Motor reflexes of stomach elicited by phenyldiguanide in the rat

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.

1978 ◽  
Vol 235 (6) ◽  
pp. H759-H766
Author(s):  
T. Shimizu ◽  
D. F. Peterson ◽  
V. S. Bishop

Two different types of circulatory reflexes evoked by electrical stimulation of afferent fibers in the left pericoronary nerves were studied in anesthetized cats. A depressor response (-32.5 mmHg) with bradycardia (-48.7 beats/min) in 21 of 31 cats was mediated by the C fibers in the right vagal cardiac nerve trunk. The efferent pathway for the bradycardia was in caudal cardiac branches of the right vagus. Neither sympathetic denervation to the heart nor atropine attenuated the hypotensive response significantly, suggesting that the depressor response results from reflex inhibition of peripheral sympathetic activity. A pressor reflex without heart rate change was observed either when the vagi were blocked or when the distribution of vagal afferents in the pericoronary nerve was considered to be small. The pressor reflex was mainly mediated by the afferent C fibers within the left cardiac sympathetic nerves. The depressor response was enhanced by sympathectomy, suggesting the sympathetic counteraction on the inhibitory vagal afferents, Similarly, an enhancement of the pressor reflex by vagal blockade was observed, indicating tonic vagal restraint on excitatory sympathetic reflexes.


2015 ◽  
Vol 70 (6) ◽  
pp. 718-726
Author(s):  
Viktor Mihajlovich Smirnov ◽  
Dmitrij Sergeevich Sveshnikov ◽  
Igor Leonidovich Myasnikov ◽  
Tat'jana Evgen'evna Kuznecova ◽  
Jurij Nikolaevich Samko

The review is devoted to the mechanism of duodenal motility activation caused by sympathetic nerves. The authors have found that stimulation of the sympathetic trunk in the thoracic cavity in dogs in most cases provide not inhibitory but excitatory motor responses of the duodenum. Excitatory effects were eliminated during 5HT-receptors blockade by promedol and lysergol. Analysis of publications showed that sympathetic trunk contains serotoninergic fibers, providing excitatory motor responses of the duodenum to electrical nerve stimulation. According to histochemical and physiological studies, amount of serotonergic fibers in the sympathetic trunk is several times more than the adrenergic. This means that the body has sertoninergic nerves. Serotoninergic nerve as well as the sympathetic is a collective notion. There are: sympathetic trunks, their ramifications and branches that innervate the internal organs. Since promedol blocks serotonergic nerves, this is plausible cause of constipation in patients after surgical treatment along with the application of this drug.


1965 ◽  
Vol 208 (2) ◽  
pp. 255-259 ◽  
Author(s):  
David E. Donald ◽  
John T. Shepherd

Following attempted denervation of the heart by the technic of regional neural ablation, dogs with incomplete cardiac denervation were shown to have the same supersensitivity to l-norepinephrine as dogs in which the denervation of the heart was complete. Dogs with chronic bilateral stellate ganglionectomy or those pretreated with reserpine had cardiac acceleration in response to the administration of tyramine or to stimulation of the stellate cardiac nerves, but did not demonstrate supersensitivity to l-norepinephrine. No supersensitivity was seen in dogs with chronic bilateral cervical vagotomy. Excision of the right stellate and caudal cervical ganglia and the immediately adjacent right vagus nerve resulted in supersensitivity to l-norepinephrine. In these animals cardiac acceleration resulted from stimulation of the left stellate cardiac nerves or from the administration of tyramine. The supersensitivity was lost after excision of the sinoatrial node. It is concluded that one can uniquely denervate the sinus node and that dogs so treated will develop supersensitivity to l-norepinephrine despite the presence of functional sympathetic nerves to the rest of the heart.


1993 ◽  
Vol 74 (1) ◽  
pp. 103-110 ◽  
Author(s):  
J. G. Pickar ◽  
J. M. Hill ◽  
M. P. Kaufman

Using electrical stimulation of the mesencephalic locomotor region, we made decerebrate unanesthetized cats walk on a treadmill. The locomotion induced by stimulation of this midbrain area was assessed before and during activation of vagal afferents by either intravenous injection of phenylbiguanide or inflation of a balloon placed in the left atrium. Inflation of a balloon, which increased left atrial pressure by 7–25 mmHg, abolished locomotion in 9 of 10 cats tested. Bilateral cervical vagotomy prevented the abolition of locomotion by balloon inflation in each of two cats tested. Intravenous phenylbiguanide (50 or 100 micrograms/kg) or serotonin (40 micrograms/kg) injections abolished or attenuated walking induced by midbrain stimulation in 11 of 13 cats tested. In addition, intravenous phenylbiguanide injections abolished or attenuated locomotion with a shorter onset time than did systemic injections of this substance in five of six cats tested. Bilateral cervical vagotomy prevented the abolition of locomotion by phenylbiguanide injection in each of five cats tested. We conclude that locomotion can be prevented by a viscerosomatic reflex arising from the lungs and heart. The afferent arm of this reflex arc is the vagus nerve. Afferents such as slowly and rapidly adapting pulmonary stretch receptors, atrial receptors, and lung C-fibers may have had a role in preventing locomotion during the increase in left atrial pressure in our experiments. On the other hand, pulmonary C-fibers had a crucial role in preventing locomotion during intravenous injection of phenyl-biguanide. We speculate that this viscerosomatic reflex may help to explain in part the intolerance for exercise displayed by patients with congestive heart failure.


1951 ◽  
Vol 28 (1) ◽  
pp. 32-40
Author(s):  
D. L. DUNCAN ◽  
A. T. PHILLIPSON

The state of motor activity of the stomach was studied in a series of foetal sheep. The non-functional period was found to end between the 50th and 60th days of gestation. Sustained activity was preceded by short periods of myogenic and neuromotor activity, and was not in evidence until the 70th day. Foetal swallowing commenced soon after this, but the pattern of suckling behaviour developed gradually over an extended period. The motor mechanisms mediated by the vagus were studied by section and electrical stimulation of the nerve.


Author(s):  
Zhenjun T TAN ◽  
Matthew Ward ◽  
Robert J Phillips ◽  
Xueguo Zhang ◽  
Deborah M Jaffey ◽  
...  

Gastric electrical stimulation (GES) is used clinically to promote proximal GI emptying and motility. In acute experiments, we measured duodenal motor responses elicited by GES applied at 141 randomly chosen electrode sites on the stomach serosal surface. Overnight-fasted (H2O available) anesthetized male rats (n = 81) received intermittent biphasic GES for 5 min (20s-on/40s-off cycles; I = 0.3mA; pw = 0.2ms; 10 Hz). A strain gauge on the serosal surface of the proximal duodenum of each animal was used to evaluate baseline motor activity and the effect of GES. Using ratios of time blocks compared to a 15-min pre-stimulation baseline, we evaluated the effects of the 5-min stimulation on concurrent activity; on the 10-min immediately after the stimulation, and on the 15-min period beginning with the onset of stimulation. We mapped the magnitude of the duodenal response (3 different motility indices) elicited from the 141 stomach sites. Post hoc electrode site maps associated with duodenal responses suggested three zones similar to the classic regions of forestomach, corpus and antrum. Maximal excitatory duodenal motor responses were elicited from forestomach sites, whereas inhibitory responses occurred with stimulation of the corpus. Moderate excitatory duodenal responses occurred with stimulation of the antrum. Complex, weak inhibitory/excitatory responses were produced by stimulation at boundaries between stomach regions. Patterns of GES efficacies coincided with distributions of previously mapped vagal afferents, suggesting that excitation of the duodenum is strongest when GES electrodes are situated over stomach concentrations of vagal intramuscular arrays, putative stretch receptors in the muscle wall.


1988 ◽  
Vol 60 (6) ◽  
pp. 2122-2137 ◽  
Author(s):  
S. N. Currie ◽  
P. S. Stein

1. A low-spinal, immobilized turtle displays a fictive scratch reflex in hindlimb motor neurons in response to tactile stimulation of the shell (17, 19). Turtles exhibit three forms of the scratch reflex: rostral, pocket, and caudal. Each form is elicited by tactile stimulation of a different receptive field on the body surface. The ventral-posterior pocket (VPP) cutaneous nerve innervates the ventral-posterior portion of the pocket scratch receptive field (Fig. 1). Natural stimulation within the VPP nerve's receptive field evoked a pocket scratch reflex (Fig. 2A). Electrical stimulation of this nerve elicited robust pocket scratch reflexes (Fig. 2, B and C). 2. A single electrical pulse to the VPP nerve delivered at a voltage (greater than 5 V, 0.1 ms) that activated all the axons in the nerve was termed a "maximal" pulse. A single maximal pulse did not evoke a scratch motor response. It raised the excitability of the pocket scratch central pattern generator for several seconds, however. We revealed such excitability changes by applying maximal pulses to the VPP nerve at multisecond intervals (Figs. 5 and 6). When we delivered maximal pulses with interpulse intervals of less than or equal to 5 s, the first pulse produced no motor response and the second pulse evoked one or more cycles of pocket scratch. 3. A stimulus pulse applied to the VPP nerve was used as a probe for studying changes in the excitability of the pocket scratch CPG following scratch motor patterns. In a rested preparation, the stimulus pulse did not activate motor output. In contrast, the stimulus pulse evoked one or two cycles of pocket scratch activity if delivered within 2.5 s after the cessation of rhythmic pocket scratch motor activity (Figs. 7-9). These results are consistent with the hypothesis that the pocket scratch CPG has elevated excitability for seconds following the cessation of pocket scratch motor output. A single pulse applied to the VPP nerve evoked no response if delivered after the cessation of rostral scratch motor activity, however (Fig. 9D). 4. We used a train of maximal pulses to the VPP nerve to probe the form-specificity of the changes in the excitability following a rostral scratch motor pattern (Fig. 10). We set the stimulus parameters so that the train evoked one or two cycles of a pocket scratch motor pattern in a preparation that had rested for over 1 min.(ABSTRACT TRUNCATED AT 400 WORDS)


1980 ◽  
Vol 239 (6) ◽  
pp. H713-H720 ◽  
Author(s):  
E. Muscholl

Activation of muscarinic cholinergic receptors located at the terminal adrenergic nerve fiber inhibits the process of exocytotic norepinephrine (NE) release. This neuromodulatory effect of acetylcholine and related compounds has been discovered as a pharmacological phenomenon. Subsequently, evidence for a physiological role of the presynaptic muscarinic inhibition was obtained on organs known to be innervated by the autonomic ground plexus (Hillarp, Acta. Physiol. Scand. 46, Suppl. 157: 1-68, 1959) in which terminal adrenergic and cholinergic axons run side by side. Thus, in the heart electrical vagal stimulation inhibits the release of NE evoked by stimulation of sympathetic nerves, and this is reflected by a corresponding decrease in the postsynaptic adrenergic response. On the other hand, muscarinic antagonists such as atropine enhance the NE release evoked by field stimulation of tissues innervated by the autonomic ground plexus. The presynaptic muscarine receptor of adrenergic nerve terminals probably restricts the influx of calcium ions that triggers the release of NE. However, the sequence of events between recognition of the muscarinic compound by the receptor and the process of exocytosis still remains to be clarified.


1970 ◽  
Vol 52 (1) ◽  
pp. 167-175
Author(s):  
P. J. MILL

1. Rhythmic bursts of motor activity associated with the expiratory phase of ventilation have been recorded from the second lateral segmental nerves of posterior abdominal ganglia in Aeshna and Anax larvae. 2. In Aeshna the rhythmic expiratory bursts contain one, or sometimes two, motor units; whereas in Anax there are almost invariably three units. In both animals only one unit is associated with action potentials in the respiratory dorso-ventral muscle. 3. Motor activity synchronized with the expiratory bursts in the second nerves has been recorded from the other lateral nerves and from the last unpaired nerve. In addition the fifth lateral nerves carry inspiratory bursts. 4. It has been confirmed that stimulation of a first segmental nerve can re-set the ventilatory rhythm by initiating an expiratory burst in the second nerves. The original frequency is immediately resumed on cessation of stimulation. 5. The nature of the ventilatory control system in dragonfly larvae is discussed in relation to other rhythmic systems in the arthropods.


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