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Group I fibers from muscle spindles and Golgi tendon organs modulate motoneuron excitabilities to coordinate smooth movements. In this study, to elucidate the effects of group I fibers of the median nerve (MN) on the excitabilities of the brachioradialis (BR), we evaluated the changes in the firing probability of a BR motor unit after electrical conditioning stimulation (CS) to MN with a post-stimulus time-histogram technique in six healthy human subjects. We tested 171 motor units: in 72 of them CS to MN at the elbow with the intensity just below the threshold of alpha motor fibers (MT) produced a facilitatory effect (facilitation), while in 43 of them it produced inhibitory one (inhibition). The facilitation and inhibition were not produced by electrical stimulation of the skin overlaying MN. The central synaptic delays of the facilitation and inhibition were on average -0.13 and 0.13 msec, respectively, longer than those of the homonymous facilitation mediated by a monosynaptic path. The thresholds of the facilitation and inhibition were less than 0.7-0.8 and 0.7-0.9 times MT, respectively. CS to MN of hand muscles produced facilitatory effects and that of the pronator teres, palmaris longus, and flexor carpi radialis inhibitory effects. The facilitatory and inhibitory effects were compatible, for latency, with the facilitation and inhibition. These findings suggest that BR motoneurons receive monosynaptic facilitation and oligosynaptic inhibition from MN in humans. Group I fibers of the hand and forearm muscles should mediate the facilitation and inhibition, respectively, to coordinate movements of the hand, forearm, and elbow. median nerve; brachioradialis; monosynaptic facilitation; oligosynaptic inhibition; humans

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previously. A routine chest roentgenogram taken during an annual check-up showed a suspicious shadow. The patient was referred to another hospital for a complete medical evaluation. Left lung cancer was diagnosed. His electrocardiogram (ECG) showed a negative T wave in leads V5 and V6, indicating a pattern of old septal and inferior myocardial infarction with mild left ventricular (LV) hypertrophy. Furthermore, epicardial echocardiography (EE) revealed interventricular septal hypertrophy (ISH) and LV outflow hypertrophy, without deterioration of LV wall motion but with mild mitral regurgitation (MR). His cardiac index (CI), ejection fraction (EF), and EE-derived LV-Ao PG were 3.85 l·min Ϫ1 ·m Ϫ2 , 86%, and 72 mmHg, respectively. Finally, HOCM accompanied with MR were diagnosed. The patient was scheduled for right upper lobectomy in the same hospital without any specific medical treatment for HOCM prior to surgery.The patient was premedicated with intramuscular atropine (0.5 mg) and hydroxyzine (50 mg) prior to the induction of anesthesia. On arrival at the operating theater, his heart rate was 78 beats·min Ϫ1 , and his systolic and diastolic blood pressure showed 132/86 mmHg. After the placement of an epidural catheter via the thoracic segment T8/9, anesthesia was induced with bolus intravenous (iv) fentanyl (0.8 µg·kg Ϫ1 ) and propofol (1 mg·kg Ϫ1 ), as well as with continuous infusion of propofol (10 mg·kg Ϫ1 ·h Ϫ1 ), followed by vecuronium (0.03 mg·kg Ϫ1 ). Hypotension (60 mmHg) and profound bradycardia (35 beats·min Ϫ1 ) were observed after anesthesia was induced. Hypotension was controlled rapidly both by volume replacement and intermittent administration of bolus iv methoxamine (1 mg), whereas bradycardia persisted at less than 40 beats·min Ϫ1 . The anesthetists discontinued the induction of anesthesia and cancelled the operation. Ten minutes later, the heart rate of the patient gradually recovered to a level of 50 beats·min Ϫ1 . Oral atenolol (50 mg·day Ϫ1 ) and disopyramide (300 mg·day Ϫ1 ) were started immediately