Cataplexy narcolepsy dogs3/2/2024 ![]() Spontaneous episodes of sleep and cataplexy occurred as the dogs rested undisturbed in the sling. No attempt was made to trigger cataplexy by presenting food, water, or other stimuli. The dogs could see only the wall of the laboratory, ~ 3 feet away. The experiments were performed between 08 h in a quiet room with a low level of natural light. The subjects were trained to stand quietly in a sling (Chatham Medical Arts) that supported most of their weight. In dog #142 respiration was recorded with a thoracic strain gauge. A cardiotachometer was employed to display heart interbeat intervals derived from the blood pressure pulse wave. Blood pressure was recorded with a Statham pressure transducer and was displayed on a polygraph along with EEG, EOG, and EMG. The catheter was flushed with heparinized saline every 12 h and a continuous flow of 4 cc/h of heparinized saline was maintained during recording sessions using a Sorenson valve. It was led subcutaneously to terminate on the dog’s head plug. A Swan-Ganz 5F catheter was inserted through the femoral artery and guided into the descending aorta. Stranded stainless steel wires were inserted into the dorsal neck musculature for recording the electromyogram (EMG). Screw electrodes were also placed in the orbit or frontal bone for recording the electro-oculogram (EOG). Using Halothane anesthesia, the dogs were implanted with screw electrodes over sensorimotor and posterior lateral cortex for recording electroencephalograms (EEGs). The dogs were Doberman and Labrador crossbreeds and were transported from the Stanford Narcoleptic Dog Colony to Los Angeles, where the studies were conducted. ![]() One male (#142) and two female (#139 and 141) puppies aged from 3 to 4 months served as subjects. In this study we have examined such changes in genetically narcoleptic dogs ( 1). Therefore, it is of considerable interest to determine if cardiovascular changes accompany cataplectic attacks. Sachs and Kaijser ( 7, 8) have reported that narcoleptic patients have reduced reactivity in the cardiovascular system. Scrima ( 6) has hypothesized that a similar activation of the baroreceptors may trigger cataplexy in human narcolepsy. This was followed by other signs of REM sleep. These workers found that in chronic encéphale isolé cats stimulation of the baroreceptors produced a loss of muscle tone resembling cataplexy. A series of studies by Puizzilout and colleagues ( 3– 5) provided some support for this hypothesis. Since such situations tend to increase heart rate, it has long been suspected that cardiovascular changes may be a triggering event in cataplexy. It is well known that cataplectic attacks in humans are often triggered by emotions such as laughter, anger, surprise, excitement, fear, and embarrassment and by sexual intercourse and athletic activity ( 1).
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