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1 Physiology, University of Auckland, Auckland, New Zealand
2 Department of Physiology, The University of Auckland, Faculty of Medical + Health Sciences, Auckland, New Zealand
3 Obstetrics & Gynaecology, University of Auckland, Auckland, New Zealand
4 Obstetrics & Gynecology, Isala Clinics, Zwolle, Netherlands
5 Physiology, The University of Auckland, Auckland, New Zealand
* To whom correspondence should be addressed. E-mail: aj.gunn{at}auckland.ac.nz.
There is limited information on whether pre-existing fetal hypoxia alters hemodynamic responses and changes in T/QRS ratio and ST waveform shape during subsequent severe asphyxia. Chronically instrumented near-term sheep fetuses (124±1 days) were identified as either normoxic PaO2 > 17 mmHg (n=9) or hypoxic PaO2 > 17 mmHg (n=5), and then received complete occlusion of the umbilical cord for 15-minutes. Umbilical cord occlusion led to sustained bradycardia, severe acidosis and transient hypertension followed by profound hypotension in both groups. Pre-existing hypoxia did not affect changes in mean arterial blood pressure, but was associated with a more rapid initial fall in femoral blood flow and vascular conductance and with transiently higher fetal heart rate at 2 minutes and from 9 to 11 minutes of occlusion compared with previously normoxic fetuses. Occlusion was associated with a significant but transient rise in T/QRS ratio; pre-existing hypoxia was associated with a significant delay in this rise (maxima 3.7 ± 0.4 vs. 6.2 ± 0.5 minutes), but a slower rate of fall. There was a similar elevation in troponin-T levels 6 hours after occlusion in the two groups (median (range) 0.43 (0.08, 1.32) vs. 0.55 (0.16, 2.32) µg/L, N.S.). In conclusion, mild pre-existing hypoxia in normally grown singleton fetal sheep is associated with more rapid centralization of circulation after umbilical cord occlusion and delayed elevation of the ST waveform and slower fall, suggesting that chronic hypoxia alters myocardial dynamics during asphyxia.
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