Left ventricular (LV) function was investigated in 16 fetal lambs (125-140 days gestation), each instrumented with an electromagnetic flow sensor on the ascending aorta and vascular catheters. Control arterial blood values were pH 7.38 ± 0.02 (SD), PCO2 46.3 ± 3.2 Torr, PO2 19.4 ± 1.3 Torr, and hematocrit 34.8 ± 4.3%. Control values for LV output (228 ± 108 ml·min-1·kg-1) and arterial pressure (AP, 47.4 ± 6.5 Torr) were unchanged by administration of atropine and propranolol. LV function curves relating stroke volume (SV) to mean left atrial pressure (LAP) were generated by rapid withdrawal and reinfusion of fetal blood with or without concomitant infusion of nitroprusside (NP) or phenylephrine hydrochloride (PE) to lower or raise mean arterial pressure (AP). The control LV function curve was composed of a steep ascending limb of 0.39 ± 0.34 ml·kg-1·Torr-1 and a plateau of 0.04 ± 0.04 ml·kg-1·Torr-1. The breakpoint joining the limbs of the control curve was LAP 3.1 ± 1.2 Torr and LVSV 1.3 ± 0.5 ml/kg, and these values were not different from control LAP and SV. Function curve slopes were not affected by PE or NP treatment. Multiple linear regression of SV, LAP, and AP showed a small but significant coefficient for AP [-0.002 ± 0.001 (SE) ml*kg-1·Torr-1] and LAP [+0.053 ± 0.004 (SE) ml·kg-1·Torr-1] at LAP greater than breakpoint. LAP was a powerful determinant of LVSV at values below the breakpoint, a weak factor above. AP had a negative effect on SV in the range tested (20-88 Torr).
|Original language||English (US)|
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|Issue number||5 (20/5)|
|State||Published - 1986|
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Physiology (medical)