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In Response

Iwata, Chihiro MD, PhD; Morita, Hironobu MD, PhD

doi: 10.1213/ANE.0000000000000393
Letters to the Editor: Letter to the Editor
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Department of Physiology, Gifu University Graduate School of Medicine, Gifu, Japan, zunzunmorita@gmail.com

As pointed out by Petrenko et al.,1 the correlation between electroencephalography (EEG) activity and clinical signs is poor, especially when median frequency or spectral edge frequency is used for EEG evaluation.2 However, since burst suppression appears just before an isoelectric EEG (electrocerebral silence) and cerebral metabolic rate of oxygen decreases progressively toward the onset of isoelectricity, the EEG (burst suppression) is a reliable marker of decreased brain metabolism.3,4 In this regard, burst suppression is thought to be a useful marker for deep anesthesia.5

The righting response used in our study might be impacted by dynamic behavior and pain threshold. Although we did not evaluate the behavior of vestibular lesion (VL) rats, the righting response latency in VL rats raised in 1 g (1G-VL) did not differ from that of sham rats (1G-sham),6 suggesting that VL itself did not cause the prolonged recovery of righting response. Furthermore, pain sensitivity was assessed using the hot plate test in the additional experiments. Following placement of each subject on a 55°C plate, no difference in latency of pain-related behavior was detected between 1 g raised rats (14.8 ± 3.8 seconds [mean ± SD]) and 3 g raised rats (12.8 ± 1.8 seconds). Thus, chronic hypergravity exposure (2 weeks) did not alter pain sensitivity, whereas acute hypergravity exposure (10 minutes) might alter pain sensitivity.7

Although Petrenko et al. comments that arterial pressure decreases in proportion to anesthetic depth,8 other factors such as autonomic disorders can augment anesthetic-induced hypotension. We have demonstrated that hypergravity exposure suppressed vestibular-mediated pressor response (vestibulo-cardiovascular reflex); however, nonvestibular-mediated pressor response was not affected by hypergravity.9 The possibility that the suppressed vestibulo-cardiovascular reflex affects propofol-induced hypotension is unlikely since hypotension measured in 1G-VL was comparable to that measured in 1G-sham.6 Sensitivity of baroreflex is the most important other factor when determining propofol-induced hypotension. To examine this, the sensitivity of baroreflex control over heart rate was assessed in rats raised in 1 g or 3 g for 2 weeks in the additional experiments, in which heart rate responses to phenylephrine- and nitroprusside-related changes in arterial pressure were plotted and fitted to the logistic function curve. There was no difference in the maximal gain between 1 g raised rats (6.9 ± 1.4 [mean ± SD]) and 3 g raised rats (6.2 ± 1.0).

The notable point of our study was that the augmenting effect of propofol was induced via the vestibular-mediated pathway because it was eliminated by the VL. As the peripheral vestibular organs are used as the gravitational sensor, it is reasonable to assume that all vestibular-mediated responses are caused by gravitational change, whether or not they are “stress responses.” Finally, the reply to Petrenko et al.’s last question1 was discussed in the introduction of our original article.6

Chihiro Iwata, MD, PhD

Hironobu Morita, MD, PhD

Department of Physiology

Gifu University Graduate School of Medicine

Gifu, Japan

zunzunmorita@gmail.com

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REFERENCES

1. Petrenko AB, Furutani K, Baba H. More solid evidence is required to validate a hypergravity-induced increase in sensitivity to propofol. Anesth Analg. 2014;119:1220
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9. Abe C, Tanaka K, Awazu C, Morita H. Impairment of vestibular-mediated cardiovascular response and motor coordination in rats born and reared under hypergravity. Am J Physiol Regul Integr Comp Physiol. 2008;295:R173–80
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