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Biomedical subjects

C Zwillich

Publications and source records attributed to C Zwillich.

11 recordsLinked to original sources
PubMed1998

Nasal congestion secondary to allergic rhinitis as a cause of sleep disturbance and daytime fatigue and the response to topical nasal corticosteroids.

BACKGROUND: Allergic rhinitis (AR) is a frequent disease affecting up to 20% of the population. AR causes a hypersensitivity reaction, which results in inflamed nasal mucosa and nasal congestion. Negative pressure generated during inspiration in the nasal airway secondary to nasal congestion may lead to nasal collapse, airway obstruction, and an increased number of sleep microarousals. Sleep disturbances and microarousals can detrimentally affect daytime energy levels, mood, and daytime function. It is unknown whether treatment directed to reduce congestion may reduce these microarousals, sleep problems, and, consequently, associated daytime fatigue. OBJECTIVE: We sought to determine whether reducing nasal congestion with nasal steroids will reduce sleep complaints and daytime sleepiness. METHOD: We enrolled 20 subjects in a double-blind, placebo-controlled study using Balaam's Design. Patients were treated with topical nasal corticosteroids or placebo. Subjective data were collected by use of a daily diary, which focused on nasal symptoms, sleep, and daytime sleepiness. RESULTS: The results demonstrated that nasal congestion and subjective sleep improved significantly in the topical corticosteroid-treated subjects but not in the placebo group. Sleepiness improved, but not significantly (p = 0.08). CONCLUSION: Often, people with perennial allergies may attribute their daytime fatigue to causes such as the side effects of medications, when in fact, the fatigue may be a result of nasal congestion and associated sleep fragmentation. Decreasing nasal congestion with nasal steroids may improve sleep, daytime fatigue, and the quality of life of patients with AR.

Administration, Topical↗
PubMed1995

Surges of muscle sympathetic nerve activity during obstructive apnea are linked to hypoxemia.

Obstructive sleep apnea (OSA) is associated with oscillations of arterial blood pressure (BP) that occur in phase with irregularities of respiration. To explore the role of the sympathetic nervous system in these responses, we studied muscle sympathetic nerve activity (MSNA; peroneal microneurography), an index of vasoconstrictor nerve traffic, and BP during awake regular breathing and during spontaneous apneas in patients with OSA. To determine the role of the arterial chemoreflex, we also examined the effects of 100% O2 (hyperoxia) on MSNA and BP. In awake regularly breathing patients with OSA (n = 12), resting MSNA was markedly higher than in an age-matched control population (n = 15) [41 +/- 23 (SD) vs. 24 +/- 17 bursts/min; P < 0.05] and was unchanged during hyperoxia (n = 9). Apneas during sleep (n = 8) were associated with surges in MSNA followed by transient rises in BP when breathing resumed. In contrast to room air apneas, hyperoxic apneas of similar duration were associated with attenuated MSNA responses (+82 +/- 84% vs. +5 +/- 25% compared with awake baseline; P < 0.05; n = 6), even though O2 did not affect sleep stage and the occurrence of arousal. Thus the BP oscillations that occur with apnea during sleep may in part be mediated by intermittent surges of sympathetic activity resulting in vasoconstriction. Because the MSNA responses to obstructive apnea are blunted during O2 administration, they appear to be linked to intermittent arterial hypoxemia and stimulation of arterial chemoreceptors.

Adult↗
PubMed1991

Norepinephrine clearance is increased during acute hypoxemia in humans.

Acute hypoxemia leads to activation of the sympathetic nervous system (SNS), yet adrenergic vasoconstriction does not occur and venous plasma norepinephrine (NE) fails to rise as expected. To examine whether this dissociation between SNS tone and plasma NE is due to altered metabolism of NE, we measured arterial NE kinetics ([3H]NE infusion technique) and sympathetic nervous outflow to muscle (peroneal microneurography) during 25-30 min of hypoxemia (spontaneous breathing, mean O2 saturation 74%) in six healthy young men. During hypoxemia, muscle sympathetic nervous activity (MSNA) rose significantly from 12.2 +/- 3.3 to 18.6 +/- 3.5 bursts/min, and the total amplitude increased from 123 +/- 36 to 255 +/- 50 mm/min. NE spillover, an index of NE release at the sympathetic nerve terminals, rose from 1.66 +/- 0.30 to 2.33 +/- 0.40 nmol.min-1.m-2 (P = 0.014). However, NE clearance increased also from 0.99 +/- 0.05 to 1.19 +/- 0.11 l.min-1.m-2 (P = 0.014), and arterial NE rose from 281 +/- 50 to 339 +/- 64 pg/ml (P = 0.023). Hypoxemia resulted in a significant rise in forearm blood flow and a decrease in forearm vascular resistance. The fact that skin blood flow and vascular resistance did not change implies that forearm vasodilation was localized to skeletal muscle. Our results suggest that during acute hypoxemia in humans the SNS is activated but the rise in plasma NE is attenuated because NE clearance is increased.

Adult↗
PubMed1982

Bradycardia during sleep apnea. Characteristics and mechanism.

To determine the characteristics of and mechanisms causing the bradycardia during sleep apnea (SA), both patients with SA and normals were studied. Evaluation of six consecutive SA patients demonstrated that bradycardia occurred during 95% of all apneas (central, obstructive, and mixed) and became marked with increased apnea length (P less than 0.01) and increased oxyhemoglobin desaturation (P less than 0.01). Heart rate slowed 9.5 beats per minute (bpm) during apneas of 10-19 s in duration, 11.4 bpm during 20-39s apneas, and 16.6 bpm during 40-59-s apneas. Sleep stage had no effect unexplained by apnea length or degree of desaturation. Oxygen administration to four SA patients completely prevented the bradycardia although apneas lengthened (P less than 0.05) in three. Sleeping normal subjects did not develop bradycardia during hypoxic hyperpnea but, instead, HR increased with hypoxia in all sleep stages, although the increase in HR was not as great as that which occurred while awake. Breath holding in awake normals did not result in bradycardia during hyperoxia (SaO2 = 99%), but was consistently (P less than 0.01) associated with heart rate slowing during room air breath-holds (-6 bpm) at SaO2 = 93%, with more striking slowing (-20 bpm) during hypoxic breath-holds (P less than 0.01) at SaO2 = 78%. Breath holding during hyperoxic hypercapnia had no significant effect on rate. Breath holding in awake SA subjects demonstrated similar findings. We conclude that the bradycardia of SA is a consistent feature of apnea and results from the combined effect of cessation of breathing plus hypoxemia.

Adult↗
PubMed1981

Lack of effects of beta sympathetic blockade on the metabolic and respiratory responses to carbohydrate feeding.

Increases in metabolic rate, heart rate and ventilation occur following carbohydrate feeding or during beta sympathetic stimulation. Furthermore, insulin secretion and hypokalemia are features common to both which raises the question as to whether these effects of carbohydrate depend upon an intact sympathetic nervous system. Accordingly, in the present study, we measured the effects of carbohydrate feeding (250 gram meal) before and after chronic beta sympathetic blockade in sex normal men. Before blockade metabolic rate (O2 consumption) rose (P less than 0.05) from a fasting mean of 248 +/- 19.7 (SEM) ML O2/min to 292 +/- 15.2 at 1 hr. 269 +/- 13.7 at 2, and 262 +/- 18.0 at 3 hr following the meal. During blockade (oral propranolol 80 mg p.o. Q 6 h for 3 days) the post-prandial increase in O2 consumption was also significant (P less than 0.05) and almost identical to that found before blockade. A similar pattern was found for ventilation, heart rate, insulin secretion and hypokalemia, where the significant postprandial changes were not altered by blockade. A transient increase in serum triiodothyronine from a mean of 92 +/- 8.4 microgram/ML to 109 +/- 9.4 occurred at 1 hr (P less than 0.05) only during blockade. No other changes in thyroid hormonal concentrations occurred as a result of the meal. We conclude that although similarities exist between beta sympathetic stimulation and carbohydrate feeding, the post-prandial effects studied do not depend on intact beta sympathetic receptors.

Dietary Carbohydrates↗
PubMed1980

Respiratory control in the parents of sudden infant death syndrome victims. Ventilatory control in SIDS parents.

To determine if a familial abnormality in the control of breathing might explain the reasons for the sudden infant death syndrome (SIDS), three groups of parents were studied. The first (N = 8 sets of parents) had one infant die of SIDS (one SIDS), whereas the second (N = 6) had a SIDS victim plus a second child with a "near-miss" occurrence (two SIDS). When compared to the third group (controls), these parents demonstrated no abnormality in the ventilatory response to hypoxia or hypercapnia. Similarly, they had normal respiratory frequency, tidal volume, inspiratory time, and arterial blood gas tensions. We conclude that a familial abnormality in breathing control measured during wakefulness is not the basis for SIDS.

Adult↗
PubMed1978

Hypoventilation in obstructive lung disease. The role of familial factors.

To determine the role of familial factors in the hypoventilation of chronic obstructive lung disease we measured chemical drives to breathe in normal offspring of two groups of patients with an equal degree of obstruction. One group of five patients had repeatedly normal arterial carbon dioxide tension (PaCO2), whereas PaCO2's were elevated in the other group of six. Two adult offspring of each patient were studied. Drives were measured as the ventilatory response to isocapnic hypoxia, and the slopes of the ventilation/PCO2 relation (the hypercapnic ventilatory response). The mean response to isocapnic hypoxia was lower (P less than 0.01) in offspring of patients with high PaCO2's than in the offspring of patients with normal levels (71 +/- 7.8 [S.E.M.] vs. 113 +/- 10.3); one offspring of each patient with high PaCO2 had a response below the range found in offspring of all patients with normal PaCO2. Lower hypercapnic ventilatory responses (P less than 0.05) were also found in the offspring of patients with high PaCO2. Familial factors in the control of breathing may be an important determinant of ventilation in chronic obstructive lung disease.

Adult↗
PubMed1976

Depressed ventilatory response in oculocraniosomatic neuromuscular disease.

Four patients with ptosis, external ophthalmoplegia, and ragged-red fibers on muscle biopsy were found to have decreased ventilatory responses to hypoxia and hypercapnia. Respiratory muscle weakness was not responsible for these findings since these responses were normal in muscle disease control patients. An altered metabolic state also can cause diminished ventilatory response, but overall oxygen consumption data in the ragged-red fiber patients were normal. The decreased ventilatory responses may be clinically significant because two of the ragged-red fiber patients had episodes suspicious of hypoventilation with poor response to hypoxia.

Adolescent↗