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Biomedical subjects

R A Parisi

Publications and source records attributed to R A Parisi.

6 recordsLinked to original sources
PubMed1992

Central respiratory carbon dioxide chemosensitivity does not decrease during sleep.

The ventilatory response to CO2 decreases during slow-wave sleep (SWS) and rapid-eye-movement (REM) sleep compared with awake levels. However, it is not known to what extent this can be attributed to decreased sensitivity of the CO2 chemoreflex. Mechanical factors during sleep may decrease ventilatory output, or PCO2 at the central chemoreceptor may not increase to the same degree as PaCO2, particularly during REM sleep when brain blood flow (BBF) is increased. In 10 goats, we measured the ventilatory (VI), diaphragmatic electromyogram (EMGdI), and BBF responses to CO2 rebreathing during each sleep-wake state. delta VI/delta PaCO2 decreased from wakefulness to SWS (p less than 0.05) and REM sleep (p less than 0.05). In contrast, delta EMGdI/delta PaCO2 was decreased only during REM sleep (p less than 0.05). Concurrently, delta BBF/delta PaCO2 increased during REM sleep (p less than 0.05) compared with the awake state or SWS. A significant reciprocal correlation existed between delta EMGdI/delta PaCO2 and delta BBF/delta PaCO2 across sleep states (r = -0.786). When EMGdI was related to directly measured cerebral venous PCO2 (n = 4), a single linear function (r = 0.894) was found, independent of sleep-wake state. Similar results were obtained during quasi-steady-state hypercapnia. We conclude that central CO2 chemosensitivity is intact during sleep.

Animals↗
PubMed1991

Responses of diaphragm and external oblique muscles to flow-resistive loads during sleep.

Although it is generally agreed that rapid respiratory compensation for externally applied inspiratory loads is impaired or absent during sleep, the individual components of the "load-compensating reflex" may not be inhibited by sleep to the same degree. We studied the effect of inspiratory flow-resistive loading (18 cm H2O/L/s) for two consecutive breaths on inspiratory (diaphragm) and expiratory (external oblique) muscle activity, and respiratory timing, in six awake and sleeping goats. During the first loaded breath in the awake state, peak integrated diaphragmatic electromyogram activity (EMGdi) increased 16.7 +/- 3.9% (p less than 0.01), peak integrated external oblique EMG activity (EMGeo) increased 21.0 +/- 7.5% (p less than 0.001), and electrical inspiratory time (Ti) increased 18.1 +/- 2.1% (p less than 0.01). In contrast, loading did not significantly change peak EMGdi or EMGeo on the first or second breaths in any sleep state. However, Ti was significantly increased during loading in all sleep states (p less than 0.01) to a similar degree seen during wakefulness. Loading did not significantly alter electrical expiratory time. No significant differences were noted between the first and second loaded breaths. We conclude that the reflex increases in peak EMG of both inspiratory and expiratory muscles in response to inspiratory flow-resistive loading during the awake state are absent during all stages of sleep; however, one aspect of load compensation, prolongation of Ti, is preserved during sleep and aids in maintaining tidal volume.

Analysis of Variance↗
PubMed1990

The role of vascular tone in the control of upper airway collapsibility.

Upper airway collapsibility may be influenced by both muscular and nonmuscular factors. Because mucosal blood volume (and therefore vascular tone) is an important determinant of nasal airway patency, vascular tone may be an important nonmuscular determinant of pharyngeal collapsibility. This hypothesis was tested in two experimental models. First, upper airway closing (CP) and opening (OP) pressures and static compliance were measured in nine anesthetized, sinoaortic-denervated, paralyzed cats with isolated upper airways. Vascular tone was decreased with either papaverine or sodium nitroprusside (NTP), and increased with phenylephrine (PE), whereas blood pressure and end-tidal CO2 were maintained constant. Vasodilation increased CP (control = -10.4 +/- 1.3, NTP = -7.3 +/- 1.2 cm H2O; p less than 0.05) and OP (control = -7.9 +/- 1.5, NTP = -3.3 +/- 1.8 cm H2O; p less than 0.05). In contrast, vasoconstriction tended to decrease CP (control = -10.7 +/- 1.5, PE = -11.7 +/- 1.4 cm H2O; p less than 0.09) and OP (control = -8.1 +/- 1.2, PE = -9.9 +/- 1.9 cm H2O; p less than 0.1). Thus, vasodilation increased and vasoconstriction tended to decrease upper airway collapsibility. Upper airway static compliance was unchanged during either drug infusion. In order to assess changes in pharyngeal cross-sectional area (CSA) that occurred during vasodilation, magnetic resonance imaging was utilized in seven cats. During vasodilation with NTP, pharyngeal CSA was reduced from 0.44 +/- 0.10 to 0.30 +/- 0.09 cm2 (p less than 0.05), and pharyngeal volume was reduced from 15.3 +/- 2.4 to 13.9 +/- 2.7 cm3 (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Airway Resistance↗
PubMed1989

Brain hypoxia preferentially stimulates genioglossal EMG responses to CO2.

Although the dominant respiratory response to hypoxia is stimulation of breathing via the peripheral chemoreflex, brain hypoxia may inhibit respiration. We studied the effects of two levels of brain hypoxia without carotid body stimulation, produced by inhalation of CO, on ventilatory (VI) and genioglossal (EMGgg) and diaphragmatic (EMGdi) responses to CO2 rebreathing in awake, unanesthetized goats. Neither delta VI/delta PCO2 nor VI at a PCO2 of 60 Torr was significantly different between the three conditions studied (0%, 25%, and 50% carboxyhemoglobin, HbCO). There were also no significant changes in delta EMGdi/delta PCO2 or EMGdi at a PCO2 of 60 Torr during progressive brain hypoxia. In contrast, delta EMGgg/delta PCO2 and EMGgg at a PCO2 of 60 Torr were significantly increased at 50% HbCO compared with either normoxia or 25% HbCO (P less than 0.05). The PCO2 threshold at which inspiratory EMGgg appeared was also decreased at 50% HbCO (45.6 +/- 2.6 Torr) compared with normoxia (55.0 +/- 1.4 Torr, P less than 0.02) or 25% HbCO (53.4 +/- 1.6 Torr, P less than 0.02). We conclude that moderate brain hypoxia (50% HbCO) in awake, unanesthetized animals results in disproportionate augmentation of EMGgg relative to EMGdi during CO2 rebreathing. This finding is most likely due to hypoxic cortical depression with consequent withdrawal of tonic inhibition of hypoglossal inspiratory activity.

Animals↗
PubMed1987

Obstructive sleep apnea following bilateral carotid body resection.

A patient who had undergone bilateral carotid body resection five years earlier for palliation of chronic airflow obstruction was found to have severe obstructive sleep apnea. He presented with hypercapnic respiratory failure, which improved after tracheostomy. A physiologic mechanism is proposed to explain this association. Previously reported studies of anesthetized animals suggest that loss of peripheral chemoreceptor activity could selectively decrease neural output to the genioglossus, the main protrusor muscle of the tongue, predisposing the upper airway to inspiratory occlusion.

Carotid Body↗