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DEVELOPMENT AND TISSUE PLASTICITY

Fetal anemia leads to augmented contractile response to hypoxic stress in adulthood

¹Department of Medicine, Division of Cardiology, and Departments of ²Physiology and Pharmacology, ⁴Surgery, and ⁵Obstetrics and Gynecology, at Oregon Health Science University, and ³Division of Cardiology, Portland Veterans Affairs Medical Center, Oregon Health & Science University, Portland, Oregon 97201

Submitted 25 November 2002 ; accepted in final form 22 May 2003

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 before birth. At 7 mo 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 and body weight, or baseline hemodynamic parameters. However, the effect of hypoxia (relative to baseline) on multiple indexes of systolic function was different between the two groups. End-systolic elastance 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 ± 0.45), which shows that the response to hypoxia was significantly different (P < 0.01) between groups. Similarly, the maximum derivative of LV pressure with respect to time increased in the in utero anemia group (486 ± 340 mmHg/s,) but on average fell in the controls (-503 ± 211 mmHg/s) 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.

phlebotomy; end-systolic elastance

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