Transient effects of forebrain ischemia on fetal heart rate variability in fetal sheep
| Autor: | Kelly Q Zhou, Mark Gunning, Tomoaki Ikeda, Michael J. Beacom, Christopher A. Lear, Alistair J. Gunn, Joanne O. Davidson, Laura Bennet, Yoshiki Maeda |
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| Rok vydání: | 2021 |
| Předmět: |
medicine.medical_specialty
Fetal Heart Rate Variability Physiology Ischemia Autonomic Nervous System Forebrain ischemia 03 medical and health sciences 0302 clinical medicine Fetus Heart Rate Physiology (medical) Internal medicine medicine Heart rate variability Animals Humans 030219 obstetrics & reproductive medicine Sheep business.industry Prenatal Care Heart Rate Fetal medicine.disease Autonomic nervous system Cardiology business 030217 neurology & neurosurgery Peripheral chemoreflex |
| Zdroj: | American journal of physiology. Regulatory, integrative and comparative physiology. 320(6) |
| ISSN: | 1522-1490 |
| Popis: | Fetal heart rate variability (FHRV) is a key index of antenatal and intrapartum fetal well-being. FHRV is well established to be mediated by both arms of the autonomic nervous system, but it remains unknown whether higher centers in the forebrain contribute to FHRV. We tested the hypothesis that selective forebrain ischemia would impair the generation of FHRV. Sixteen chronically instrumented near-term fetal sheep were subjected to either forebrain ischemia induced by bilateral carotid occlusion or sham-ischemia for 30 min. Time, frequency, and nonlinear measures of FHRV were assessed during and for seven days after ischemia. Ischemia was associated with profound suppression of electroencephalographic (EEG) power, which remained suppressed throughout the recovery period ( P < 0.001). During the first 5 min of ischemia, multiple time and frequency domain measures were increased (all P < 0.05) before returning back to sham levels. A delayed increase in sample entropy was observed during ischemia ( P < 0.05). For the first 3 h after ischemia, there was moderate suppression of two measures of FHRV (very-low frequency power and the standard deviation of RR-intervals, both P < 0.05) and increased sample entropy ( P < 0.05). Thereafter, all measures of FHRV returned to control levels. In conclusion, profound forebrain ischemia sufficient to lead to severe neural injury had only transient effect on multiple measures of FHRV. These findings suggest that the forebrain makes a limited contribution to FHRV. FHRV therefore primarily originates in the hindbrain and is unlikely to provide meaningful information on forebrain neurodevelopment or metabolism. |
| Databáze: | OpenAIRE |
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