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1 Cardiology/Medicine, Oregon Health and Science University, Portland, OR, USA
2 Cardiology/Medicine, Oregon Health and Science University, Portland, OR, USA; Physiology and Pharmacology, Oregon Health and Sciences University, Portland, OR, USA; Division of Cardiology, Portland Veterans Affairs Medical Center, Portland, OR, USA
3 Surgery, Oregon Health and Sciences University, Portland, OR, USA
4 Cardiology/Medicine, Oregon Health and Science University, Portland, OR, USA; Obstetrics and Gynecology, Oregon Health and Science University, Portland, OR, USA; Physiology and Pharmacology, Oregon Health and Sciences University, Portland, OR, USA
5 Obstetrics and Gynecology, Oregon Health and Science University, Portland, OR, USA; Physiology and Pharmacology, Oregon Health and Sciences University, Portland, OR, USA
6 Obstetrics and Gynecology, Oregon Health and Science University, Portland, OR, USA
* To whom correspondence should be addressed. E-mail: davislo{at}ohsu.edu.
In response to chronic fetal anemia, coronary blood flow, maximal coronary conductance and coronary reserve increase. We sought to determine whether chronic fetal anemia alters left ventricular (LV) function in adulthood. We studied adult sheep that had been made anemic for 20 days in utero by phlebotomy. They were transfused just prior to birth. At 7 months of age, LV function was measured by pressure-volume loops at rest and during hypoxic stress. The in utero anemia group (n = 8) did not differ from controls (n = 5) with respect to hematocrit, heart/body weight, or baseline hemodynamic parameters. However, the effect of hypoxia (relative to baseline) on multiple indices of systolic function was different between the two groups. End-systolic elastance (E max) increased in the in utero anemia group (baseline to hypoxia) by 4.15 ± 3.47 mmHg/ml (mean ± SD) but changed little in controls (0.24 ±.45), the response to hypoxia being significantly different (P < 0.01) between the groups. Similarly, the maximum derivative of LV pressure with respect to time (dP/dtmax) increased in the in utero anemia group (486 ± 340 mmHg/s,) but on average fell in the controls (-503 ± 211) with the response again being significantly different (P < 0.03). We conclude that in sheep, perinatal anemia can alter cardiac responses to hypoxic stress in the adult long after restoration of normocythemia.
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