Rebuttal from Ryan L. Hoiland and Philip N. Ainslie

Brothers & Zhang (2016) provide a relevant CrossTalk discussion on the measurement of middle cerebral artery (MCA) diameter during alterations in arterial blood pressure (ABP) and gases. While in support of a constant MCA diameter, they nonetheless judiciously acknowledge that several previous studies indicating a constant MCA diameter, specifically during alterations in arterial blood gases, are confounded by subject co‐morbidities, anesthesia, and/or suffer from poor resolution (1.5 T MRI) (Schreiber et al. 2000; Serrador et al. 2000). They speculate that elevations in ABP and the associated autoregulatory response concurrent to hypercapnia may explain the increases in diameter reported by the more recent and higher resolution MRI studies (3 and 7 T) assessing MCA diameter (Verbree et al. 2014; Coverdale et al. 2014). The rationale for this hypothesis is unclear as the available data in humans indicate an increase in ABP will increase cerebral vascular resistance in large cerebral arteries (Liu et al. 2013; Warnert et al. 2016). Collectively, these findings indicate that any engagement of autoregulatory mechanisms would more likely lead to an underestimation of vasodilatation, not overestimation.

In their discussion of arterial blood gases, Brothers & Zhang fail to discuss the potential for hypoxia‐induced vasomotion of the MCA. Previous study has indicated MCA dilatation in hypoxia (Wilson et al. 2011), in addition to more recent evidence that continues to highlight a tendency for increased MCA diameter (Sagoo et al. 2016). Overall there is a strong body of data supporting hypoxia‐induced dilatation at the level of the MCA.

It is noted by Brothers & Zhang that the study by Serrador et al. (2000) provides insight into MCA diameter during mild hypotension; however, a statistical change in BP did not occur during their simulated orthostasis trial (see Table 2 in Serrador et al. 2000). This renders the study by Giller et al. (1993) the only one to date that has directly imaged MCA diameter during alterations in ABP. Thus, while it remains difficult to definitively conclude the effect of ABP on MCA diameter, a large body of evidence now supports the notion that MCA diameter does change during alterations in arterial blood gases. Although we acknowledge that much utility still exists in the employment of transcranial Doppler ultrasound, we encourage the complimentary addition of multi‐modal imaging to provide important new insight into cerebrovascular regulation in humans.

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The authors declare no conflict of interest, financial or otherwise.

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Comments.

Last words by Brothers and Zhang.