Cross-talk along gastrointestinal tract during electrical stimulation: effects and mechanisms of gastric/colonic stimulation on rectal tone in dogs

2005 ◽  
Vol 288 (6) ◽  
pp. G1195-G1198 ◽  
Author(s):  
Shi Liu ◽  
Lijie Wang ◽  
J. D. Z. Chen

Gastric electrical stimulation (GES) has been shown to alter motor and sensory functions of the stomach. However, its effects on other organs of the gut have rarely been investigated. The study was performed in 12 dogs implanted with two pairs of electrodes, one on the serosa of the stomach and the other on the colon. The study was composed of two experiments. Experiment 1 was designed to study the effects of GES on rectal tone and compliance in nine dogs compared with colonic electrical stimulation (CES). Rectal tone and compliance were assessed before and after GES or CES. Experiment 2 was performed to study the involvement of sympathetic pathway in 8 of the 12 dogs. The rectal tone was recorded for 30–40 min at baseline and 20 min after intravenous guanethidine. GES or CES was given for 20 min 20 min after the initiation of the infusion. It was found that both GES and CES reduced rectal tone with comparable potency. Rectal compliance was altered neither with GES, nor with CES. The inhibitory effect of GES but not CES on rectal tone was abolished by an adrenergic blockade, guanethidine. GES inhibited rectal tone with a comparable potency with CES but did not alter rectal compliance. The inhibitory effect of GES on rectal tone is mediated by the sympathetic pathway. It should be noted that electrical stimulation of one organ of the gut may have a beneficial or adverse effect on another organ of the gut.

2010 ◽  
Vol 59 (6) ◽  
pp. 452-459 ◽  
Author(s):  
Alexander Friedman ◽  
Elad Lax ◽  
Yahav Dikshtein ◽  
Lital Abraham ◽  
Yakov Flaumenhaft ◽  
...  

1987 ◽  
Vol 96 (4) ◽  
pp. 349-361 ◽  
Author(s):  
Mark J. Maslan ◽  
Josef M. Miller

As a result of practical considerations, histopathologic findings of the temporal bone in humans with cochlear prosthesis implants have been limited. This project attempts to better define safe parameters of electrical stimulation of the inner ear and compare the safe limits of intracochlear vs. extracochlear stimulation sites. Guinea pigs were implanted with single electrodes either on the promontory or in the scala tympani and were stimulated relative to a remote indifferent for 12 hours distributed over a 4-week period. Electrical auditory brainstem evoked responses (EABRs) were tested before and after each of four 3-hour stimulation sessions. Six weeks after implantation, the animals were killed, and their cochleas were examined under the scanning electron microscope. Intracochlear electrodes exhibited thresholds for damage well below one half of that found for most extracochlear stimulation sites. The function-relating damage threshold (in amperes) to frequency of intracochlear stimulation is represented by two straight lines, with an intercept of 1 kHz. The low-frequency limb exhibited a slope of 3 to 4 dB/octave, whereas the high-frequency limb exhibited a slope of 9 to 10 dB/octave. Extracochlear results were too variable to permit speculation. Changes in EABRs were only variably related to histopathologic findings.


1990 ◽  
Vol 259 (5) ◽  
pp. H1511-H1517 ◽  
Author(s):  
N. Toda ◽  
T. Okamura

Relaxant responses to transmural electrical stimulation and nicotine of cerebral artery strips obtained from dogs and Japanese monkeys were abolished by tetrodotoxin and hexamethonium, respectively, and suppressed by treatment with NG-monomethyl-L-arginine (L-NMMA), a nitric oxide (NO) synthesis inhibitor. The inhibitory effect was prevented and reversed by L-arginine but not by D-arginine. The relaxations suppressed by L-NMMA were not increased by exogenously applied NO. Endothelium denudation did not alter the response to transmural stimulation and nicotine or the inhibitory effect of L-NMMA. D-NMMA did not inhibit the response to vasodilator nerve stimulation. Dog coronary artery relaxations caused by transmural stimulation were not inhibited by L-NMMA but reversed to contractions by propranolol. Relaxations caused by substance P of dog cerebral arteries treated with indomethacin were dependent on endothelium and inhibited by L-NMMA, whereas those by NO and nitroglycerin, endothelium-independent relaxations, were unaffected. It is concluded that chemical and electrical stimulation of vasodilator nerves relaxes dog and monkey cerebral arteries, possibly by a mediation of NO rather than a stimulating action of NO on the release of vasodilator transmitter. Endothelium-dependent relaxations by substance P of dog cerebral arteries appear to be mediated by NO.


1987 ◽  
Vol 63 (3) ◽  
pp. 912-917 ◽  
Author(s):  
J. C. Connelly ◽  
L. W. McCallister ◽  
M. P. Kaufman

Although the role played by the caudal ventrolateral medulla in the regulation of the cardiovascular system has been extensively investigated, little is known about the role played by this area in the regulation of airway caliber. Therefore, in alpha-chloralose-anesthetized dogs, we used both electrical and chemical means to stimulate the caudal ventrolateral medulla while we monitored changes in total lung resistance breath by breath. We found that electrical stimulation (25 microA) of 26 sites in this area significantly decreased total lung resistance from 7.1 +/- 0.4 to 5.7 +/- 0.3 cmH2O.1'1.s (P less than 0.001). The bronchodilation evoked by electrical stimulation was unaffected by beta-adrenergic blockade but was abolished by cholinergic blockade. In addition, chemical stimulation of seven sites in the caudal ventrolateral medulla with microinjections of DL-homocysteic acid (0.2 M; 66 nl), which stimulates cell bodies but not fibers of passage, also decreased total lung resistance from 8.3 +/- 1.1 to 6.5 +/- 0.8 cmH2O.l'1.s (P less than 0.01). In contrast, microinjections of DL-homocysteic acid into the nucleus ambiguus (n = 6) increased total lung resistance from 7.5 +/- 0.5 to 9.2 +/- 0.4 cmH2O.l'1.s (P less than 0.05). We conclude that the caudal ventrolateral medulla contains a pool of cell bodies whose excitation causes bronchodilation by withdrawing cholinergic input to airway smooth muscle.


2001 ◽  
Vol 90 (4) ◽  
pp. 1570-1576 ◽  
Author(s):  
Jalal M. Abu-Shaweesh ◽  
Ismail A. Dreshaj ◽  
Musa A. Haxhiu ◽  
Richard J. Martin

Stimulation of the superior laryngeal nerve (SLN) results in apnea in animals of different species, the mechanism of which is not known. We studied the effect of the GABAA receptor blocker bicuculline, given intravenously and intracisternally, on apnea induced by SLN stimulation. Eighteen 5- to 10-day-old piglets were studied: bicuculline was administered intravenously to nine animals and intracisternally to nine animals. The animals were anesthetized and then decerebrated, vagotomized, ventilated, and paralyzed. The phrenic nerve responses to four levels of electrical SLN stimulation were measured before and after bicuculline. SLN stimulation caused a significant decrease in phrenic nerve amplitude, phrenic nerve frequency, minute phrenic activity, and inspiratory time ( P < 0.01) that was proportional to the level of electrical stimulation. Increased levels of stimulation were more likely to induce apnea during stimulation that often persisted beyond cessation of the stimulus. Bicuculline, administered intravenously or intracisternally, decreased the SLN stimulation-induced decrease in phrenic nerve amplitude, minute phrenic activity, and phrenic nerve frequency ( P < 0.05). Bicuculline also reduced SLN-induced apnea and duration of poststimulation apnea ( P < 0.05). We conclude that centrally mediated GABAergic pathways are involved in laryngeal stimulation-induced apnea.


2021 ◽  
Author(s):  
Y.Y. Bikbaeva ◽  
D.A. Pavlov ◽  
A.S. Kuznetsov ◽  
E.S. Balykina ◽  
I.V. Antipov

The effect of percutaneous electrical stimulation of the spinal cord on the reactions of the autonomic nervous system in patients after acute cerebral circulatory disorders was evaluated. Patients in the acute period of rehabilitation treatment underwent a course of percutaneous electrical stimulation for 10 days. Before and after rehabilitation, vegetative reactions were assessed using an orthoclinostatic test, an A.M.Wein questionnaire, and neurological disorders on the Scandinavian scale. The inclusion of the course of percutaneous electrical stimulation in the program of physical rehabilitation of patients who have suffered an ischemic stroke indicates an improvement in the motor status of patients and a decrease in the imbalance of sympathetic and parasympathetic influences Keywords: ischemic stroke, percutaneous electrical stimulation of the spinal cord, vegetative reactions


Hypertension ◽  
2013 ◽  
Vol 61 (2) ◽  
pp. 450-456 ◽  
Author(s):  
Masaomi Chinushi ◽  
Daisuke Izumi ◽  
Kenichi Iijima ◽  
Katsuya Suzuki ◽  
Hiroshi Furushima ◽  
...  

2004 ◽  
Vol 286 (6) ◽  
pp. G1009-G1014 ◽  
Author(s):  
Giovanni Sarnelli ◽  
Pieter Vanden Berghe ◽  
Petra Raeymaekers ◽  
Jozef Janssens ◽  
Jan Tack

Galanin modulates gastrointestinal motility by inhibiting the release of ACh from enteric neurons. It is, however, not known whether galanin also inhibits neuronal cholinergic transmission postsynaptically and whether galanin also reduces the action of other excitatory neurotransmitters. The aim of the present study was thus to investigate the effect of galanin on the evoked intracellular Ca2+ concentration ([Ca2+]i) responses in myenteric neurons. Cultured myenteric neurons from small intestine of adult guinea pigs were loaded with the Ca2+ indicator fluo-3 AM, and the [Ca2+]i responses following the application of different stimuli were quantified by confocal microscopy and expressed as a percentage of the response to high-K+ solution (75 mM). Trains of electrical pulses (2 s, 10 Hz) were applied to stimulate the neuronal fibers before and after a 30-s superfusion with galanin (10−6 M). Substance P (SP), 5-HT, 1,1-dimethyl-4-phenyl-piperazinium iodide (DMPP), and carbachol were used as direct postsynaptic stimuli (10−5 M, 30 s) and were applied alone or after galanin perfusion. Galanin significantly reduced the responses induced by electrical fiber stimulation (43 ± 2 to 35 ± 3%, P = 0.01), SP (15.4 ± 1 to 8.0 ± 0.3%, P < 0.01), and 5-HT (26 ± 2 to 21.4 ± 1.5%, P < 0.05). On the contrary, galanin did not affect the responses induced by local application of DMPP and carbachol. We conclude that in cultured myenteric neurons, galanin inhibits the excitatory responses induced by electrical stimulation, SP, and 5-HT. Finally, the inhibitory effect of galanin on electrical stimulation, but not on DMPP- and carbachol-induced responses, suggests that, at least for the cholinergic component, galanin acts at the presynaptic level.


1981 ◽  
Vol 241 (1) ◽  
pp. R55-R61 ◽  
Author(s):  
B. G. Celler ◽  
L. P. Schramm

Integrated sympathetic activity was recorded on anterior or posterior divisions of the greater splanchnic nerve (GSN) in anesthetized, acutely spinalized, artificially respired Wistar rats before and after ganglionic blockade by hexamethonium. Focal electrical stimulation of spinal sympathoexcitatory pathways elicited large increases in splanchnic sympathetic activity. Ganglionic blockade showed that the anterior and posterior divisions of the GSN are predominantly preganglionic and postganglionic, respectively. Histological examination of excised splanchnic nerves and sympathetic chains indicated that splanchnic postganglionic cell bodies must lie in the chain ganglia rather than within the GSN. Postganglionic responses were calculated for each rat by subtracting responses recorded after ganglionic blockade from responses recorded before ganglionic blockade. As expected, postganglionic responses exhibited longer onset latencies than preganglionic responses. However, evoked activity increased and decreased more rapidly in postganglionic fibers than in preganglionic fibers. Responses to stimulus trains were also better maintained in postganglionic than in preganglionic fibers.


1980 ◽  
Vol 186 (1) ◽  
pp. 105-109 ◽  
Author(s):  
F M Clarke ◽  
F D Shaw ◽  
D J Morton

The extent of binding of glycolytic enzymes to the particulate fraction of homogenates was measured in bovine psoas muscle before and after electrical stimulation. In association with an accelerated glycolytic rate on stimulation, there was a significant increase in the binding of certain glycolytic enzymes, the most notable of which were phosphofructokinase, aldolase, glyceraldehyde 3-phosphate dehydrogenase and pyruvate kinase. From the known association of glycolytic enzymes with the I-band of muscle it is proposed that electrical stimulation of anaerobic muscle increases enzyme binding to actin filaments. Calculations of the extent of enzyme binding suggest that significant amounts of enzyme protein, particularly aldolase and glyceraldehyde 3-phosphate dehydrogenase, are associated with the actin filaments. The results also imply that kinetic parameters derived from considerations of the enzyme activity in the soluble state may not have direct application to the situation in the muscle fibre, particularly during accelerated glycolysis.


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