The role of the vagus nerves in the respiratory response to CO2 under hyperoxic conditions

1972 ◽  
Vol 336 (2) ◽  
pp. 147-170 ◽  
Author(s):  
W. Wiemer ◽  
P. Kiwull
1984 ◽  
Vol 56 (6) ◽  
pp. 1614-1620 ◽  
Author(s):  
E. E. Lawson ◽  
W. A. Long

During exposure to hypoxia newborns hypoventilate following a brief period of hyperventilation. Failure of integration of the afferent signals from peripheral O2 chemoreceptors due to immaturity of the central respiratory centers could explain this paradoxical respiratory response. To test this hypothesis we have utilized anesthetized, paralyzed, mechanically ventilated newborn piglets and lambs (less than 11 days) and old piglets (19–35 days). The vagus nerves were cut in each animal. Respiratory activity was quantified by integration of phrenic neural activity. A carotid sinus nerve (CSN) was isolated and electrically stimulated for periods of 1–6 min. In all three groups of animals respiratory activity was continuously elevated throughout the period of CSN stimulation. After CSN stimulation respiratory activity immediately declined about 25% from the stimulated value. Thereafter respiratory activity declined in an exponential fashion toward the initial control level of respiratory activity. The time constant of this latter decay was 84.2 s in the young piglets, 83.2 s in the old piglets, and 63.0 s in the lambs. These results indicate that the respiratory centers of newborn piglets and lambs can maintain integration of continuous afferent CSN activity. Further, the respiratory afterdischarge that follows CSN stimulus cessation is similar to that of adults. These studies indicate that, during periods of O2 sufficiency, the central respiratory centers of newborns respond in a qualitatively similar manner to CSN stimulation as do adult cats.


1963 ◽  
Vol 204 (5) ◽  
pp. 825-828 ◽  
Author(s):  
Michael E. Fritz ◽  
Frank P. Brooks

Rate of flow and composition of bile were measured in three unanesthetized, cholecystectomized dogs. One of these animals and one other dog were also studied after bilateral vagotomy. Bile flow and output of solids were increased by intravenous insulin and feeding. Tolbutamide had a similar choleretic effect. The anticholinergic drug, pipenzolate methylbromide blocked the choleretic effect of insulin. After bilateral vagotomy, the choleretic effect of both feeding and insulin-hypoglycemia was lost. Commercial pancreozymin had a choleretic action which may indicate a role of intestinal hormones in the response to feeding. Intraduodenal injection of hydrochloric acid was followed by an increase in only the volume of bile. Glucagon produced a hydrochloresis and an increase in bilirubin output. The results suggest that normal bile production in the dog after eating may be controlled in part by a mechanism involving the vagus nerves. The data also show that the insulin-hypoglycemia-induced choleresis differs from that of secretin. The composition of hepatic bile obtained from the common duct is consistent with an absorptive function of the ductal epithelium in the dog without a gallbladder.


1981 ◽  
Vol 241 (3) ◽  
pp. R163-R166
Author(s):  
R. F. Munzner ◽  
D. G. Ward ◽  
D. S. Gann

To examine the role of right atrial receptors in mediating reflex vascular responses we measured, in cats anesthetized with chloralose/urethan, changes in mean arterial pressure (MAP) in response to volume pulsation of the right atrium (+/- 1 ml, 1 Hz). Changes in MAP were measured 1) with pressure in the carotid arteries normal and vagus nerves intact: right atrial pulsation led to a very small and transient fall in MAP; 2) with pressure in the carotid arteries at 75 mmHg and the vagus nerves intact: right atrial pulsation led to a larger and sustained fall in MAP; 3) with pressure in the carotid arteries at 75 mmHg and the vagus nerves cooled or sectioned bilaterally: right atrial pulsation of the right atrium led only to a very small and transient fall in MAP. These data suggest strongly that signals from right atrial receptors traveling in the vagus nerves mediate a reflex change in MAP that is normally masked by signals from carotid receptors.


1998 ◽  
Vol 28 (6) ◽  
pp. 678-685 ◽  
Author(s):  
V. G. Kassil' ◽  
L. A. Vataeva ◽  
G. V. Makukhina

CHEST Journal ◽  
1985 ◽  
Vol 87 (5) ◽  
pp. 197S-201S ◽  
Author(s):  
Homer A. Boushey
Keyword(s):  

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