Initiation of esophageal secondary peristalsis by slow fluid infusion in the opossum: effect of hydrochloric acid

1996 ◽  
Vol 270 (6) ◽  
pp. G927-G931 ◽  
Author(s):  
M. Kusano ◽  
W. J. Hogan ◽  
I. M. Lang ◽  
J. L. Bonnevier ◽  
B. T. Massey ◽  
...  

We investigated the mechanisms of slow fluid infusion-induced secondary peristalsis and the effects of hydrochloric acid on this response. In 13 chronically esophagostomized opossum, acidic and neutral barium sulfate were infused into the distal esophagus at a rate of 1.1 ml/min, while recording the esophageal dimension by videofluoroscopy and esophageal intraluminal pressure concurrently. The effects of atropine, tetrodotoxin, capsaicin, and bilateral cervical vagotomy on the response to slow fluid infusion were examined. Acidic barium initiated secondary peristalsis more frequently and at shorter latency with less increase of preperistaltic intraesophageal pressure than neutral barium (P < 0.05). Atropine abolished secondary peristalsis initiated by neutral barium. For acidic barium, atropine decreased the incidence of secondary peristalsis, increased the latency for initiation of secondary peristalsis, and initiated secondary peristalsis more distally (P < 0.05). Tetrodotoxin or vagotomy and capsaicin abolished activation of secondary peristalsis. We concluded that secondary peristalsis can be stimulated in response to slow distension by minute amounts of fluid. This peristalsis is atropine and capsaicin sensitive and vagally mediated. The presence of acid significantly lowers the threshold for stimulation of secondary peristalsis induced by slow fluid distension. This effect seems to be atropine resistant.

1992 ◽  
Vol 72 (6) ◽  
pp. 2311-2316 ◽  
Author(s):  
H. Miki ◽  
W. Hida ◽  
Y. Kikuchi ◽  
T. Chonan ◽  
M. Satoh ◽  
...  

We examined the effect of electrical stimulation of the hypoglossal nerve and pharyngeal lubrication with artificial surfactant (Surfactant T-A) on the opening of obstructed upper airway in nine anesthetized supine dogs. The upper airway was isolated from the lower airway by transecting the cervical trachea. Upper airway obstruction was induced by applying constant negative pressures (5, 10, 20, and 30 cmH2O) on the rostral cut end of the trachea. Peripheral cut ends of the hypoglossal nerves were electrically stimulated by square-wave pulses at various frequencies from 10 to 30 Hz (0.2-ms duration, 5–7 V), and the critical stimulating frequency necessary for opening the obstructed upper airway was measured at each driving pressure before and after pharyngeal lubrication with artificial surfactant. The critical stimulation frequency for upper airway opening significantly increased as upper airway pressure became more negative and significantly decreased with lubrication of the upper airway. These findings suggest that greater muscle tone of the genioglossus is needed to open the occluded upper airway with larger negative intraluminal pressure and that lubrication of the pharyngeal mucosa with artificial surfactant facilitates reopening of the upper airway.


1981 ◽  
Vol 240 (1) ◽  
pp. R23-R28 ◽  
Author(s):  
D. R. Kostreva ◽  
F. A. Hopp ◽  
J. P. Kampine

In dogs and monkeys anesthetized with pentobarbital sodium, stimulation of the cut central ends of the stellate cardiac nerve, the left and right anterior ansae subclavia, and the stellate ganglia resulted in a depressor response when stimulating fibers with conduction velocities in the range of 2.5-10 m/s. These afferents are in the A delta-fiber-type range. Pressor responses could be elicited by stimulating afferent fibers with conduction velocities in the range of 0.5-3.0 m/s. These fibers are in the C-fiber-type range. Stimulation of the abdominal sympathetic afferents always resulted in a depressor response regardless of the conduction velocities of the fibers. No changes in heart rate were observed. Bilateral cervical vagotomy did not alter the pressor or depressor responses.


2000 ◽  
Vol 279 (5) ◽  
pp. H2549-H2557 ◽  
Author(s):  
De-Pei Li ◽  
Hui-Lin Pan

Ischemic stimulation of cardiac receptors reflexly excites the cardiovascular system. However, the supraspinal mechanisms involved in this reflex are not well defined. This study examined the responses of barosensitive neurons in the rostral ventrolateral medulla (RVLM) to stimulation of cardiac receptors and the afferent pathways involved in these responses. Single-unit activity of RVLM neurons was recorded in α-chloralose-anesthetized rats. Cardiac receptors were stimulated by epicardial application of 10 μg/ml of bradykinin (BK). Barosensitive neurons were silenced by stimulation of baroreceptors. Application of BK increased the mean arterial pressure from 65.2 ± 1.9 to 89.3 ± 2.9 mmHg and excited RVLM barosensitive neurons from 6.2 ± 0.7 to 10.7 ± 0.9 impulses/s ( P < 0.05, n = 40). BK had no effect on 21 nonbarosensitive neurons. Blockade of stellate ganglia abolished the response of barosensitive neurons to BK. Cervical vagotomy significantly increased the baseline discharges of RVLM barosensitive neurons but had no effect on their responses to BK. Thus this study indicates that stimulation of cardiac receptors selectively activates RVLM barosensitive neurons through sympathetic afferent pathways. This information suggests that the RVLM barosensitive neurons are likely involved in the sympathetic control of circulation during myocardial ischemia.


1987 ◽  
Vol 253 (2) ◽  
pp. G165-G170 ◽  
Author(s):  
H. E. Raybould ◽  
M. E. Roberts ◽  
G. J. Dockray

The actions of intravenous sulfated cholecystokinin octapeptide (CCK-8) on intraluminal pressure in the body of the stomach were studied in urethan-anesthetized rats. There was a dose-related decrease in pressure in response to CCK-8 over the range 0.3-33 pmol. Bilateral cervical vagotomy alone reduced the response to CCK-8 and together with splanchnic section abolished it. Hexamethonium also reduced the response. Vagotomy did not change the response to CCK-8 in hexamethonium-treated rats, but celiac ganglionectomy abolished it. Guanethidine and phentolamine, but not propranolol, significantly decreased the response to CCK-8; subsequent vagotomy abolished the response. Similarly, depletion of tissue catecholamines by pretreatment with 6-OH dopamine, reserpine, or celiac ganglionectomy together with vagal section abolished the effect of CCK-8. It concluded that CCK-8 decreases mean intragastric pressure in the rat by pathways involving both vagal and splanchnic nerves. The splanchnic pathway involves an alpha-adrenergic mechanism but is hexamethonium resistant. The vagal pathway is hexamethonium sensitive and nonadrenergic. Similar pathways may mediate the effect of CCK on gastric emptying.


1995 ◽  
Vol 269 (4) ◽  
pp. G558-G569 ◽  
Author(s):  
C. H. Malbert ◽  
C. Mathis ◽  
J. P. Laplace

Pyloric resistance is probably a major factor regulating gastric emptying of liquids, but its nervous control is unknown. The role of efferent vagal pathways in pyloric resistance was evaluated in 13 anesthetized pigs. Pyloric resistance was assessed by simultaneous recording of gastropyloroduodenal motility and transpyloric flow during gastric emptying of saline. Cervical vagotomy suppressed all antral pressure events, increased the number of pressure events localized at the pylorus, and decreased the frequency of the flow pulses (P < 0.05), without affecting either pyloric resistance or the characteristics of flow pulses. Electrical stimulation of the cervical and the thoracic vagi both decreased pyloric resistance by about 60% and increased the stroke volume of flow pulses (P < 0.05). The reduced pyloric resistance was mainly related to an alteration of the temporal relationship between flow pulses and pyloric pressure events. These results indicate that vagal efferents could provide inhibitory inputs to pyloric resistance. A reduction in pyloric resistance contributes to the increased flow rate observed during vagal stimulation.


1975 ◽  
Vol 39 (3) ◽  
pp. 411-416 ◽  
Author(s):  
D. Heistad ◽  
F. M. Abboud ◽  
A. L. Mark ◽  
P. G. Schmid

This study tested the hypothesis that ventilatory responses to chemoreceptor stimulation are affected by the level of arterial pressure and degree of baroreceptor activation. Carotid chemoreceptors were stimulated by injection of nicotine into the common carotid artery of anesthetized dogs. Arterial pressure was reduced by bleeding the animals and raised by transient occlusion of the abdominal aorta. The results indicate that ventilatory responses to chemoreceptor stimulation were augmented by hypotension and depressed by hypertension. In additional studies we excluded the possibility that the findings were produced by a direct effect of changes in arterial pressure on chemoreceptors. Both carotid bifurcations were perfused at constant flow. In one carotid bifurcation, perfusion pressure was raised to stimulate carotid sinus baroreceptors. In the other carotid bifurcation, pressure was constant and nicotine was injected to stimulate carotid chemoreceptors. Stimulation of baroreceptors on one side attenuated the ventilatory response to stimulation of contralateral chemoreceptors. This inhibition was observed before and after bilateral cervical vagotomy. We conclude that there is a major central interaction between baroreceptor and chemoreceptor reflexes so that changes in baroreceptor activity modulate ventilatory responses to chemoreceptor stimulation.


1980 ◽  
Vol 58 (4) ◽  
pp. 352-359 ◽  
Author(s):  
K. S. Rao

Intragastric pressure (IGP) as an index of gastric motor activity was used to investigate gastric motor responses elicited by phenyldiguanide (PDG) in rats under pentobarbitone anaesthesia. Phenyldiguanide injected into the atrium produced an inhibitory gastric motor response whereas an aortic injection resulted in an increase in IGP. Intracarotid injections were without effect. Atropine reduced the response to atrial PDG but not to aortic PDG. Cervical vagotomy abolished the response to both atrial and aortic PDG. Guanethidine and spinal transection abolished the response to atrial PDG only. It is concluded that PDG acts by stimulation of nonmedullated vagal afferents. The efferent pathway for PDG-evoked gastric relaxation is through sympathetic nerves and the efferent system for gastric contraction involves a noncholinergic, nonadrenergic excitatory mechanism.


1975 ◽  
Vol 20 (7) ◽  
pp. 607-612 ◽  
Author(s):  
T. E. Bynum ◽  
Leonard R. Johnson

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