to the ipsilateral sciatic nerve. The fatigue-resistance test (5 sets with a 2-min rest in between) was evaluated in terms of tension attenuation (fatigue) from the initial to the last tension (A) during each set, attenuation of the initial (B) or last tension (C) in each set, as compared to the first set under the presence or absence of ischemia or h-LEH (10 mL/kg). While ischemia significantly enhanced fatigue only in PLT, h-LEH showed no effect regardless of perfusion pattern (normal/ischemia) or muscle type (PLT/SOL) during each set (A). In parameter (B), set-by-set fatigue development was observed in PLT, whereas h-LEH-SOL showed a trend of advanced fatigue resistance. Such trends became clearer in parameter C (last tension), because h-LEH-SOL exerted tension enhancement (rather than decrease) regardless of the presence or absence of ischemia, whereas there were no h-LEH effects in PLT. In addition, faster recovery of nicotinamide adenine dinucleotide content in the muscle after 10 min of all fatigue tests was observed in h-LEH-SOL, while saline-SOL still showed significantly higher value than that of control. These results suggested that additional O₂ supply by h-LEH may accelerate the tricarboxylic-acid cycle/electron transport chain in slow-type aerobic SOL muscle containing abundant mitochondria and contribute to faster removal of muscle fatigue substances such as lactate. This article is protected by copyright. All rights reserved.