Aerospace medicine and biology: A continuing bibliography with indexes, supplement 162, January 1977

This bibliography lists 189 reports, articles, and other documents introduced into the NASA scientific and technical information system in December 1976

Circadian Modulation Of Breathing Stability And Respiratory Plasticity

Purpose: Our project was designed to determine the effect of time of day on multiple mechanisms influencing breathing stability and respiratory plasticity. We investigated if the number and duration of breathing events coupled to upper airway collapsibility, as well as the carbon dioxide reserve, chemoreflex sensitivity and arousal threshold during non-rapid eye movement (NREM) sleep were affected by the time of day. In addition, we examined if mild intermittent hypoxia (IH) initiates long-term facilitation of upper airway muscle activity leading to a reduction in the therapeutic continuous positive airway pressure required to eliminate breathing events. Methods: Male participants with obstructive sleep apnea completed a constant routine protocol that consisted of sleep sessions in the evening (10 PM to 1 AM), morning (6 AM to 9 AM), and afternoon (2 PM to 5 PM). On one occasion the number and duration of breathing events was ascertained for each sleep session. For breathing events detected during these sessions the rate of change of respiratory effort, maximum respiratory effort immediately prior to termination of an event, and the maximum tidal volume and the minimum partial pressure of end-tidal carbon dioxide (PETCO2) immediately following an event were measured Participants then completed the same protocol on two additional occasions, where the critical closing pressure that demarcated upper airway collapsibility was determined on one, and baseline levels of carbon dioxide PET(CO2) and minute ventilation, as well as the PET(CO2) that demarcated the apneic threshold and hypocapnic ventilatory response were measured on the other (the order of these 2 visits was randomized). In the second aim of the study, male participants with obstructive sleep apnea were treated with twelve 2-minute episodes of hypoxia (PETO2 ≈ 50 mmHg) separated by 2-minute intervals of normoxia in the presence of PETCO2 that was sustained 3 mmHg above baseline. During recovery from the last episode the positive airway pressure was reduced in a step-wise fashion until flow limitation was evident. The participants also completed a sham protocol under normocapnic conditions, which mimicked the timeframe of the IH protocol. Results: The duration of breathing events was consistently greater in the morning compared with the evening and afternoon during N1 and N2, while an increase in event frequency was evident during N1. The critical closing pressure was increased in the morning (2.68 ± 0.98 cmH2O) compared with the evening (1.29 ± 0.91 cmH2O; P ≤ 0.02) and afternoon (1.25 ± 0.79; P ≤ 0.01). The increase in the critical closing pressure was correlated to the decrease in the baseline partial pressure of carbon dioxide in the morning compared with the afternoon and evening (r = −0.73, P ≤ 0.005).. The nadir of core body temperature during sleep occurred in the morning and was accompanied by reductions in minute ventilation and PETCO2 compared with the evening and afternoon (minute ventilation: 5.3 ± 0.3 vs. 6.2 ± 0.2 vs. 6.1 ± 0.2 l/min, P lt; 0.02; PET(CO2): 39.7 ± 0.4 vs. 41.4 ± 0.6 vs. 40.4 ± 0.6 Torr, P \u3c 0.02). The carbon dioxide reserve was reduced, and the hypocapnic ventilatory response increased in the morning compared with the evening and afternoon (carbon dioxide reserve: 2.1 ± 0.3 vs. 3.6 ± 0.5 vs. 3.5 ± 0.3 Torr, P \u3c 0.002; hypocapnic ventilatory response: 2.3 ± 0.3 vs. 1.6 ± 0.2 vs. 1.8 ± 0.2 l·min(-1)·mmHg(-1), P \u3c 0.001). The rate of change of respiratory effort was similar in N2 compared to N1 but the maximum respiratory effort immediately prior to event termination was greater (-10.7 ± 1.2 vs. -9.6 ± 1.0 cmH2O/s, P \u3c 0.05). Likewise, tidal volume was increased (1169 ± 105 vs. 1082 ± 100 ml, P \u3c 0.05) and PETCO2 was decreased (37.0 ± 0.8 vs. 37.7 ± 0.8 mmHg P \u3c 0.05) following events in N2 compared to N1. A similar tidal volume and PETCO2 response was evident following events in the morning compared to the evening independent of sleep stage. After exposure to IH the therapeutic pressure was significantly reduced (Δ CPAP = - 4.95 ± 0.5 cmH2O, p \u3c 0.001) without evidence of flow limitation (P \u3e 0.2) or increases in upper airway resistance (P \u3e 0.4). In contrast, a similar decrease in pressure was accompanied by significant flow limitation (P \u3c 0.003) and an increase in upper airway resistance (P \u3c 0.01) following completion of the sham protocol. Conclusion: Our findings indicate that time of day affects the duration and frequency of events, coupled with alterations in upper airway collapsibility and chemoreflex properties during sleep, which may contribute to increases in breathing instability in the morning compared with other periods throughout the day/night cycle in individuals with sleep apnea. We propose that increases in airway collapsibility in the morning may be linked to an endogenous modulation of baseline carbon dioxide levels and chemoreflex sensitivity, which are independent of the consequences of sleep apnea. We also conclude that alterations in the arousal threshold, reflected by an increase in respiratory effort at event termination, coupled to increases in tidal volume and reductions in PETCO2 contribute to modifications in event duration and frequency associated with variations in sleep state or time of night. In addition, Exposure to IH decreases the therapeutic pressure required to eliminate apneic events which could improve treatment compliance. This possibility coupled with the direct beneficial effects of IH on co-morbidities linked to sleep apnea suggests that IH may have a multipronged therapeutic effect on sleep apnea

Aerospace Medicine and Biology: A continuing bibliography with indexes (supplement 133)

This special bibliography lists 276 reports, articles, and other documents introduced into the NASA Scientific and Technical Information System in September 1974

Aerospace Medicine and Biology: A continuing bibliography with indexes (supplement 255)

This bibliography lists 278 reports, articles and other documents introduced into the NASA scientific and technical information system in January 1984

A reversal of fate : unravelling the role of central 5-HT in cardiorespiratory control in neonatal and adult rodents

We seek to address the extent to which a specific loss of 5-hydroxytryptamine (5-HT) affects the control of respiration, arterial blood pressure (ABP) and heart rate (HR) across vigilance-states based on existing evidence suggesting that 5-HT defects increase the risk for Sudden Infant Death Syndrome (SIDS) and neurogenic hypertension. SIDS is the leading cause of infant mortality between 1 month and 1 year of age, occurs during sleep, and up to 70% of all SIDS cases have at least one 5-HT system abnormality. Neonatal rodents lacking central 5-HT exhibit severe apneas, and a reduced ABP and HR. Central 5-HT has been implicated in the etiology of neurogenic hypertension, presumably due to projections of 5-HT neurons within the midline raphe to vagal and presympathetic regions of the brain. However, data from studies examining the specific role of central 5-HT function is conflicting or inconclusive. Neurogenic hypertension accounts for more than 90% of all hypertensive cases and the normal fall in ABP that occurs during non-rapid eye movement sleep is absent in some patients with hypertension. Understanding the mechanisms associated with the development of hypertension is critical not only to lower blood pressure, but to lower its associated cardiovascular events. The purpose of this dissertation is to examine the role of central 5-HT in the control of ABP during sleep and reveal, mechanistically, the physiological role of 5-HT in the autonomic control of ABP in neonatal and adult rodents. The overarching hypothesis for this dissertation is that central 5-HT is required for the maintenance of ABP and autonomic tone at rest in both neonatal and adult rodents.Includes bibliographical reference

Aerospace medicine and biology: A continuing bibliography with indexes (supplement 333)

This bibliography lists 122 reports, articles and other documents introduced into the NASA Scientific and Technical Information System during January, 1990. Subject coverage includes: aerospace medicine and psychology, life support systems and controlled environments, safety equipment, exobiology and extraterrestrial life, and flight crew behavior and performance

Aerospace Medicine and Biology: A continuing bibliography with indexes (supplement 141)

This special bibliography lists 267 reports, articles, and other documents introduced into the NASA scientific and technical information system in April 1975

Modeling Post Stroke Respiratory Dysfunction, Apneas and Cognitive Decline

Modeling Post Stroke Respiratory Dysfunction, Apneas and Cognitive Decline Anthony Patrizz, B.A. Advisory Professor: Louise McCullough M.D., Ph.D. Stroke is a major cause of mortality and the leading cause of long-term disability in the US. More than 60% of individuals suffering a first time stroke develop respiratory dysfunction, prolonging recovery and increasing mortality. Post-stroke cognitive decline is a major contributor to disability and nursing home placement, therefore the cognitive consequences of Stroke Induced Respiratory Dysfunction (SIRD) need to be explored if we hope to enhance functional recovery. The first step towards treatment of the negative consequences of SIRD is the development of appropriate animal models that will allow us to explore the pathophysiology of SIRD and provide the opportunity to test potential pharmacological agents. We developed and characterized an animal model of stroke induced respiratory dysfunction recapitulating the respiratory phenotype witnessed in the clinical population, characterized by incidences of apnea and hypoventilation. Interestingly, mice with high incidence of apneas display signs of progressive cognitive decline compared to those with low/no incidence of apneas. Histological analysis of vital brainstem respiratory control sites unveiled reactive astrocytosis, an important cell type in the neurovascular unit and an essential component of chemoreception. Respiratory dysfunction and brainstem astrocytosis was reproduced in mice that underwent intracerebroventricular injections of TGF-b. Suggesting the TGF-b signaling pathway contributes to the onset of astrogliosis and respiratory dysfunction. Our data suggests that stroke disrupts basal breathing rather than increasing chemoreceptor gain. Therefore, we predict treatments designed to stimulate breathing independent of chemoreceptor gain will improve respiratory instability, behavior, cognition and mortality. Systemic application of acetazolamide eliminated apneas while preventing further cognitive decline. This work not only developed a model of stroke induced respiratory dysfunction that recapitulates the respiratory phenotype witnessed in the clinical population, but also providing translational relevance to the field of stroke, aging, and cognitive decline. Successful treatment of SIRD may lead to significant improvements in post-stroke recovery and cognition