ACUTE PLASMA EXPANSION - LEFT-VENTRICULAR HEMODYNAMICS AND ENDOCRINE FUNCTION DURING EXERCISE

In 11 healthy subjects (8 males and 3 females, age 21-59 yr) left ventricular end-diastolic (LVEDV) and end systolic (LVESV) volumes were measured in the supine position by isotope cardiography at rest and during two submaximal one-legged exercise loads before and 1 h after acute plasma expansion (PE) by use of a 6% dextran solution (500-750 ml). After PE, blood volume increased from 5.22 +/- 0.92 to 5.71 +/- 1.02 (SD) liters (P < 0.01). At rest, cardiac output increased 30% (5.3 +/- 1.0 to 6.9 +/- 1.6 l/min; P < 0.01), stroke volume increased from 90 +/- 20 to 100 +/- 28 ml (P < 0.05), and LVEDV increased from 134 +/- 29 to 142 +/- 40 ml (NS). LVESV was unchanged (44 +/- 11 and 42 +/- 14 ml). Heart rate rose from 60 +/- 7 to 7 +/- 10 beats/min (P < 0.01). The cardiac preload [central venous pressure (CVP)] was insignificantly elevated (4.9 +/- 2.1 and 5.3 +/- 3.0 mmHg); systemic vascular resistance and arterial pressures were significantly reduced (mean pressure fell from 91 +/- 11 to 85 +/- 11 mmHg, P < 0.01). Left ventricular peak filling and peak ejection rates both increased (19 and 14%, respectively; P < 0.05). During exercise, cardiac output remained elevated after PE compared with the control situation, predominantly due to a 10- to 14-ml rise in stroke volume caused by an increased LVEDV, whereas LVESV was unchanged. CVP increased after PE by 2.1 and 3.0 mmHg, respectively (P < 0.05). CVP remained unchanged during exercise compared with rest after PE in contrast to the fall in the control experiment. Systemic vascular resistance was significantly reduced after PE. Atrial natriuretic factor (ANF) and guanosine 3',5'-cyclic monophosphate increased with exercise but with great individual variations. After PE, a rise was seen compared with the control situations (P < 0.05 during exercise). Changes in ANF and guanosine 3',5'-cyclic monophosphate were highly correlated (r = 0.89). It is concluded that PE-induced rises in cardiac output at rest and during exercise are caused mainly by increased cardiac filling (increased preload), which leads to increased LVEDV and stroke volume. ANF concentration is increased concomitantly with the increased cardiac preload, but exercise-induced increases in heart rate and sympathetic nervous activity seem to be an even stronger stimulus for ANF release.