Abstract
Sella, Hiestand and others 1 , 2 , 3 , 4 have demonstrated gasping phenomena in the isolated ischemic rat head and determined the variations with age and drug administration prior to decapitation. In duplicating these experiments a single edge razor blade held vertically in a blade holder was used, 4 and the section made from the dorsal surface as far cephalad as possible. Subsequent examination of the heads revealed that the section had passed caudal to the carotid sinus-body region leaving this mechanism intact. To evaluate the possible role of this structure in the gasping phenomena, male rats were anesthetized with chloralose (0.4 g per kg body weight), previously shown to increase the survival time and total number of gasps more than 250% in rats of a younger age group, 1 and the carotid sinus body located bilaterally through a midline incision. Decapitation was then performed in one group of 10 animals caudal to these structures and in another group of 10 above them, the surgical technic being as identical as possible in all cases. The rats weighed from 50 g to 64 g, a range previously shown to have a characteristic and fairly constant gasping response. The results shown in Table I indicate that only when the carotid mechanism remains connected to the brain does gasping occur.
Since rats of this weight group show both an initial aerobic series of gasps and a later anaerobic series 4 it must be concluded that the carotid drive is essential to both.
In 2 dogs (7.6 and 11.3 kg) under nembutal anesthesia gasping (depression of the mandible) was produced by occluding the trachea which was subsequently released and artificial respiration instituted to restore the animals when respiratory efforts had ceased. After removal of the carotid sinus-body region by resecting this area of the common carotid artery and its branches (ext. carotid, int. carotid and occipital artery), tracheal occlusion caused marked diaphragmatic and intercostal hyperpneic efforts, but no mandibular movements occurred.
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