Myocardial relaxation. III. Reoxygenation mechanics in the intact dog heart.

Abstract
Reoxygenation of hypoxic isolated cardiac muscle results in prolonged duration of contraction-relaxation. To determine whether similar mechanical changes occur in the intact left ventricle (LV), and especially to assess the influence of prolonged relaxation on LV diastolic stiffness, we examined LV pressure transients (micromanometer) and changes in myocardial segment length (ultrasonic transit time) during reoxygenation in 22 anesthetized dogs following 15 minutes of hypoxia (PaO2 = 21 +/- 2 mm Hg). The time constant (T) of LV isovolumic exponential pressure decline was used as an index of myocardial relaxation; LV end-diastolic stiffness was assessed from stiffness constants derived from multiple coordinates of end-diastolic pressure and segment length (volume loading). During reoxygenation, after LV systolic pressure and segment length measurements had returned to control levels, relaxation was prolonged; T increased from a control of 32 +/- 2 to 44 +/- 3 msec at 5 minutes of reoxygenation (P less than 0.01). Prolonged relaxation resulted in a consistent increase in LV early-diastolic pressures. Furthermore, calculated values for LV end-diastolic stiffness increased during reoxygenation when the next beat began less than 3.5 T after maximum negative dP/dt; this condition was present more frequently at a heart rate of 150 beats/min than at 120 beats/min. Thus, rapid correction of acute hypoxia in the dog results in prolonged LV relaxation; prolonged relaxation can influence LV end-diastolic stiffness when relaxation is sufficiently slow and/or when diastole is sufficiently short.