Heart rate variability (HRV) was studied in 19 patients with severe obstructive sleep apnea syndrome (OSAS), 17 with mild OSAS and 19 control subjects. A very low frequency (VLF) component during sleep in frequency-domain analysis was significantly higher in patients with severe OSAS, but not in patients with mild OSAS, compared with controls. It suggests that VLF is useful for the screening of severe OSAS, but not for mild OSAS. In addition, a low frequency (LF) component during sleep was also elevated in patients with severe OSAS. Further investigation is needed to understand the underlying causes of the LF elevation.

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Two patients with idiopathic central sleep apnea (ICSA), which is an uncommon condition, were recently encountered. This study examines the polysomnographic features of ICSA. The characteristic findings of ICSA are summarized as follows: (i) central apneas and hypopneas are progressively less frequent as sleep state deepens from stage 1 to stage 2 to stage 3 + 4 to stage REM (rapid eye movement); (ii) desaturation related to apneas and hypopneas is mild; and (iii) periodic breathing is commonly observed. However, the two patients demonstrated apparently different findings. It is suggested that the mechanisms underlying apnea and hypopnea in ICSA are heterogeneous.

Heart rate variability was studied in 11 sleep apnea syndrome (SAS) patients. Two types of control groups were chosen; one group comprises patients having sleep disturbances other than SAS (SAS (–)) and the other group comprises patients who sleep normally (S(–)). Very low frequency (VLF) in frequency‐domain analysis was significantly higher in the SAS group than in the control groups. Two parameters in time‐domain analysis were significantly higher in the SAS group than in the S(–) group, but were not significantly higher in the SAS (–) group. The frequency component of VLF might serve as a screening method for SAS. Time‐domain analyses were more ambiguous.

We previously reported that the injection of neostigmine, an acetylcholine esterase inhibitor, into the dorsal hippocampus produced hepatic venous plasma hyperglycemia associated with an increase of epinephrine and glucagon in anesthetized fed rats. To evaluate the relative contribution of these glucoregulatory hormones and the nervous system to the net hyperglycemic response, we unilaterally injected neostigmine (5 × 10^–8 mol) into the dorsal hippocampus in the following groups of rats: intact rats with bilateral adrenalectomy to eliminate the action of epinephrine, and rats receiving a constant infusion of somatostatin and insulin to prevent the glucagon response and to maintain the basal insulin level. Hepatic venous plasma levels of glucose, immunoreactive glucagon, immunoreactive insulin, epinephrine, and norepinephrine were determined. The area under the glucose curve during the 120-min period following the injection of neostigmine was compared between groups. The areas under the glucose curve for rats receiving somatostatin and insulin, adrenalectomy rats, and adrenalectomy rats receiving somatostatin and insulin were, respectively, 82, 31, and 61% of that for intact rats. The fashion of hippocampal stimulated hyperglycemia with neostigmine was similar to that after injection of neostigmine into the third cerebral ventricle. Therefore, we investigated hyperglycemia in rats with lesions of ventromedial hypothalamus and found that the response to hippocampal neostigmine was significantly inhibited by the hypothalamic lesion. These findings suggest that the glucoregulatory hippocampal activity evoked by neostigmine may be transmitted to peripheral organs via the ventromedial hypothalamus.