The development of left ventricular ischaemic
contracture and its correlation with ultrastructural and sarcolemmal permeability defects were studied in isolated rat hearts during global subtotal ischaemia. With
acetate as substrate the hearts exhibited a rise in diastolic tension after 8-10 min at which time small foci of contracted myocytes were scattered throughout the myocardium. In hearts with 5% of the maximum diastolic tension (termed 5%
contracture), the foci were situated predominantly in the subendocardium and papillary muscle. Contracted myocytes in these foci were capable of excluding ionic
lanthanum thus demonstrating retention of normal sarcolemmal permeability properties. With 30%
contracture ultrastructural damage had spread to the subepicardium and with further
contracture there was an associated increase in the number and size of foci in all regions. In these foci, swelling of the tubular sarcolemmal system and occasionally of the sarcoplasmic reticulum appeared to precede myofibrillar contraction. At 50%
contracture lanthanum influx into contracted cells became more frequent. Hearts developed full
contracture by 15-18 min at which time most myocytes were contracted and retained
lanthanum intracellularly. The heterogeneity of the response at a cellular level may offer a possible explanation for the lack of correlation between
contracture and tissue
ATP. A possible sequence of structural injury leading to impaired
calcium homeostasis is also suggested.