Canine model of obstructive sleep apnea: model description and preliminary application

Kimoff, R. John; Makino, Hideo; Horner, Richard L.; Kozar, L. F.; Lue, Franklin A.; Slutsky, A. S.; Phillipson, Eliot A.

doi:10.1152/jappl.1994.76.4.1810

Cited by 72 publications

(40 citation statements)

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“…The studies by PHILIPSON and co-workers [36,37] using a dog model of OSA suggest that recurrent intermittent hypoxia is the more likely mechanism for the sustained hypertension of OSA, rather than sleep fragmentation [38], which is the more likely explanation for the transient BP rises seen following each apnoea. Studies in rats [39] also suggest that hypoxia may be the causal link, although BP elevation is seen in only some rat strains after exposure to chronic episodic hypoxia for 35 days.…”

Section: Discussionmentioning

confidence: 99%

Continuous positive airway pressure does not reduce blood pressure in nonsleepy hypertensive OSA patients

Robinson

Smith²,

Langford³

et al. 2006

European Respiratory Journal

279

171

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Obstructive sleep apnoea (OSA) is associated with high cardiovascular morbidity and mortality. Several randomised controlled trials have shown that continuous positive airway pressure (CPAP) treatment of OSA reduces blood pressure (BP). This randomised, sham-placebo controlled crossover trial assesses whether CPAP produces a similar clinically significant fall in BP in hypertensive OSA patients, but without hypersomnolence.Thirty-five, nonsleepy, hypertensive patients with OSA were treated with CPAP for 1 month, randomised first to either therapeutic or sham-placebo (subtherapeutic CPAP, about 1 cmH 2 O pressure). The second months' alternative treatment followed a 2-week washout period. BP was measured over 24 h, before and at the end of the two treatment periods: mean 24-h BP was the primary outcome variable.There was no overall significant difference in mean 24-h BP: the change in mean 24-h BP on therapeutic CPAP was -2.1 mmHg (SD 8.1), and -1.1 mmHg (SD 8.1) on subtherapeutic CPAP, with a difference of 0.7 mmHg (95% confidence interval (CI) +2.9--4.4). There was a small significant fall in Epworth Sleepiness Score, therapeutic (-1.4) versus sham (-0.3), and difference -1.2 (95% CI -2.0--0.4), but no change in objective sleepiness.In nonhypersomnolent hypertensive patients with obstructive sleep apnoea, there is no significant fall in mean 24-h blood pressure with continuous positive airway pressure, in contrast to the fall seen in hypersomnolent patients with obstructive sleep apnoea.

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Section: Discussionmentioning

confidence: 99%

Continuous positive airway pressure does not reduce blood pressure in nonsleepy hypertensive OSA patients

Robinson

Smith²,

Langford³

et al. 2006

European Respiratory Journal

279

171

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“…OSA was produced in four dogs (three female, one male, 23-31 kg) using a modification of a model developed in our laboratory (7). All surgical and experimental procedures were approved by the Animal Care Committee of the University of Toronto.…”

Section: Methodsmentioning

confidence: 99%

“…The dogs were trained to sleep in the laboratory and then underwent two surgical procedures at least 2 mo before initiation of studies. The first was to create a permanent side-hole tracheostomy, and the second was to implant a three-channel telemetry unit (TLM11M3D70-CCP; Data Sciences, St. Paul, MN) for monitoring of arterial BP, the electroencephalogram (EEG) from implanted skull electrodes, and nuchal electromyogram (EMG; 7,8). Surgery was performed under general anesthesia and aseptic conditions.…”

Section: Methodsmentioning

confidence: 99%

“…The EEG and EMG signals were converted to analogue signals, amplified, filtered, and relayed to a microcomputer through an analogue-to-digital board. The computer produced a judgment of sleep-wake state every 6 s, based on the frequencies in the EEG signal and the amplitude of the averaged EMG signal (7). Whenever a period of sleep of predetermined length (generally 18 s) was identified by the computer, it generated a radio signal that was detected by a receiver controller unit housed in a jacket worn by the dog.…”

Section: Methodsmentioning

confidence: 99%

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Obstructive sleep apnea as a cause of systemic hypertension. Evidence from a canine model.

Brooks¹,

Horner²,

Kozar³

et al. 1997

J. Clin. Invest.

608

310

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Several epidemiological studies have identified obstructive sleep apnea (OSA) as a risk factor for systemic hypertension, but a direct etiologic link between the two disorders has not been established definitively. Furthermore, the specific physiological mechanisms underlying the association between OSA and systemic hypertension have not been identified. The purpose of this study was to systematically examine the effects of OSA on daytime and nighttime blood pressure (BP). We induced OSA in four dogs by intermittent airway occlusion during nocturnal sleep. Daytime and nighttime BP were measured before, during, and after a 1-3-mo long period of OSA. OSA resulted in acute transient increases in nighttime BP to a maximum of 13.0 Ϯ 2.0 mmHg (mean Ϯ SEM), and eventually produced sustained daytime hypertension to a maximum of 15.7 Ϯ 4.3 mmHg. In a subsequent protocol, recurrent arousal from sleep without airway occlusion did not result in daytime hypertension. The demonstration that OSA can lead to the development of sustained hypertension has considerable importance, given the high prevalence of both disorders in the population. ( J. Clin. Invest. 1997. 99:106-109.)

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“…One major advance, although the experiments were difficult to perform on a long-term basis, was the canine model, in which upper airway obstruction and sleep fragmentation were compared in terms of the acute and chronic cardiovascular consequences [46][47][48]. However, much more research in the field of hypoxia has been performed using wild-type or genetically modified rodents [49].…”

Section: Cellular and Molecular Consequences Of Ihmentioning

confidence: 99%

Intermittent hypoxia and sleep-disordered breathing: current concepts and perspectives

Lévy¹,

Pépin²,

Arnaud³

et al. 2008

European Respiratory Journal

168

111

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There are three major types of sleep-disordered breathing (SDB) with respect to prevalence and health consequences, i.e. obstructive sleep apnoea syndrome (OSAS), CheyneStokes respiration and central sleep apnoea (CSR-CSA) in chronic heart failure, and obesity hypoventilation syndrome (OHS). In all three conditions, hypoxia appears to affect body functioning in different ways. Most of the molecular and cellular mechanisms that occur in response to SDB-related hypoxia remain unknown.In OSAS, an inflammatory cascade mainly dependent upon intermittent hypoxia has been described. There is a strong interaction between haemodynamic and inflammatory changes in promoting vascular remodelling. Moreover, during OSAS, most organ, tissue or functional impairment is related to the severity of nocturnal hypoxia. CSR-CSA occurring during heart failure is primarily a consequence of cardiac impairment. CSR-CSA has deleterious consequences for cardiac prognosis and mortality since it favours sympathetic activation, ventricular ectopy and atrial fibrillation. Although correction of CSR-CSA seems to be critical, there is a need to establish therapy guidelines in large randomised controlled trials.Finally, OHS is a growing health concern, owing to the worldwide obesity epidemic and OHS morbidities. The pathophysiology of OHS remains largely unknown. However, resistance to leptin, obesity and severe nocturnal hypoxia lead to insulin resistance and endothelial dysfunction. In addition, several adipokines may be triggered by hypoxia and explain, at least in part, OHS morbidity and mortality.Overall, chronic intermittent hypoxia appears to have specific genomic effects that differ notably from continuous hypoxia. Further research is required to fully elucidate the molecular and cellular mechanisms.

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Canine model of obstructive sleep apnea: model description and preliminary application

Cited by 72 publications

References 0 publications

Continuous positive airway pressure does not reduce blood pressure in nonsleepy hypertensive OSA patients

Continuous positive airway pressure does not reduce blood pressure in nonsleepy hypertensive OSA patients

Obstructive sleep apnea as a cause of systemic hypertension. Evidence from a canine model.

Intermittent hypoxia and sleep-disordered breathing: current concepts and perspectives

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