Reduced chemosensitivity to hypoxia and blunted perception of dyspnea may predispose patients to fatal asthma attacks.

1. An attempt has been made to test the hypothesis that, in the caudal part of nucleus tractus solitarii (NTS) where carotid sinus nerve (CSN) The carotid body is the major peripheral chemoreceptor for hypoxia in humans and other animals, and it plays an important role in augmenting ventilation during hypoxia (Martin-Body, Robson & Sinclair, 1986). In the rat, chemoreceptor afferents from the carotid body travel along the carotid sinus nerve (CSN) and terminate mainly in the caudal nucleus tractus solitarii (NTS; Lipski, McAllen & Spyer, 1977;Donoghue, Felder, Jordan & Spyer, 1984;Housley & Sinclair, 1988). Several neurotransmitters have been found in NTS (Cherniack, Prabhakar, Haxhiu & Runold, 1991). Among them, substance P (Prabhakar, Runold, Yamamoto, Lagercrantz & Euler, 1984;Henry & Sessle, 1985;Lindefors, Yamamoto, Pantaleo, Lagercrantz, Brodin & Ungerstedt, 1986), dopamine (Goiny, Lagercrantz, Srinivasan, Ungerstedt & Yamamoto, 1991) and L-glutamate (Glut; Kazemi, Chiang & Hoop, 1989) are considered to mediate chemoreceptor inputs to NTS. However, which neurotransmitter is released from the CSN in response to peripheral chemoreceptor activation and to what extent it is involved in regulation of respiration has not been determined.In the present study we used unanaesthetized, freely moving rats in which ventilation and in vivo release of Glut in the caudal NTS by microdialysis were measured during peripheral chemoreceptor stimulation by hypoxic hypoxia or doxapram (Dox) infusion in sham-operated and peripherally chemodenervated (carotid body denervated; CBD) rats. Moreover, the effects on ventilation of a local injection of Glut and during hypoxia, of pretreatment with the NMDA-type receptor antagonist MK-801 or the ionotropic receptor antagonist kynurenate into the caudal NTS (Housley & Sinclair, 1988) were investigated. MS 2462, pp. 55-65 55

No abstract

We studied the quality of life of obesity hypoventilation syndrome (OHS) by comparing it with age- and body mass index-matched patients without hypoventilation and age-matched obstructive sleep apnea (OSA) patients with body mass index (BMI) under 30, and the efficacy of nasal continuous positive airway pressure (CPAP) therapy for 3 to 6 months on the quality of life in these patients. Prospectively recruited patients from six sleep laboratories in Japan were administered assessments of the general health status by the Short-Form 36 Health Survey (SF-36) and subjective sleepiness by the Epworth Sleepiness Scale (ESS). Compared with matched healthy subjects, OHS and OSA patients not yet treated had worse results on the ESS scores and the SF-36 subscales for physical functioning, role limitations due to physical problems, general health perception, energy/vitality, role limitations due to emotional problems, and social functioning. The ESS scores of OHS patients were worse than those of the OSA groups including the age- and BMI-matched OSA patients. In the SF-36 subscales of OHS patients, only the subscale of social functioning showed worse results compared with that of BMI-matched OSA patients. After 3 to 6 months of treatment, ESS scores and these SF-36 subscales in all three patient groups improved to the normal level. These results suggested that the quality of life of OHS before nasal CPAP was significantly impaired and that nasal CPAP for OHS improved the quality of life associated with the improvement of daytime sleepiness to the level of the other OSA patients.

The purpose of this study was to examine our hypothesis that gamma-aminobutyric acid (GABA) in the nucleus tractus solitarii (NTS) may be related to the hypoxic ventilatory decline (HVD) and that chemoreceptor stimulation was essential to activate this mechanism. We used unanesthetized, freely moving rats in this study. An in vivo microdialysis technique was used to measure the extracellular GABA concentration ([GABA]o), and an in vivo microinjection technique was used to examine the effects of the GABA agonists and antagonists on the ventilation during hypoxia. The GABA agonists injected into the NTS attenuated the ventilation during hypoxia. By hypoxic exposure, [GABA]o was increased during the HVD. However, by carotid body denervation (CBD), this GABA increase was abolished. Although GABA antagonists microinjected into the NTS during the HVD phase significantly increased the depressed ventilation, this effect on the ventilation was abolished by CBD. These results suggest that the GABA in the NTS has a pivotal role in the HVD and that this mechanism is not activated without chemoreceptor stimulation.

Japanese male OSAHS patients had specific anatomical features in the bottom part of the mandible; however, obesity seemed to be a less significant risk factor. Investigators and clinicians must realize that ethnicity may modify the effects of obesity and abnormal craniofacial anatomy as risk factors for the pathogenesis of OSAHS.

Sudden death is common in patients with multiple system atrophy (MSA). In its early stages, the cerebellar presentation MSA-C can be indistinguishable from idiopathic late-onset cerebellar ataxia. We studied the hypoxic ventilatory response in MSA-C and idiopathic late-onset cerebellar ataxia patients. Six patients with idiopathic late-onset cerebellar ataxia that later evolved to MSA had impaired hypoxic ventilatory response when minimal autonomic failure was still present, whereas for patients with unimpaired hypoxic ventilatory response their diagnosis remained idiopathic late-onset cerebellar ataxia. The demonstration of impaired hypoxic ventilatory response appears to be a good marker enabling earlier diagnosis of MSA in patients presenting with idiopathic late-onset cerebellar ataxia.

We examined the effects of multiple repetitive airway obstruction (RAO) on arterial oxygen saturation (SaO2) and pulmonary and systemic arterial pressure in eight anesthetized spontaneously breathing dogs. SaO2 was monitored at the tongue with a pulse oximeter. RAO created by an electrical valve that was attached to a tracheal cannula was alternated with seven consecutive spontaneous breaths until the nadir SaO2 (nSaO2) became constant or decreased to less than 35%. Tracheal occlusion durations of 15, 30, 45 and 60 s were chosen arbitrarily. In each animal nSaO2 decreased with every trial number in an exponential fashion, and the rate of nSaO2 fall was greater for the longer occlusion duration. In each animal the increases in pulmonary arterial pressure (PAP) and systemic arterial pressure (SAP) were inversely related to the nSaO2 values, and the relationship between nSaO2 and PAP or SAP was identical for all occlusion durations. Moreover, when the animals breathed pure oxygen and SaO2 did not decrease, there were no significant increases in the PAP and SAP at similar levels of pleural pressure (Ppl). In another six dogs, the effects of RAO on PAP and SAP were compared with those of intermittent hypoxic exposure without apnea, which was achieved by the inhalation of hypoxic gas (4 to 6% O2, 5% CO2 in N2) instead of RAO, to examine the effects of interruption of ventilation. The relationships between nSaO2 and both pressures did not differ significantly from those during RAO.(ABSTRACT TRUNCATED AT 250 WORDS)