Objective: In a sheep model we tested the hypothesis that the fetal left ventricle is less tolerant to worsening acidemia than the right ventricle. Study design: At 106-124/145 days of gestation, 12 fetuses were instrumented. After a 4-day recovery, placental vascular resistance was increased by fetal angiotensin (AT) II infusion. After a 2 h ATII infusion, to further deteriorate fetal oxygenation, maternal hypoxemia was induced. Fetal cardiac function and hemodynamics were assessed by tissue Doppler imaging (TDI) and pulsed Doppler imaging. Ultrasonography was performed at baseline, at 1 and 2 h after the beginning of ATII infusion and during the ATII + hypoxemia phase. Results: Fetal pH and pO 2 decreased significantly and progressively during the experiment. Left ventricular TDI-derived isovolumic relaxation velocity (IVRV) was lower during ATII 2 h and ATII + hypoxemia phases than at baseline. The IVRV deceleration was significantly less during the ATII + hypoxemia phase than at baseline. Right ventricular IVRV was significantly lower during the ATII + hypoxemia phase than at baseline. IVRV deceleration did not change. Only left ventricular IVRV deceleration correlated with fetal pO 2 (R = 0.36, p < 0.05). Fetal right and left ventricular cardiac outputs, as well as umbilical artery, aortic isthmus and ductus venosus pulsatility indices remained unchanged during the experiment. Conclusion: Our results show that signs of cardiac dysfunction develop earlier in the left ventricle than in the right ventricle. The fetal left ventricle seems to be more sensitive to progressively worsening hypoxemia and acidemia than the right ventricle.
|Original language||English (US)|
|Number of pages||5|
|Journal||European Journal of Obstetrics and Gynecology and Reproductive Biology|
|State||Published - Apr 2013|
ASJC Scopus subject areas
- Reproductive Medicine
- Obstetrics and Gynecology