Effect of fetal anaemia on myocardial ischaemia-reperfusion injury and coronary vasoreactivity in adult sheep

Q. Yang, Alan (Roger) Hohimer, George Giraud, D. M. Van Winkle, M. J. Underwood, G. W. He, Lowell Davis

Research output: Contribution to journalArticle

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Abstract

Aims: We investigated whether chronic fetal anaemia affects myocardial infarct in adulthood and elicits functional modifications in adult coronary vasoreactivity. Methods: Seven-month-old sheep that were made anaemic in utero and transfused to normal haematocrit before birth were studied. Infarct size was determined by tetrazolium after 1-h ischaemia (occlusion of the mid of left anterior descending artery) and 2-h reperfusion. The dose-response to vasoconstrictors and vasodilators was assessed in small resistance coronary arteries. Results: There were no significant differences between the animals previously subjected to in utero anaemia and the control animals regarding the percentage infarct size and the area-at-risk to the left ventricle. The ventricular function (dP/dt) was preserved. The percentage infarct size of the area-at-risk (70.7 ± 3.5%) was larger than that in the controls (49.8 ± 4.5%) (P = 0.006). The vascular responses were not altered. Endothelium-dependent relaxation to bradykinin (96.0 ± 2.6% vs. 98.8 ± 1.0%) was not affected by PGI2 inhibitor (94.6 ± 2.6% vs. 98.5 ± 1.0%) but significantly reduced by the inhibition of nitric oxide (NO) in both anaemic (P <0.05) and control (P <0.001) groups with a significant right shift of EC50 (P <0.01). The non-NO-non-PGI2-mediated relaxation was slightly potentiated in anaemic animals. Conclusions: Exposing fetal sheep to in utero anaemia in late gestation for 3 weeks may increase the susceptibility of adult hearts to ischaemia-reperfusion injury without major alterations in coronary vasomotor responsiveness. The impact of in utero anaemia at earlier period of pregnancy and on the earlier or later life of the adult is yet to be further investigated.

Original languageEnglish (US)
Pages (from-to)325-334
Number of pages10
JournalActa Physiologica
Volume194
Issue number4
DOIs
StatePublished - Dec 2008

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Myocardial Reperfusion Injury
Reperfusion Injury
Myocardial Ischemia
Anemia
Sheep
Pregnancy
Ventricular Function
Bradykinin
Vasoconstrictor Agents
Epoprostenol
Vasodilator Agents
Hematocrit
Oxides
Reperfusion
Heart Ventricles
Endothelium
Blood Vessels
Coronary Vessels
Nitric Oxide
Ischemia

Keywords

  • Coronary circulation
  • Endothelial function
  • Fetal anaemia
  • Ischaemia
  • Myocardial infarct
  • Reperfusion

ASJC Scopus subject areas

  • Physiology

Cite this

Effect of fetal anaemia on myocardial ischaemia-reperfusion injury and coronary vasoreactivity in adult sheep. / Yang, Q.; Hohimer, Alan (Roger); Giraud, George; Van Winkle, D. M.; Underwood, M. J.; He, G. W.; Davis, Lowell.

In: Acta Physiologica, Vol. 194, No. 4, 12.2008, p. 325-334.

Research output: Contribution to journalArticle

Yang, Q. ; Hohimer, Alan (Roger) ; Giraud, George ; Van Winkle, D. M. ; Underwood, M. J. ; He, G. W. ; Davis, Lowell. / Effect of fetal anaemia on myocardial ischaemia-reperfusion injury and coronary vasoreactivity in adult sheep. In: Acta Physiologica. 2008 ; Vol. 194, No. 4. pp. 325-334.
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abstract = "Aims: We investigated whether chronic fetal anaemia affects myocardial infarct in adulthood and elicits functional modifications in adult coronary vasoreactivity. Methods: Seven-month-old sheep that were made anaemic in utero and transfused to normal haematocrit before birth were studied. Infarct size was determined by tetrazolium after 1-h ischaemia (occlusion of the mid of left anterior descending artery) and 2-h reperfusion. The dose-response to vasoconstrictors and vasodilators was assessed in small resistance coronary arteries. Results: There were no significant differences between the animals previously subjected to in utero anaemia and the control animals regarding the percentage infarct size and the area-at-risk to the left ventricle. The ventricular function (dP/dt) was preserved. The percentage infarct size of the area-at-risk (70.7 ± 3.5{\%}) was larger than that in the controls (49.8 ± 4.5{\%}) (P = 0.006). The vascular responses were not altered. Endothelium-dependent relaxation to bradykinin (96.0 ± 2.6{\%} vs. 98.8 ± 1.0{\%}) was not affected by PGI2 inhibitor (94.6 ± 2.6{\%} vs. 98.5 ± 1.0{\%}) but significantly reduced by the inhibition of nitric oxide (NO) in both anaemic (P <0.05) and control (P <0.001) groups with a significant right shift of EC50 (P <0.01). The non-NO-non-PGI2-mediated relaxation was slightly potentiated in anaemic animals. Conclusions: Exposing fetal sheep to in utero anaemia in late gestation for 3 weeks may increase the susceptibility of adult hearts to ischaemia-reperfusion injury without major alterations in coronary vasomotor responsiveness. The impact of in utero anaemia at earlier period of pregnancy and on the earlier or later life of the adult is yet to be further investigated.",
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T1 - Effect of fetal anaemia on myocardial ischaemia-reperfusion injury and coronary vasoreactivity in adult sheep

AU - Yang, Q.

AU - Hohimer, Alan (Roger)

AU - Giraud, George

AU - Van Winkle, D. M.

AU - Underwood, M. J.

AU - He, G. W.

AU - Davis, Lowell

PY - 2008/12

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N2 - Aims: We investigated whether chronic fetal anaemia affects myocardial infarct in adulthood and elicits functional modifications in adult coronary vasoreactivity. Methods: Seven-month-old sheep that were made anaemic in utero and transfused to normal haematocrit before birth were studied. Infarct size was determined by tetrazolium after 1-h ischaemia (occlusion of the mid of left anterior descending artery) and 2-h reperfusion. The dose-response to vasoconstrictors and vasodilators was assessed in small resistance coronary arteries. Results: There were no significant differences between the animals previously subjected to in utero anaemia and the control animals regarding the percentage infarct size and the area-at-risk to the left ventricle. The ventricular function (dP/dt) was preserved. The percentage infarct size of the area-at-risk (70.7 ± 3.5%) was larger than that in the controls (49.8 ± 4.5%) (P = 0.006). The vascular responses were not altered. Endothelium-dependent relaxation to bradykinin (96.0 ± 2.6% vs. 98.8 ± 1.0%) was not affected by PGI2 inhibitor (94.6 ± 2.6% vs. 98.5 ± 1.0%) but significantly reduced by the inhibition of nitric oxide (NO) in both anaemic (P <0.05) and control (P <0.001) groups with a significant right shift of EC50 (P <0.01). The non-NO-non-PGI2-mediated relaxation was slightly potentiated in anaemic animals. Conclusions: Exposing fetal sheep to in utero anaemia in late gestation for 3 weeks may increase the susceptibility of adult hearts to ischaemia-reperfusion injury without major alterations in coronary vasomotor responsiveness. The impact of in utero anaemia at earlier period of pregnancy and on the earlier or later life of the adult is yet to be further investigated.

AB - Aims: We investigated whether chronic fetal anaemia affects myocardial infarct in adulthood and elicits functional modifications in adult coronary vasoreactivity. Methods: Seven-month-old sheep that were made anaemic in utero and transfused to normal haematocrit before birth were studied. Infarct size was determined by tetrazolium after 1-h ischaemia (occlusion of the mid of left anterior descending artery) and 2-h reperfusion. The dose-response to vasoconstrictors and vasodilators was assessed in small resistance coronary arteries. Results: There were no significant differences between the animals previously subjected to in utero anaemia and the control animals regarding the percentage infarct size and the area-at-risk to the left ventricle. The ventricular function (dP/dt) was preserved. The percentage infarct size of the area-at-risk (70.7 ± 3.5%) was larger than that in the controls (49.8 ± 4.5%) (P = 0.006). The vascular responses were not altered. Endothelium-dependent relaxation to bradykinin (96.0 ± 2.6% vs. 98.8 ± 1.0%) was not affected by PGI2 inhibitor (94.6 ± 2.6% vs. 98.5 ± 1.0%) but significantly reduced by the inhibition of nitric oxide (NO) in both anaemic (P <0.05) and control (P <0.001) groups with a significant right shift of EC50 (P <0.01). The non-NO-non-PGI2-mediated relaxation was slightly potentiated in anaemic animals. Conclusions: Exposing fetal sheep to in utero anaemia in late gestation for 3 weeks may increase the susceptibility of adult hearts to ischaemia-reperfusion injury without major alterations in coronary vasomotor responsiveness. The impact of in utero anaemia at earlier period of pregnancy and on the earlier or later life of the adult is yet to be further investigated.

KW - Coronary circulation

KW - Endothelial function

KW - Fetal anaemia

KW - Ischaemia

KW - Myocardial infarct

KW - Reperfusion

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