Induction of fine structural alteration in cardiac Purkinje cells by ischaemic metabolites depends on oxygen tension.

The effects of major ischaemic metabolites on the fine structure of false tendon Purkinje cells from the dog heart were investigated in vitro under oxygenated and oxygen-deficient conditions. High levels of potassium ion induced potentially reversible alteration consisting of moderate cell swelling, swelling of sarcoplasmic reticulum, and nuclear swelling with moderate aggregation of chromatin irrespective of gas tension. Other metabolites induced alteration only in oxygen-deficient solutions. Ischaemic levels of lactate and inorganic phosphate both caused mitochondrial swelling, which was most severe in the presence of lactate. At acidic pH intramitochondrial dense inclusions, the hallmark of irreversible injury, also developed. Severe aggregation of nuclear chromatin and gross dilatations of the sarcoplasmic reticulum were focal and much less prominent than in contractile myocardium exposed to excess hydrogen ion. These observations indicate that the efflux of ischaemic metabolites from a developing infarct may be arrhythmogenic by impairing the function of the subjacent Purkinje network without damaging its cell structure, since luminal blood flow ensures it is always adequately oxygenated.