{'fraction_non_alphanumeric': 0.02280633938925396, 'fraction_numerical': 0.0030923850019327404, 'mean_word_length': 5.176610978520286, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Effects of anesthetics on central vagal tone.

I read with interest the recent paper by Drs. Yamamura, Kimura, and Furukawa (1) on the effects of anesthetics on sympathetic and vagal tone. Although their aim is a commendable one, their conclusions deserve comment for methodological and analytical reasons. The authors’ conclusions regarding changes in the balance of the autonomic tone by anesthetics and the effects of these changes on the cardiovascular system are based on the assumption that the recorded compound action potentials are the neurophysiological correlate of the sympathetic and vagal drive to effector organs. I would like to point out, however, that this assumption does not apply to vagal tone. The cervical vagus contains several quite different categories of efferent nerve fibers depending on target organs as well as functions (2) and, according to our recent studies, there are definite differences in responses to some drugs among various categories of vagal fibers (e.g., ketamine consistently inhibited cardiac vagal efferents but activated or did not influence noncardiac vagal efferents (3); while fentanyl activated only cardiac vagal efferents, whereas other types of vagal efferents were inhibited or not affected (4)). I consider it, therefore, indispensable to identify target organs or fiber categories using single fiber preparations to study the effects of a drug on cervical vagal activity. One may ask, however, whether the compound action potentials represented the activity of any particular kind of vagal efferents. I would say it is unlikely that the activity of cardiac vagal efferents was recorded: based on a histological study in cats, only 8% of all efferent vagal fibers are cardiac (5) and, in accordance with this, the majority of efferent vagal fibers whose activity can be recorded in cats is not cardiac (6, unpublished results). Even if the activity of the cardiac vagus is accurately measured, the combined effects of sympathetic and vagal components on an effector organ may not be derived simply by adding and subtracting percent changes in their nerve activities because any given percent change in one component may not show the same effect (in the opposite direction) as the same percent change in the other component. For example, in the resting condition, the increase of heart rate by complete vagolysis is much larger than the decrease produced by complete sympathetic blockade (7). For these reasons, the authors’ claim that their results may explain some of the cardiovascular effects of anesthetics is not acceptable.