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Endotoxin Augments Cerebral Hyperemic Response to Halothane by Inducing Nitric Oxide Synthase

Nagase, Kiyoshi MD; Ando-Nagase, Kaori MSc

doi: 10.1097/00000539-200104000-00060
Letters To The Editor: Letters & Announcements

Department of Anesthesiology & Critical Care Medicine, Gifu University School of Medicine, Gifu City, Japan

School of Human Life & Environment, Nara Women’s University, Nara City, Japan

To the Editor:

We would like to pose a few questions on the interesting report by Okamoto et al. (1). First, they used 0.6% halothane as a basal anesthetic throughout the study period, whereas Sjakstae et al. (2) reported that 1.5% halothane increased nitric oxide (NO) content time-dependently in the rat cortex about six times 60 min after exposure. Okamoto et al. (1) concluded that NO produced by inducible NO synthase is relevant to augment halothane-mediated cerebral hyperemia. However, the effect of the NO produced by basal anesthesia was not discussed and they did not measure the content of NO in the brain. Second, the degree of increase in regional cerebral blood flow (rCBF) by halothane was elevated according to the level of rCBF at 4 h after endotoxin treatment. The result may be influenced by baseline elevation because the baseline rCBF affects the degree of response to hyperemia. Brian (3) concluded that inhaled anesthetics enhanced the response of cerebral circulation to hypocapnia because it increases normocapnic CBF.

Kiyoshi Nagase, MD

Kaori Ando-Nagase, MSc

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1. Okamoto H, Roman RJ, Kampine JP, et al. Endotoxin augments cerebral hyperemic response to halothane by inducing nitric oxide synthase and cyclooxygenase. Anesth Analg 2000; 91: 896–903.
2. Sjakste N, Baumane L, Meirena D, et al. Drastic increase in nitric oxide content in rat brain under halothane anesthesia revealed by EPR method. Biochem Pharmacology 1999; 58: 1955–9.
3. Brian JE Jr. Carbon dioxide and the cerebral circulation. Anesthesiology 1998; 88: 1365–86.
© 2001 International Anesthesia Research Society