{'fraction_non_alphanumeric': 0.016321406151914627, 'fraction_numerical': 0.005649717514124294, 'mean_word_length': 5.811965811965812, '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}}
Cardiovascular control mechanisms during anesthesia.

Acute homeostatic control of arterial blood pressure is mediated in part by the baroreceptor reflex. Any disorders that produce change in arterial blood pressure from its set point are compensated by reflex responses which operate through alterations in heart rate, myocardial contractility, venous tone, and arterial resistance. These responses are mediated by sympathetic and vagal systems. Since autonomic reflexes are under the control of the central nervous system, it can be expected that anesthesia will alter baroreflex function, and indeed, Bristow et al. (1) showed 20 years ago that anesthesia depressed baroreflex control of heart rate in humans (1). This finding has important implications in the clinical interpretation of blood pressure and heart rate changes which are used daily by anesthesiologists to monitor surgical patients during anesthesia. The analysis of circulatory parameters to assess, for instance, the adequacy of blood replacement to compensate blood loss during surgical procedures, must take into account that homeostatic regulation of arterial blood pressure may be altered by the anesthetic drugs used. In the 1970s, Vatner and Braunwald (2) emphasized the consequences of the disruptive effect of anesthesia on sympathetic contribution to cardiovascular control mechanisms and particularly the difficulties encountered in the interpretation of experiments designed in anesthetized animals to investigate cardiac physiology or cardiac pharmacology. In addition, they showed that impairment of baroreflex