Gastric distension alters frequency and regularity but not amplitude of the gastric slow wave

Zhu, Hongbing; Chen, J. D. Z.

doi:10.1111/j.1365-2982.2004.00571.x

Cited by 21 publications

(29 citation statements)

References 36 publications

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“…Food‐induced slowing of SWR is also likely to be multifactorial in origin. Previous studies have shown that gastric distension diminishes SWR, 4 in a volume‐dependent manner 17,18 . As with impedance, we observed that changes in SWR were correlated with balloon volume, but significantly diminished only with the largest volume.…”

Section: Discussionsupporting

confidence: 75%

The use of gastric electrical signals for algorithm for automatic eating detection in dogs

Aviv

Sanmiguel

Kliger

et al. 2008

Neurogastroenterology Motil

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Food ingestion increases fundic impedance (FI) and reduces antral slow wave rate (SWR). Our aim was to determine if such changes can be integrated into an algorithm for automatic eating detection (AED). When incorporated in implantable medical devices, AED can time treatment to food intake without need for patient input. Four dogs were implanted with fundic and antral electrodes, connected to an implantable recording device. Changes in FI and SWR induced by fixed meals of different weights were determined, and were used to build an AED algorithm. Its performance was then tested on the same animals given an ad libitum access to food. The effects of gastric balloon distension and nitroglycerin on SWR and FI were also tested. Fixed meals reduced SWR in a weight-dependent manner, R(2) = 0.936, P < 0.05 baseline compared to 50, 100, 200 and 400 g. Meals increased FI above baseline in a weight-dependent manner; R(2) = 0.994, P < 0.05 baseline compared to 200 and 400 g. During ad libitum intake, the AED algorithm detected 86% of all meals > or =15 g. Gastric distension reduced SWR and increased FI. Nitroglycerin reduced SWR. AED, using changes in FI and gastric SWR is feasible. Changes in FI and SWR are induced primarily by the presence of food in the stomach.

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Section: Discussionsupporting

confidence: 75%

The use of gastric electrical signals for algorithm for automatic eating detection in dogs

Aviv

Sanmiguel

Kliger

et al. 2008

Neurogastroenterology Motil

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“…This result provides further evidence that the MGG and EGG record different phenomena than intraluminal manometry. It remains unclear to what extent the postprandial amplitude increases can be ascribed to gastric distension as opposed to an actual increase in gastric activity, but other authors have addressed this question 10,45,46 . The consensus appears to be that postprandial signal power increases may or may not correspond to actual increases in slow wave activity, but postprandial amplitude decreases are generally considered pathological 47 .…”

Section: Discussionmentioning

confidence: 99%

“…These issues have led some to suggest that temporal characteristics of the EGG signal such as slow wave frequency are the only potentially reliable information obtainable from cutaneous recordings 5–9 . Postprandial increases in EGG power may be attributed to either increased motility or decreased source‐to‐electrode separation caused by gastric distension; however, it is not currently possible to determine the relative degree each factor contributes to the increased power 10 . A recent study by Chen et al.…”

Section: Introductionmentioning

confidence: 99%

Biomagnetic characterization of spatiotemporal parameters of the gastric slow wave

Bradshaw

Irimia

Sims

et al. 2006

Neurogastroenterology Motil

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Certain gastric disorders affect spatiotemporal parameters of the gastric slow wave. Whereas the electrogastrogram (EGG) evaluates electric potentials to determine primarily temporal parameters, fundamental physical limitations imposed by the volume conduction properties of the abdomen suggest the evaluation of gastric magnetic fields. We used a multichannel superconducting quantum interference device magnetometer to study the magnetogastrogram (MGG) in 20 normal human subjects before and after a test meal. We computed the frequency and amplitude parameters of the gastric slow wave from MGG. We identified normal gastric slow wave activity with a frequency of 2.6 ± 0.5 cycles per minute (cpm) preprandial and 2.8 ± 0.3 cpm postprandial. In addition to frequency and amplitude, the use of surface current density mapping applied to the multichannel MGG allowed us to visualize the propagating slow wave and compute its propagation velocity (6.6 ± 1.0 mm s )1 preprandial and 7.4 ± 0.4 mm s )1 postprandial). Whereas MGG and EGG signals exhibited strong correlation, there was very little correlation between the MGG and manometry. The MGG not only records frequency dynamics of the gastric slow wave, but also characterizes gastric propagation. The MGG primarily reflects the underlying gastric electrical activity, but not its mechanical activity.

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“…Gastric contractility is closely coupled to the mechanosensitivity located in the gastric wall [12, 23, 24]. The myogenic response of the gastric smooth muscle and efferent neurogenic contraction are regulated by mechanoreceptors: afferent and efferent vagus nerves [1, 6, 9, 11, 12, 23, 24].…”

Section: Discussionmentioning

confidence: 99%

“…The myogenic response of the gastric smooth muscle and efferent neurogenic contraction are regulated by mechanoreceptors: afferent and efferent vagus nerves [1, 6, 9, 11, 12, 23, 24]. The relation between afferent vagus signals and gastric distension was identified decades ago [6, 9, 11, 12].…”

Section: Discussionmentioning

confidence: 99%

Distension-Induced Gastric Contraction is Attenuated in an Experimental Model of Gastric Restraint

Guo

Mattar

et al. 2010

OBES SURG

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BackgroundGastric distension has important implications for motility and satiety. The hypothesis of this study was that distension affects the amplitude and duration of gastric contraction and that these parameters are largely mediated by efferent vagus stimulation.MethodsA novel isovolumic myograph was introduced to test these hypotheses. The isovolumic myograph isolates the stomach and records the pressure generated by the gastric contraction under isovolumic conditions. Accordingly, the phasic changes of gastric contractility can be documented. A group of 12 rats were used under in vivo conditions and isolated ex vivo conditions and with two different gastric restraints (small and large) to determine the effect of degree of restraint.ResultsThe comparison of the in vivo and ex vivo contractility provided information on the efferent vagus mediation of gastric contraction, i.e., the in vivo amplitude and duration reached maximum of 12.6 ± 2.7 mmHg and 19.8 ± 5.6 s in contrast to maximum of 5.7 ± 0.9 mmHg and 7.3 ± 1.3 s in ex vivo amplitude and duration, respectively. The comparison of gastric restraint and control groups highlights the role of distension on in vivo gastric contractility. The limitation of gastric distension by restraint drastically reduced the maximal amplitude to below 2.9 ± 0.2 mmHg.ConclusionsThe results show that distension-induced gastric contractility is regulated by both central nervous system and local mechanisms with the former being more substantial. Furthermore, the gastric restraint significantly attenuates gastric contractility (decreased amplitude and shortened duration of contraction) which is mediated by the efferent vagus activation. These findings have important implications for gastric motility and physiology and may improve our understanding of satiety.

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Gastric distension alters frequency and regularity but not amplitude of the gastric slow wave

Cited by 21 publications

References 36 publications

The use of gastric electrical signals for algorithm for automatic eating detection in dogs

The use of gastric electrical signals for algorithm for automatic eating detection in dogs

Biomagnetic characterization of spatiotemporal parameters of the gastric slow wave

Distension-Induced Gastric Contraction is Attenuated in an Experimental Model of Gastric Restraint

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