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

Craig Broberg, George Giraud, Jess M. Schultz, Kent Thornburg, Alan (Roger) Hohimer, Lowell Davis

Research output: Contribution to journalArticle

32 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume285
Issue number3 54-3
StatePublished - Sep 1 2003

Fingerprint

Anemia
Left Ventricular Function
Sheep
Phlebotomy
Ventricular Pressure
Hematocrit
Hemodynamics
Body Weight
Parturition
Pressure
Hypoxia

Keywords

  • End-systolic elastance
  • Phlebotomy

ASJC Scopus subject areas

  • Physiology

Cite this

@article{3e5249eec41c4682b97758f17cf86ec0,
title = "Fetal anemia leads to augmented contractile response to hypoxic stress in adulthood",
abstract = "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.",
keywords = "End-systolic elastance, Phlebotomy",
author = "Craig Broberg and George Giraud and Schultz, {Jess M.} and Kent Thornburg and Hohimer, {Alan (Roger)} and Lowell Davis",
year = "2003",
month = "9",
day = "1",
language = "English (US)",
volume = "285",
journal = "American Journal of Physiology - Renal Fluid and Electrolyte Physiology",
issn = "1931-857X",
publisher = "American Physiological Society",
number = "3 54-3",

}

TY - JOUR

T1 - Fetal anemia leads to augmented contractile response to hypoxic stress in adulthood

AU - Broberg, Craig

AU - Giraud, George

AU - Schultz, Jess M.

AU - Thornburg, Kent

AU - Hohimer, Alan (Roger)

AU - Davis, Lowell

PY - 2003/9/1

Y1 - 2003/9/1

N2 - 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.

AB - 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.

KW - End-systolic elastance

KW - Phlebotomy

UR - http://www.scopus.com/inward/record.url?scp=0042130539&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0042130539&partnerID=8YFLogxK

M3 - Article

C2 - 12775557

AN - SCOPUS:0042130539

VL - 285

JO - American Journal of Physiology - Renal Fluid and Electrolyte Physiology

JF - American Journal of Physiology - Renal Fluid and Electrolyte Physiology

SN - 1931-857X

IS - 3 54-3

ER -