Electrical stimulation of gastric electrical control activity

Sarna, S. K.; Daniel, E. E.

doi:10.1152/ajplegacy.1973.225.1.125

Cited by 71 publications

(34 citation statements)

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“…Entrainment of gastric slow waves or pacing has been reported in a number of studies with GES of long pulses with a pulse width in the order of a few hundred milliseconds. 26,[28][29][30][31][32] Typically, GES was performed at a frequency slightly higher than the measured intrinsic frequency of gastric slow waves. When entrainment or pacing occurs, the natural slow waves are phase-locked with stimuli.…”

Section: Alterations Of Gastric Slow Wavesmentioning

confidence: 99%

Systematic review: applications and future of gastric electrical stimulation

Zhang

Chen

2006

Aliment Pharmacol Ther

105

114

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Section: Alterations Of Gastric Slow Wavesmentioning

confidence: 99%

Systematic review: applications and future of gastric electrical stimulation

Zhang

Chen

2006

Aliment Pharmacol Ther

105

114

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“…It requires the release of ACh during membrane depolarization to generate an RPC (57). Furthermore, electrical stimulation can increase slow-wave frequency only marginally, and when the slow-wave frequency is increased, the distance over which they are phase locked decreases in the small intestine (61,62), resulting in reduced distance of propagation of RPCs. On the contrary, reversing the direction of propagation of slow waves in the stomach or the duodenum or by stimulating them in pyloric smooth muscle cells to disrupt antro-pyloro-duodenal coordination can effectively retard the rate of gastric emptying (35,80).…”

Section: Strategies In the Selection Of Molecular And Pharmacologicalmentioning

confidence: 99%

Molecular, functional, and pharmacological targets for the development of gut promotility drugs

Sarna

2006

American Journal of Physiology-Gastrointestinal and Liver Physi

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. Molecular, functional, and pharmacological targets for the development of gut promotility drugs. Am J Physiol Gastrointest Liver Physiol 291: G545-G555, 2006. First published March 24, 2006 doi:10.1152/ajpgi.00122.2006.-The science of gastrointestinal motility has made phenomenal advances during the last fifty years. Yet, there is a paucity of effective promotility drugs to treat functional bowel disorders that affect 10 -29% of the U.S. population. A part of the reason for the lack of effective drugs is our limited understanding of the etiology of these diseases. In the absence of this information, mostly an ad hoc approach has been used to develop the currently available drugs, which are modestly effective or effective in only a subset of the patients with functional bowel disorders. This review discusses a grounds-up approach for development of the next generation of promotility drugs. The approach is based on our current understanding of 1) the different types of contractions that produce overall motility function of mixing and orderly net distal propulsion in major gut organs, 2) the regulatory mechanisms of these contractions, 3) which receptors and intracellular signaling molecules could be targeted to stimulate specific types of contractions to accelerate or retard transit, and 4) the strengths and limitations of animal models and experimental approaches that could screen potential promotility drugs for their efficacy in human gut propulsion in functional bowel disorders. smooth muscle; slow waves; enteric neurons; excitation-contraction coupling; peristaltic reflex; irritable bowel syndrome; prokinetic agents; gastroparesis; functional bowel disorders THE SCIENCE OF GASTROINTESTINAL MOTILITY has made phenomenal advances during the last fifty years. Our understanding of the individual regulatory mechanisms of motility function [excitation-contraction coupling in smooth muscle cells; enteric motor, sensory, and interneurons; enteric neurotransmitters, neuromodulators, and hormones; extrinsic neurons including spinal cord and central nervous system (CNS)] has matured (7, 18 -20, 26, 28, 39, 42, 53, 54, 57, 59, 60, 76, 78). However, significant gaps remain in our understanding of how and when the inputs from these mechanisms integrate to produce the normal mixing and propulsive motor functions of the gut; defects in these regulatory mechanisms result in motility dysfunction in diseases such as irritable bowel syndrome, inflammatory bowel disease, gastroparesis, and gastroesophageal reflux. Finally, our understanding of which receptors and intracellular signaling molecules in circular smooth muscle cells and enteric neurons could be targeted to normalize function in motility disorders is still rudimentary.Most currently available promotility drugs or those under development seem to have their origins in a known physiological or pharmacological effect or in their established role in a different system. For example, CCK receptor antagonists (loxiglumide and deloxyglumide) are thought to be potential promotil...

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“…Later, Sarna et al used a modi"ed set of Van der Pol oscillators to simulate di!erent aspects of the GI tract activity (Sarna et al, 1971(Sarna et al, , 1972a}c, 1976Sarna & Daniel, 1973, 1975. The pioneering works by these authors had an essential impact on the terminology and approaches used in later studies.…”

Section: Introductionmentioning

confidence: 99%