Abstract
Following our failure to reproduce the renal effects of crush syndrome in rabbits, whose muscles are virtually devoid of myoHb., we have injected solutions containing this pigment into rabbits in doses equivalent to the amount excreted in human crushing injury.1. In normal rabbits no lesion results.2. If myoHb. is injected after release of a standardised leg compression, renal impairment may follow.3. In rabbits with acid urine (pH 4·5‐6·1) the injection of myoHb. solutions led to more severe renal failure, with death in uræmia in 4/25 cases. This renal damage was associated with pigment retention to a significant degree.4. Experiments with limb compression and rabbit (non‐pigmented) muscle extract injections in “acidified” rabbits gave negative results.5. It is concluded, by analogy with these experiments, that myohæmoglobin excreted in an acid urine such as occurs in the crush syndrome may play an important role in the genesis of the renal failure seen in that type of injury. Analogies with the mismatched transfusion kidney are pointed out.
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