LETTERS TO THE EDITOR: Letters & Announcements
Thank you for the valuable comments regarding our article (1). We would like to reply to the comments concerning methodological issues.
As criticized, a moderate increase in mean arterial pressure (MAP) (20mmHg) induced with phenylephrine may cause an increase in intracranial pressure (ICP), even in patients without intracranial pathology. However, Strebel et al. have shown that phenylephrine does not directly affect intracranial hemodynamics in anesthetized patients, but rather that hemodynamic changes caused with phenylephrine reflect the effect of the background anesthetic agents on cerebral pressure autoregulation (2). Propofol, which is known to produce a “hyper-regulated” state of cerebral vessels (3), was used in our study as background anesthesia. Thus, in our study, the influence of phenylephrine on ICP seems to be minimal, supporting our methodology based on MAP, not cerebral perfusion pressure. On the other hand, we evaluated the influence of nitroglycerin in this study (1). Nitroglycerin is known to possess potent venous dilating properties, presumably resulting in an increased ICP. However, our previous study showed that, during nitroglycerin-induced hypotension, critical closing pressure, representing effective downstream pressure rather than ICP, was not significantly changed from baseline (4), which also may support our methodology based on MAP.
Essentially, the index of static rate of regulation (SRoR) only assesses the gradient of the autoregulatory plateau, because SRoR is calculated from the percentage change in cerebral vascular resistance per percentage change in MAP. Furthermore, because the changes induced in MAP are only moderate (20mmHg), SRoR cannot assess changes in the width of the plateau (5). Ideally, as criticized, cerebral pressure autoregulation should be assessed from the entire autoregulatory curve: the upper and lower thresholds, the slope, and the width of plateau. However, such assessment needs a large change in MAP, which seems ethically unacceptable, and to ensure that assessment at the upper threshold is not a clinical concern during induced hypotension. Indeed, SRoR cannot distinguish between the change of slope and the upward shift of lower threshold. However, in a broader sense, both scenarios mean impaired cerebral pressure autoregulation. Thus, our findings still remain clinically relevant.
Thank you again for your valuable comments.
Hiroshi Endoh, MD
1. Endoh H, Honda T, Ohashi S, et al. The influence of nicardipine-, nitroglycerin-, and prostaglandin E(1)-induced hypotension on cerebral pressure autoregulation in adult patients during propofol-fentanyl anesthesia. Anesth Analg 2002; 94: 169–73.
2. Strebel SP, Kindler C, Bissonnette B, et al. The impact of systemic vasoconstrictors on the cerebral circulation of anesthetized patients. Anesthesiology 1998; 89: 67–72.
3. Harrison JM, Girling KJ, Mahajan RP. Effects of target-controlled infusion of propofol on the transient hyperaemic response and carbon dioxide reactivity in the middle cerebral artery. Br J Anaesth 1999; 83: 839–44.
4. Endoh H, Honda T, Ohashi S, et al. The influence of nitroglycerin and prostaglandin E1 on dynamic cerebral autoregulation in adult patients during propofol and fentanyl anaesthesia. Anaesthesia 2001; 56: 947–52.
5. Panerai RB. Assessment of cerebral pressure autoregulation in humans—a review of measurement methods. Physiol Meas 1998; 19: 305–38.