Mechanisms of burn-induced impairment in gastric slow waves and emptying in rats

2010 ◽  
Vol 299 (1) ◽  
pp. R298-R305 ◽  
Author(s):  
Hanaa S. Sallam ◽  
Hermes M. Oliveira ◽  
Suhuan Liu ◽  
Jiande D. Z. Chen
Keyword(s):  
Gastric Emptying ◽  
Slow Wave ◽  
Delayed Gastric Emptying ◽  
Burn Injury ◽  
Wave Activity ◽  
Cyclooxygenase 2 ◽  
Slow Waves ◽  
Gastric Slow Wave ◽  
Gastric Slow Waves ◽  
Gastric Dysrhythmias

Delayed gastric emptying is common following severe large cutaneous burns; however, the mechanisms of burn-induced delayed gastric emptying remain unknown. The aim of this study was to explore the possible involvement of hyperglycemia and cyclooxygenase-2 receptors in the burn-induced gastric dysrhythmias. Gastric slow waves and gastric emptying were assessed in rats 6 h following sham or burn injury. Animals were randomized to one sham-burn and seven burn groups: untreated; two groups of saline treated (control); insulin treated (5 IU/kg); cyclooxygenase-2 inhibitor treated (10 mg/kg); ghrelin treated (2 nmol/rat); and gastric electrical stimulation treated. It was found that 1) severe burn injury impaired gastric slow waves postprandially and delayed gastric emptying; 2) the impairment in gastric slow waves included a decrease in the slow-wave frequency and in the percentage of normal slow waves, and an increase in the percentage of bradygastria ( P = 0.001, 0.01, and 0.01, respectively vs. preburn values). None of the gastric slow-wave parameters was significantly correlated with gastric emptying; 3) cyclooxygenase-2 inhibitor normalized burn-induced delayed gastric emptying ( P = 0.3 vs. sham-burn), but not gastric dysrhythmias ( P < 0.002 vs. sham), whereas insulin normalized both gastric emptying ( P = 0.4 vs. sham-burn) and gastric dysrhythmias ( P = 0.3 vs. sham-burn); 4) both gastric electrical stimulation and ghrelin accelerated burn-induced delayed gastric emptying ( P = 0.002 and 0.04, respectively, vs. untreated burn). In conclusion, hyperglycemia alters gastric slow-wave activity and delayed gastric emptying, while cyclooxygenase-2 inhibition delays gastric emptying without altering gastric slow-wave activity.

scholarly journals Abnormal gastric slow waves in patients with functional dyspepsia assessed by multichannel electrogastrography

2001 ◽  
Vol 280 (6) ◽  
pp. G1370-G1375 ◽  
Author(s):  
Xuemei Lin ◽  
Jiande Z. Chen
Keyword(s):  
Wave Propagation ◽  
Functional Dyspepsia ◽  
Slow Wave ◽  
Single Channel ◽  
Slow Waves ◽  
Lower Percentage ◽  
Healthy Controls ◽  
Fasting State ◽  
Gastric Slow Wave ◽  
Gastric Slow Waves

The aim of this study was to utilize multichannel electrogastrography to investigate whether patients with functional dyspepsia had impaired propagation or coordination of gastric slow waves in the fasting state compared with healthy controls. The study was performed in 10 patients with functional dyspepsia and 11 healthy subjects. Gastric myoelectrical activity was measured by using surface electrogastrography with a specially designed four-channel device. The study was performed for 30 min or more in the fasting state. Special computer programs were developed for the computation of the propagation and coupling of the gastric slow wave. It was found that, compared with the healthy controls, the patients showed a significantly lower percentage of slow wave propagation (58.0 ± 8.9 vs. 89.9 ± 2.6%, P < 0.002) and a significantly lower percentage of slow wave coupling (46.9 ± 4.4 vs. 61.5 ± 6.9%, P < 0.04). In addition, the patients showed inconsistencies in the frequency and regularity of the gastric slow wave among the four-channel electrogastrograms (EGGs). It was concluded that patients with functional dyspepsia have impaired slow wave propagation and coupling. Multichannel EGG has more information than single-channel EGG for the detection of gastric myoelectrical abnormalities.

Quantitative cellular description of gastric slow wave activity

2008 ◽  
Vol 294 (4) ◽  
pp. G989-G995 ◽  
Author(s):  
Alberto Corrias ◽  
Martin L. Buist
Keyword(s):  
Slow Wave ◽  
Interstitial Cells Of Cajal ◽  
Quantitative Description ◽  
Wave Activity ◽  
Slow Waves ◽  
Slow Wave Activity ◽  
Good Correspondence ◽  
Gastric Slow Wave ◽  
Intracellular Ca ◽  
Cells Of Cajal

Interstitial cells of Cajal (ICC) are responsible for the spontaneous and omnipresent electrical activity in the stomach. A quantitative description of the intracellular processes whose coordinated activity is believed to generate electrical slow waves has been developed and is presented here. In line with recent experimental evidence, the model describes how the interplay between the mitochondria and the endoplasmic reticulum in cycling intracellular Ca2+ provides the primary regulatory signal for the initiation of the slow wave. The major ion channels that have been identified as influencing slow wave activity have been modeled according to data obtained from isolated ICC. The model has been validated by comparing the simulated profile of the slow waves with experimental recordings and shows good correspondence in terms of frequency, amplitude, and shape in both control and pharmacologically altered conditions.

Gastric myoelectric and motor activity in dogs with gastric dilatation-volvulus

1993 ◽  
Vol 265 (4) ◽  
pp. G646-G653
Author(s):  
J. A. Hall ◽  
T. N. Solie ◽  
H. B. Seim ◽  
D. C. Twedt
Keyword(s):  
Wave Propagation ◽  
Gastric Emptying ◽  
Slow Wave ◽  
Propagation Velocity ◽  
Delayed Gastric Emptying ◽  
Solid Phase ◽  
Phase Iii ◽  
Gastric Dilatation ◽  
Wave Propagation Velocity ◽  
Gastric Slow Wave

Electrical and contractile properties of the stomach were assessed in six adult dogs after recovery from surgical treatment for gastric dilatation-volvulus (GDV), a disorder characterized by delayed gastric emptying of the solid phase. Electrodes and strain-gauge force transducers were sutured to the serosa of the antrum and pylorus at the time of surgical intervention for GDV. Ten days after implantation, electrical and mechanical activities were recorded before and after a standardized meal. The analog FM tape recordings of the electrical and mechanical signals were converted to digital time series for analysis by computer. Recordings from dogs after GDV showed increased slow wave propagation velocity in both the fasting and the fed states compared with controls. In addition, the GDV dogs had atypical fasting state phase III activity fronts. We found no difference in gastric slow wave frequency, dysrhythmia, or electromechanical coupling between the two groups. These results indicate that delayed gastric emptying in this syndrome is associated with increased gastric slow wave propagation velocity.

Effects of pacing parameters on entrainment of gastric slow waves in patients with gastroparesis

1998 ◽  
Vol 274 (1) ◽  
pp. G186-G191 ◽  
Author(s):  
Z. Y. Lin ◽  
R. W. McCallum ◽  
B. D. Schirmer ◽  
J. D. Z. Chen
Keyword(s):  
Slow Wave ◽  
Pulse Width ◽  
Cardiac Pacing ◽  
Slow Waves ◽  
Effective Parameters ◽  
Gastric Pacing ◽  
Gastric Slow Wave ◽  
Gastric Slow Waves ◽  
Baseline Recording ◽  
Ectopic Pacemaker

The aim of this study was to investigate the effect of pacing parameters on the entrainment of gastric slow waves in patients with gastroparesis. Four pairs of cardiac pacing wires were placed on the serosal surface of the stomach in 13 patients with gastroparesis. After a baseline recording for 30 min, gastric pacing was performed in a number of sessions with different effective parameters, each lasting for 30 min. The following parameters were found to be effective for the entrainment of the gastric slow wave: a pacing frequency 10% higher than the intrinsic gastric slow wave frequency (IGF), 300 ms pulse width, and 4 mA pacing amplitude. A reduction of pacing amplitude from 4 to 2 mA and 1 mA reduced the percentage of entrainment of the gastric slow wave to 79 ± 10% and 50 ± 11%, respectively. Pacing with a pulse width of 30 or 3 ms was not able to entrain the gastric slow wave in any of the patients. An ectopic pacemaker of tachygastria found in three patients was reversed with gastric pacing. It was concluded that gastric pacing at a frequency up to 10% higher than the IGF and with an amplitude of 4 mA and a pulse width of 300 ms is able to completely entrain the gastric slow wave and normalize gastric dysrhythmias in patients with gastroparesis.

Effect of cromakalim and lemakalim on slow waves and membrane currents in colonic smooth muscle

1991 ◽  
Vol 260 (2) ◽  
pp. C375-C382 ◽  
Author(s):  
J. M. Post ◽  
R. J. Stevens ◽  
K. M. Sanders ◽  
J. R. Hume
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Slow Wave ◽  
Outward Current ◽  
Wave Activity ◽  
Slow Waves ◽  
Slow Wave Activity ◽  
Ca Current ◽  
K Current ◽  
Stimulation Of

The effects of cromakalim (BRL 34915) and its optical isomer lemakalim (BRL 38227) were investigated in intact tissue and freshly dispersed circular muscle cells from canine proximal colon. Cromakalim and lemakalim hyperpolarized resting membrane potential, shortened the duration of slow waves by abolishing the plateau phase, and decreased the frequency of slow waves. Glyburide, a K channel blocker, prevented the effect of cromakalim on slow-wave activity. The mechanisms of these alterations in slow-wave activity were studied in isolated myocytes under voltage-clamp conditions. Cromakalim and lemakalim increased the magnitude of a time-independent outward K current, but cromakalim also reduced the peak outward K current. Glyburide inhibited lemakalim stimulation of the time-independent background current. Nisoldipine also reduced the peak outward current, and in the presence of nisoldipine, cromakalim did not affect the peak outward component of current. This suggested that cromakalim may block a Ca-dependent component of the outward current. Lemakalim did not affect the peak outward current. We tested whether the effects of cromakalim on outward current might be indirect due to an effect on inward Ca current. Cromakalim, but not lemakalim, was found to inhibit L-type Ca channels; however, glyburide did not alter cromakalim inhibition of inward Ca current. We conclude that the effects of cromakalim and lemakalim on membrane potential and slow waves in colonic smooth muscle appear to result primarily from stimulation of a time-independent background K conductance. The effects of these compounds on channel activity may explain the inhibitory effect of these compounds on contractile activity.

Selective lesioning of interstitial cells of Cajal by methylene blue and light leads to loss of slow waves

1994 ◽  
Vol 266 (3) ◽  
pp. G485-G496 ◽  
Author(s):  
L. W. Liu ◽  
L. Thuneberg ◽  
J. D. Huizinga
Keyword(s):  
Methylene Blue ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Electrical Activity ◽  
Slow Wave ◽  
Interstitial Cells Of Cajal ◽  
Wave Activity ◽  
Slow Waves ◽  
Slow Wave Activity ◽  
Cells Of Cajal

Incubation with 50 microM methylene blue (MB) and subsequent intense illumination resulted in abolition of the slow-wave activity in the submuscular interstitial cells of Cajal-circular muscle (ICC-CM) preparations of canine colon. This was often accompanied by a decrease in resting membrane potential. Repolarization of cells back to -70 mV did not restore the slow-wave activity, indicating that MB plus light directly interrupted the generation mechanism of slow waves. After MB incubation, a 2-min illumination consistently changed the mitochondrial conformation in ICCs from very condensed to orthodox, without inducing any obvious changes in smooth muscle cells. After 4- to 10-min illumination, ICCs became progressively more damaged with swollen and ruptured mitochondria, loss of cytoplasmic contrast and detail, loss of caveolae, and rupture of the plasma membrane. No damage was seen in smooth muscle cells or nerves. Gap junctional ultrastructure was preserved. Intense illumination without preincubation with MB left the slow waves and the ultrastructure of ICC-CM preparations unaffected. In CM preparations, without the submuscular ICC-smooth-muscle network, MB plus light induced no changes in electrical activity. We conclude that the correlation between selective damage to the submuscular ICCs (relative to smooth muscle) and selective loss of the slow-wave activity (relative to other electrical activity of the CM) strongly indicates that the ICCs play an essential role in the generation of slow waves.

scholarly journals High-resolution mapping of gastric slow-wave recovery profiles: biophysical model, methodology, and demonstration of applications

2017 ◽  
Vol 313 (3) ◽  
pp. G265-G276 ◽  
Author(s):  
N. Paskaranandavadivel ◽  
L. K. Cheng ◽  
P. Du ◽  
J. M. Rogers ◽  
G. O’Grady
Keyword(s):  
Wave Propagation ◽  
Wavelet Transform ◽  
High Resolution ◽  
Slow Wave ◽  
Recovery Phase ◽  
Slow Waves ◽  
Gastric Slow Wave ◽  
High Resolution Mapping ◽  
Resolution Mapping ◽  
Extracellular Potentials

Slow waves play a central role in coordinating gastric motor activity. High-resolution mapping of extracellular potentials from the stomach provides spatiotemporal detail on normal and dysrhythmic slow-wave patterns. All mapping studies to date have focused exclusively on tissue activation; however, the recovery phase contains vital information on repolarization heterogeneity, the excitable gap, and refractory tail interactions but has not been investigated. Here, we report a method to identify the recovery phase in slow-wave mapping data. We first developed a mathematical model of unipolar extracellular potentials that result from slow-wave propagation. These simulations showed that tissue repolarization in such a signal is defined by the steepest upstroke beyond the activation phase (activation was defined by accepted convention as the steepest downstroke). Next, we mapped slow-wave propagation in anesthetized pigs by recording unipolar extracellular potentials from a high-resolution array of electrodes on the serosal surface. Following the simulation result, a wavelet transform technique was applied to detect repolarization in each signal by finding the maximum positive slope beyond activation. Activation-recovery (ARi) and recovery-activation (RAi) intervals were then computed. We hypothesized that these measurements of recovery profile would differ for slow waves recorded during normal and spatially dysrhythmic propagation. We found that the ARi of normal activity was greater than dysrhythmic activity (5.1 ± 0.8 vs. 3.8 ± 0.7 s; P < 0.05), whereas RAi was lower (9.7 ± 1.3 vs. 12.2 ± 2.5 s; P < 0.05). During normal propagation, RAi and ARi were linearly related with negative unit slope indicating entrainment of the entire mapped region. This relationship was weakened during dysrhythmia (slope: −0.96 ± 0.2 vs −0.71 ± 0.3; P < 0.05). NEW & NOTEWORTHY The theoretical basis of the extracellular gastric slow-wave recovery phase was defined using mathematical modeling. A novel technique utilizing the wavelet transform was developed and validated to detect the extracellular slow-wave recovery phase. In dysrhythmic wavefronts, the activation-to-recovery interval (ARi) was shorter and recovery-to-activation interval (RAi) was longer compared with normal wavefronts. During normal activation, RAi vs. ARi had a slope of −1, whereas the weakening of the slope indicated a dysrhythmic propagation.

scholarly journals Broadband slow-wave modulation in posterior and anterior cortex tracks distinct states of propofol-induced unconsciousness

2019 ◽  
Author(s):  
Emily P. Stephen ◽  
Gladia C. Hotan ◽  
Eric T. Pierce ◽  
P. Grace Harrell ◽  
John L. Walsh ◽  
...  
Keyword(s):  
Frontal Cortex ◽  
Slow Wave ◽  
Time Course ◽  
Wave Activity ◽  
Slow Waves ◽  
Brain State ◽  
Posterior Cortex ◽  
Anterior Cortex ◽  
Wave Modulation ◽  
Up And Down States

A controversy 5 has developed in recent years over the role that frontal and posterior cortices play in mediating consciousness and unconsciousness. One hypothesis proposes that posterior sensory and association cortices are the principal mediators of consciousness, citing evidence that strong slow-wave activity over posterior cortex during sleep disrupts the contents of dreaming. A competing hypothesis proposes that frontal-posterior interactions are critical to ignite a conscious percept, since activation of frontal cortex appears necessary for perception and can reverse unconsciousness under anesthesia. In both cases, EEG slow-waves (< 1 Hz) are considered evidence that up- and down-states are disrupting cortical activity necessary for consciousness. Here, we used anesthesia to study the interaction between the slow-wave and higher frequency activity in humans. If slow-waves are derived from underlying up and down-states, then they should modulate activity across a broad range of frequencies. We found that this broadband slow-wave modulation does occur: broadband slow-wave modulation occurs over posterior cortex when subjects initially become unconscious, but later encompasses both frontal and posterior cortex when subjects are more deeply anesthetized and likely unarousable. Based on these results, we argue that unconsciousness under anesthesia comprises several shifts in brain state that disrupt the sensory contents of consciousness distinct from arousal and awareness of those contents.Significance StatementThe roles of frontal and posterior cortices in mediating consciousness and unconsciousness are controversial. Disruption of posterior cortex during sleep appears to suppress the contents of dreaming, yet activation of frontal cortex appears necessary for perception and can reverse unconsciousness under anesthesia. We studied the time course of regional cortical disruption, as mediated by slow-wave modulation of broadband activity, during anesthesia-induced unconsciousness in humans. We found that broadband slow-wave modulation covered posterior cortex when subjects initially became unconscious, but later encompassed both frontal and posterior cortex when subjects were deeply anesthetized and likely unarousable. This suggests that unconsciousness under anesthesia comprises several shifts in brain state that disrupt the contents of consciousness distinct from arousal and awareness of those contents.

VI. Pathogenesis and therapeutic approaches to human gastric dysrhythmias

2002 ◽  
Vol 283 (1) ◽  
pp. G8-G15 ◽  
Author(s):  
Chung Owyang ◽  
William L. Hasler
Keyword(s):  
Slow Wave ◽  
Animal Studies ◽  
Nausea And Vomiting ◽  
Causative Role ◽  
Therapeutic Approaches ◽  
Receptor Antagonists ◽  
Gastric Slow Wave ◽  
Dopamine Receptor Antagonists ◽  
Gastric Dysrhythmias ◽  
Intestinal Delivery

This review describes recent advances in our knowledge about the pathogenesis and therapeutic approaches to human gastric dysrhythmias. A number of clinical conditions has been found to be associated with gastric slow-wave rhythm disturbances that may relate to the induction of nausea and vomiting. Human and animal studies indicate that multiple neurohumoral factors are involved in the generation of gastric dysrhythmias. Antral distension and increased intestinal delivery of lipids may cause slow-wave disruption and development of nausea. This may be mediated by cholinergic and serotonergic pathways. Similarly, progesterone and estrogen may also disrupt gastric slow-wave rhythm in susceptible individuals. Prostaglandin overproduction in gastric smooth muscle appears to mediate slow-wave disruption in diabetes and with tobacco smoking. On the other hand, central cholinergic pathways play an important role in the genesis of gastric dysrhythmias associated with motion sickness. This may be mediated by vasopressin released from the pituitary. Although it is difficult to ascribe with certainty a causative role of slow-wave rhythm disturbances in the genesis of nausea and vomiting, the search has begun for novel antiemetic therapies based on their abilities to ablate or prevent gastric dysrhythmia formation. This includes the use of prostaglandin synthesis inhibitors, central muscarinic receptor antagonists, and dopamine receptor antagonists. Finally direct gastric electrical stimulation using a surgically implanted neurostimulator has shown promise in reducing emesis in patients with gastroparesis and gastric dysrhythmias.

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