Abstract

Strength-interval curves (SIC) were evaluated using computerized techniques each minute during five minutes of hypoxia and ten minutes of reoxygenation in ten isolated muscle preparations paced at 50 beats/minute. The falling limb of the SIC was measured at six 15 msec intervals during repolarization. At five minutes of hypoxia, the SIC was shifted to the left, indicating marked shortening of refractoriness (p<0.001). Following one minute of reoxygenation, the SIC approached control values; at 2–3 minutes of reoxygenation, the SIC reversed its movement from the one observed at one minute of reoxygenation and moved sharply to the left with refractoriness significantly shorter than five minutes of hypoxia (p<0.001). Recovery occurred at 6–10 minutes of reoxygenation. Eight muscles were exposed to 1, 5, 10, and 20 μg/ml of lidocaine. The control SIC at each concentration of lidocaine was shifted upward and to the right, indicting prolonged refractoriness and increasing diastolic threshold. During hypoxia, 1 μg/ml had little affect on the SIC. Five μg/ml reduced the SIC shift to the left while 10–20 μg/ml reversed the SIC shift from leftward to rightward, thus increasing refractoriness and diastolic threshold of the hypoxic muscle. Lidocaine only modified the reoxygenation phase without abolishing the supernormal refractory period phase. It is concluded that: 1) shifts in the SIC of isolated heart muscle during hypoxia and reoxygenation are similar to those previously reported in the intact dog heart; 2) in concentrations of 5 μg/ml or greater, lidocaine displaces the SIC during hypoxia upward and to the right; and 3) electrical instability during reoxygenation is characterized by oscillatory shifts in the SIC which are not abolished by lidocaine.

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