Education  |   July 2018
Baseline Cerebral Metabolic Rate Is a Critical Determinant of the Cerebral Vasodilating Potency of Volatile Anesthetic Agents
Author Notes
  • From the Department of Anesthesiology, University of California, San Diego, California; and the Anesthesia Service, the Veterans Affairs San Diego Healthcare System, San Diego, California.
  • Submitted for publication March 10, 2018. Accepted for publication March 15, 2018.
    Submitted for publication March 10, 2018. Accepted for publication March 15, 2018.×
  • Address correspondence to Dr. Drummond: Veterans Affairs Medical Center, 3350 La Jolla Village Drive, Anesthesia Service – 125, San Diego, California 92161. jdrummond@ucsd.edu. Information on purchasing reprints may be found at www.anesthesiology.org or on the masthead page at the beginning of this issue. Anesthesiology’s articles are made freely accessible to all readers, for personal use only, 6 months from the cover date of the issue.
Article Information
Education / Central and Peripheral Nervous Systems / Endocrine and Metabolic Systems / Pharmacology
Education   |   July 2018
Baseline Cerebral Metabolic Rate Is a Critical Determinant of the Cerebral Vasodilating Potency of Volatile Anesthetic Agents
Anesthesiology 7 2018, Vol.129, 187-189. doi:10.1097/ALN.0000000000002219
Anesthesiology 7 2018, Vol.129, 187-189. doi:10.1097/ALN.0000000000002219
Abstract

A Comparison of the Direct Cerebral Vasodilating Potencies of Halothane and Isoflurane in the New Zealand White Rabbit. By Drummond JC, Todd MM, Scheller MS, and Shapiro HM. Anesthesiology 1986; 65:462–7. Reprinted with permission.

Halothane is commonly viewed as a more potent cerebral vasodilator than isoflurane. It was speculated that the lesser vasodilation caused by isoflurane might be the result of the greater reduction in cerebral metabolic rate (CMR) that it causes, and that the relative vasodilating potencies of halothane and isoflurane would be similar if the two agents were administered in a situation that precluded volatile-agent–induced depression of CMR. To test this hypothesis, cerebral blood flow (CBF) and the cerebral metabolic rate for oxygen (CMRO2) were measured in two groups of rabbits before and after the administration of 0.75 MAC halothane or isoflurane. One group received a background anesthetic of morphine and N2O, which resulted in an initial CMRO2 of 3.21 ± 0.17 (SEM) ml · 100 g–1 · min–1; second group received a background anesthetic of high-dose pentobarbital, which resulted in an initial CMRO2 of 1.76 ± 0.16 ml · 100 g–1 · min–1. In rabbits receiving a background of morphine sulfate/N2O, halothane resulted in a significantly greater CBF (65 ± 10 ml · 100 g–1 · min–1) than did isoflurane (40 ± 5 ml · 100 g–1 · min–1). Both agents caused a reduction in CMRO2, but CMRO2 was significantly less during isoflurane administration. By contrast, with a background of pentobarbital anesthesia, CBF increased by significant and similar amounts with both halothane and isoflurane. With halothane, CBF increased from 22 ± 2 ml · 100 g–1 · min–1 in the control stage to 39 ± 3, and with isoflurane from 24 ± to 38 ± 2 ml · 100 g–1 · min–1. CMRO2 was not depressed further by either halothane or isoflurane. These results suggest that the relative effects of halothane and isoflurane on CBF are dependent on the CMR present prior to their administration. When the preexistent CMR is not markedly depressed, isoflurane decreases CMR and causes less cerebral vasodilation than does halothane. When initial CMR is depressed, halothane and isoflurane have similar vasodilating potencies.