Disease relevance of Peristalsis

• CONCLUSIONS: Ang II has a salutary effect of protecting kidneys from hydronephrosis during partial ureteral obstruction through its ability to augment ureteral peristalsis [1].
• Return of esophageal peristalsis after nifedipine therapy in patients with idiopathic esophageal achalasia [2].
• We hypothesized that neostigmine would restore peristalsis in patients with acute colonic pseudo-obstruction [3].
• BACKGROUND: Laparoscopic adjustable gastric banding has become the prefered method for the surgical treatment of morbid obesity in Europe. It is not known whether this procedure may induce gastroesophageal reflux and whether it may impair esophageal peristalsis [4].
• Using trans-synaptic tracing with pseudorabies virus (PRV), immunocytochemistry and histochemistry, we have demonstrated the expression of NMDAR1 and nitric oxide synthase (NOS) within brain stem neurons controlling esophageal peristalsis [5].

Psychiatry related information on Peristalsis

• Motor activity of the rat duodenum in vivo: evidence for the existence of an atropine-resistant peristalsis [6].

High impact information on Peristalsis

• We administered 1 mg of glucagon intravenously immediately before CT scanning to minimize the degree of smooth-muscle spasm and peristalsis and to reduce the patient's discomfort [7].
• Isolated lower esophageal sphincter (LES) relaxation, defined as a transient sphincteric relaxation unaccompanied by esophageal peristalsis, has been shown to precede most episodes of gastroesophageal reflux in humans [8].
• Brain-derived neurotrophic factor augments peristalsis by augmenting 5-HT and calcitonin gene-related peptide release [9].
• CONCLUSIONS: Our results indicate that endogenous 5-HT is involved in the modulation of circular muscle accommodation during the preparatory phase of peristalsis via the activation of 5-HT7 receptors expressed by neurons in addition to smooth muscle cells [10].
• Blockade of muscarinic or nicotinic receptors by hyoscine or hexamethonium decelerated peristalsis up to propulsion arrest [11].

Chemical compound and disease context of Peristalsis

• Pathologic processes that affect the intestine generally result in decreased peristalsis and bowel wall thickening, both of which tend to decrease the luminal gas content [12].
• Despite receiving metoclopramide, barium studies revealed gastroparesis, a significant decrease in gastric peristalsis, and reflux [13].
• The effect of pentagastrin on esophageal peristalsis in patients with diffuse esophageal spasm may be explained as denervation supersensitivity [14].
• X-rays of ethosuximide-treated rats showed GI hypotonia, disturbed peristalsis and decreased evacuation activity [15].
• If not formally demonstrated in this study, it is suggested that metabolic and hepatic changes observed during the peripartum, could result in a disruption of the intestinal ecosystem (pH, volatile fatty acids, NH3, peristalsis) and in the emergence of a Salmonella population [16].

Biological context of Peristalsis

• Nitric oxide (NO) is associated with functions as diverse as peristalsis, blood flow, neuroendosecretion, visual transduction, smooth muscle relaxation, and microbial killing (H. H. W. H. Schmidt and V. Walter, Cell 78:919-925, 1994) [17].
• To elucidate the possible functional significance of sensory neuropeptides in visceral organs of mammals and birds the distribution, binding sites and the effects on ureteric peristalsis of substance P and calcitonin gene-related peptide (CGRP) were investigated in the ureter of guinea-pigs and chickens [18].
• In this paper, we show that a small deletion, which eliminates H2.0, has no detectable effect on normal gut morphogenesis, visceral muscle actin organization, or larval peristalsis [19].
• 1. Since the cyclo-oxygenase (COX) isoform-nonselective inhibitor indomethacin is known to modify intestinal motility, we analysed the effects of COX-1 and COX-2 inhibition on intestinal peristalsis [20].
• Metoclopramide causes a small and nonsignificant increase in LES pressure, has no effect on esophageal peristalsis, and increases the rate of gastric emptying of a liquid meal [21].

Anatomical context of Peristalsis

• After GER the esophagus was generally cleared of refluxed acid by primary peristalsis and less frequently by secondary peristalsis [22].
• (2) L-NMMA given ICV significantly reduced the number of oropharyngeal swallows and the incidence of primary peristalsis in both smooth and striated muscle, but the reduction in amplitude was significant only for the smooth muscle contraction [23].
• Recent human studies suggest that oesophageal HCO3- secretion, in conjunction with salivary HCO3- secretion and secondary oesophageal peristalsis, is important for the protection of oesophageal mucosa from refluxed gastric contents [24].
• It is concluded that P2X3 subunit-containing receptors participate in neural pathways underlying peristalsis in the mouse intestine in vitro [25].
• RESULTS: CCh (0.1 to 1.0 microg/kg intravenously) dose dependently decreased elevated pressure and peristalsis in completely and partially obstructed ureters, respectively, and increased intravesical isovolumetric pressure [26].

Associations of Peristalsis with chemical compounds

• Radiologically, segmental tertiary activity (complete luminal obliteration) was always associated with disrupted primary peristalsis, but nonsegmental tertiary activity was often seen with normal bolus transit and did not have a specific manometric correlate [27].
• METHODS: (1) The effect of intravenous (IV) NOS inhibitor N(G)-nitro-L-arginine (L-NNA) on swallowing and swallowing-induced peristalsis was examined [23].
• There were no changes in sphincter relaxation or in peristalsis, velocity, or duration of contraction with any dose of nifedipine [28].
• BACKGROUND & AIMS: Nitric oxide controls lower esophageal sphincter (LES) relaxation and esophageal peristalsis in opossums, but its role in the control of esophageal motility in humans is not defined [29].
• The effect of L-NMMA was evaluated on water swallow-evoked primary peristalsis (n = 8; single-blind, placebo-controlled) and on the rate of TLESRs during gastric distention (n = 8; double-blind, placebo-controlled) [30].

Gene context of Peristalsis

• NT-3 is required for the differentiation, maintenance and proper physiological function of late-developing enteric neurons that are important for the control of gut peristalsis [31].
• Small (nanomolar) quantities of NO produced by calcium-dependent nNOS play a physiological role in peristalsis and sphincter function of the intestine [32].
• In summary, NK1 receptors play a role in normal development of peristalsis and NK1 receptor activation markedly increases propulsive peristaltic contractile activity [33].
• c-kit and ureteral peristalsis [34].
• Inhibition of motility by CGRP could be important for setting the frequency of ureteral peristalsis and suppression of latent pacemakers to prevent the occurrence of antiperistaltic waves [35].

Analytical, diagnostic and therapeutic context of Peristalsis

• Lower esophageal sphincter pressure and relaxation and esophageal contraction amplitude, peristalsis, velocity, and duration after wet swallows were determined before and for 120 min after the sublingual/buccal administration of placebo and of nifedipine in doses of 10, 20, 30, and 40 mg [28].
• Intravenous infusion of prostaglandin F2alpha (0-05 to 0-8 mug kg-minus1) produced marked, dose-related and sustained elevation of cardiac sphincter pressure without significantly affecting oesophageal peristalsis or gastric fundal motility [36].
• Esophageal manometry demonstrated decreased lower esophageal sphincter pressures and low amplitude peristalsis; 24-hour esophageal pH monitoring revealed significant gastroesophageal reflux [37].
• Metoclopramide effect on esophageal peristalsis in normal human volunteers [38].
• In six greyhound dogs, ureteral peristalsis transiently ceased following the intravenous injection of glucagon [39].

References