Anesthesiology:
doi: 10.1097/ALN.0000000000000167
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Brady, Ken M.D.; Rhee, Christopher J. M.D.; Hogue, Charles W. M.D.

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We thank Dr. Schwartz et al.1–3 for his contribution to the understanding of cerebral blood flow during cardiopulmonary bypass. We are pleased that our citation is in agreement with his own published results. We disagree, however, on the interpretation of our previous study on renal blood flow.4 Although it is true that cardiac output was not measured in the referenced article, our position that “the kidney can be hypoperfused at normal mean arterial pressure if cardiac output is compromised” is supported by the citation in question.5
In that study, piglets with a baseline mean arterial pressure between 50 and 60 mmHg underwent continuous slow hemorrhage over 3 to 4 h to demise. Cerebral blood flow was trended as a percentage of baseline using continuous laser-Doppler red cell flux monitoring with probes surgically placed against the cerebral cortex through a dural incision. Renal blood flow was similarly trended using laser-Doppler probes placed surgically against the renal capsule. Red cell flux monitoring was plotted against cerebral and renal perfusion pressure respectively as a definitive standard pressure autoregulation curve. The aim of the study was to test the accuracy of separately measured metrics of dynamic vascular reactivity derived from near-infrared spectroscopy: the hemoglobin volume index describing cerebral vascular reactivity and the renovascular reactivity index to describe vascular reactivity in the kidney. Although not the primary aim of that study, it was observed in some animals that renal blood flow fell during hemorrhagic shock before any change in arterial blood pressure occurred. Although, cardiac output was not directly monitored, these findings of reduced renal blood flow despite no change in blood pressure can be explained only by a reduced cardiac output. This was demonstrated by the example data shown in the figures of the article. Thus, these findings support our contention that renal blood flow is dependent on both blood flow (cardiac output or cardiopulmonary bypass) and blood pressure as we state in our editorial.
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Acknowledgments

Dr. Hogue is funded by the National Institutes of Health, Bethesda, Maryland (R01HL092259).
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Competing Interests

The authors declare no competing interests.
Ken Brady, M.D., Christopher J. Rhee, M.D., Charles W. Hogue, M.D.
The Johns Hopkins University School of Medicine, Baltimore, Maryland (C.W.H.). chogue2@jhmi.edu
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References

1. Schwartz AE, Kaplon RJ, Young WL, Sistino JJ, Kwiatkowski P, Michler RE. Cerebral blood flow during low-flow hypothermic cardiopulmonary bypass in baboons. ANESTHESIOLOGY. 1994;81:959–64

2. Schwartz AE, Minanov O, Stone JG, Adams DC, Sandhu AA, Pearson ME, Kwiatkowski P, Young WL, Michler RE. Phenylephrine increases cerebral blood flow during low-flow hypothermic cardiopulmonary bypass in baboons. ANESTHESIOLOGY. 1996;85:380–4

3. Schwartz AE, Sandhu AA, Kaplon RJ, Young WL, Jonassen AE, Adams DC, Edwards NM, Sistino JJ, Kwiatkowski P, Michler RE. Cerebral blood flow is determined by arterial pressure and not cardiopulmonary bypass flow rate. Ann Thorac Surg. 1995;60:165–9; discussion 169–70

4. Brady K, Hogue CW. Intraoperative hypotension and patient outcome: Does “one size fit all?”. ANESTHESIOLOGY. 2013;119:495–7

5. Rhee CJ, Kibler KK, Easley RB, Andropoulos DB, Czosnyka M, Smielewski P, Brady KM. Renovascular reactivity measured by near-infrared spectroscopy. J Appl Physiol. 2012;113:307–14

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