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

Abstract

This report describes a canine model of obstructive sleep apnea (OSA) developed in our laboratory and the results of its preliminary short-term application. Healthy adult dogs were prepared with a tracheostomy and with implanted electroencephalographic and nuchal electromyographic recording electrodes. A silent occlusion valve was attached to the outer end of the endotracheal tube. The electroencephalogram and electromyogram were monitored continuously by a computer that determined sleep-wake state using software developed in our laboratory. At a predetermined time (e.g., 12 s) after each sleep onset, a signal was transmitted from the computer to the valve controller, resulting in airway occlusion. When the dog aroused from sleep, the occlusion was released. These events therefore mimic those that occur in human OSA. Successful operation of the model was confirmed during 5-day continuous trials in two dogs. During the trials, the dogs became increasingly somnolent both by behavioral observation and objective measurement. The frequency of occlusions increased, and measures of apnea severity, including apnea duration and end-apneic arterial oxygen saturation, worsened. We conclude that this experimental model of repeated airway occlusion during sleep provides a potentially powerful tool for investigating the sequelae of OSA.

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

“…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.…”

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

“…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.…”

“…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.…”

“…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.…”

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

“…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].…”