Transient effects of forebrain ischemia on fetal heart rate variability in fetal sheep

Author(s):  
Yoshiki Maeda ◽  
Christopher A. Lear ◽  
Michael J. Beacom ◽  
Joanne O Davidson ◽  
Kelly Q Zhou ◽  
...  

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. 16 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 non-linear 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.

2014 ◽  
Vol 307 (4) ◽  
pp. R387-R395 ◽  
Author(s):  
Christopher A. Lear ◽  
Joanne O. Davidson ◽  
Lindsea C. Booth ◽  
Guido Wassink ◽  
Robert Galinsky ◽  
...  

Perinatal exposure to infection is highly associated with adverse outcomes. Experimentally, acute, severe exposure to gram-negative bacterial lipopolysaccharide (LPS) is associated with increased fetal heart rate variability (FHRV). It is unknown whether FHRV is affected by subclinical infection with or without acute exacerbations. We therefore tested the hypothesis that FHRV would be associated with hypotension after acute on chronic exposure to LPS. Chronically instrumented fetal sheep at 0.7 gestation were exposed to a continuous low-dose LPS infusion ( n = 12, 100 ng/kg over 24 h, followed by 250 ng·kg−1·24 h−1 for a further 96 h) or the same volume of saline ( n = 10). Boluses of either 1 μg LPS or saline were given at 48, 72, and 96 h. Low-dose infusion was not associated with hemodynamic or FHRV changes. The first LPS bolus was associated with tachycardia and suppression of nuchal electromyographic activity in all fetuses. Seven of twelve fetuses developed hypotension (a fall in mean arterial blood pressure ≥5 mmHg). FHRV was transiently increased only at the onset of hypotension, in association with increased cytokine induction and electroencephalogram suppression. FHRV then fell before the nadir of hypotension, with transient suppression of short-term FHRV. After the second LPS bolus, the hypotension group showed a biphasic pattern of a transient increase in FHRV followed by more prolonged suppression. These findings suggest that infection-related hypotension in the preterm fetus mediates the transient increase in FHRV and that repeated exposure to LPS leads to progressive loss of FHRV.


2004 ◽  
Vol 287 (4) ◽  
pp. R925-R933 ◽  
Author(s):  
Sherly George ◽  
Alistair J. Gunn ◽  
Jenny A. Westgate ◽  
Christine Brabyn ◽  
Jian Guan ◽  
...  

This study was undertaken to determine the mechanisms mediating changes in fetal heart rate variability (FHRV) during and after exposure to asphyxia in the premature fetus. Preterm fetal sheep at 0.6 of gestation (91 ± 1 days, term is 147 days) were exposed to either sham occlusion ( n = 10) or to complete umbilical cord occlusion for either 20 ( n = 7) or 30 min ( n = 10). Cord occlusion led to a transient increase in FHRV with abrupt body movements that resolved after 5 min. In the 30 min group there was a marked increase in FHRV in the final 10 min of occlusion related to abnormal atrial activity. After reperfusion, FHRV in both study groups was initially suppressed and progressively increased to baseline levels over the first 4 h of recovery. In the 20 min group this improvement was associated with return of normal EEG activity and movements. In contrast, in the 30 min group the EEG was abnormal with epileptiform activity superimposed on a suppressed background, which was associated with abnormal fetal movements. As the epileptiform activity resolved, FHRV fell and became suppressed for the remainder of the study. Histological assessment after 72 h demonstrated severe brain stem injury in the 30 min group but not in the 20 min group. In conclusion, during early recovery from asphyxia, epileptiform activity and associated abnormal fetal movements related to evolving neural injury can cause a confounding transient increase in FHRV, which mimics the normal pattern of recovery. However, chronic suppression of FHRV was a strong predictor of severe brain stem injury.


2018 ◽  
Vol 596 (23) ◽  
pp. 6093-6104 ◽  
Author(s):  
Kyohei Yamaguchi ◽  
Christopher A. Lear ◽  
Michael J. Beacom ◽  
Tomoaki Ikeda ◽  
Alistair J. Gunn ◽  
...  

1995 ◽  
Vol 12 (04) ◽  
pp. 259-261 ◽  
Author(s):  
Adam Hiett ◽  
Lawrence Devoe ◽  
Haywood Brown ◽  
Joy Watson

1977 ◽  
Vol 128 (4) ◽  
pp. 381-392 ◽  
Author(s):  
Russell K. Laros ◽  
Wilson S. Wong ◽  
David C. Heilbron ◽  
Julian T. Parer ◽  
Sol M. Shnider ◽  
...  

2006 ◽  
Vol 51 (4) ◽  
pp. 248-250 ◽  
Author(s):  
Uwe Schneider ◽  
Anja Fiedler ◽  
Mario Liehr ◽  
Christiane Kähler ◽  
Ekkehard Schleussner

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