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New Review of Traction Therapy 's ability to treat Delayed Gastric Emptying

Posted by screeb , 19 February 2012 · 167 views

Abstract -- Delayed gastric emptying (GE) is called gastroparesis (associated with Irritable Bowel Syndrome -constipation). The following procedure was developed to produce gastric emptying. Drinking coffee is a pre-requisite for the anti-gastro paretic effects of the procedure. The procedure, in a nutshell, is this: for one hour after taking coffee and rocking on one’s side, gastric emptying of coffee is induced (and palpable). The above steps are necessary for the cervical traction device (TD) to function after the application of TD, in which one lies on one’s side while performing neck pulls. The following analysis of the inputs of the procedure uses known research about how the steps of the procedure work
Pathophysiology—Rapid gastric emptying, rather than delayed gastric emptying, might provoke functional dyspepsia (FD) with gastroparesis. Abnormal gastric emptying in patients with FD had profiles in which rapid gastric emptying during the midpostcibal period, which means abnormal inhibition in the middle phase, and rapid gastric emptying during the early postcibal period, which means overly rapid emptying in the early phase, were present. As the result of hastened gastric emptying, plasma glucose is elevated postprandially. Hyperglycemia led to a significant reduction in adipocyte apoE (apolipoprotein E) mRNA levels. ApoE is important in modulating triglyceride metabolism in adipocytes. In ApoE-KO (knock-out) mice, the superoxide derived from NADPH oxidase reacts with NO to form peroxynitrite wnich induces oxidative degradation of tetrahydrobiopterin (BH4). BH4, a co-factor for nNOS, restores gastric emptying and nNOS expression. Pyloric sphincter manometry was performed in wild-type controls, and neuronal nitric oxide synthase-deficient (nNos(-/-)) mice. In nNOS(-/-) mice, loss of nitrergic pyloric inhibition (sphincter relaxation), leads to gastric stasis.
Cholecystokinin (CCK) controls nutrient delivery to the small intestine by inhibiting gastric emptying. Vagal afferent neurons are a primary target of CCK and are now recognized as an important site of integration of peripheral signals regulating ingestion. With obesity, there is decreased stimulation of vagal afferent neurons by CCK (cholecystokinin), and there is reduced stimulation of jejunal afferent fibers by CCK. The reduced glutaminergic input from vagal afferent neurons decreases NTS (brain stem) gliotransmitter projection to the DMV.
The objective to stimulate gut and bowel motility is to activate the DMV. The process is analogous to a vacuum tube circuit with the emitter being afferent vagal input (which is decreased by decreased sensitivity to CCK), the control grid being the NTS (being either amplifying or suppressing) depending on the upstream glutamate (electron-like) flow, and finally, the DMV is the collector of glutamate, which allows glutamate flow depending on IRS-2 stimulation by INS at the liver.
The nucleus of the solitary tract (NTS), located in the dorsal medulla, plays a significant role tor NTS astrocytes in the modulation of homeostatic reflexes, in particular gastric reflexes. The relationship of glia to neurons is not merely supportive but potentially interactive. Neuronally driven increases in astrocytic intracellular calcium ([Ca2]i) can lead to modulation of synaptic strength produced by the release of neuroactive compounds by astrocytes, often referred to as ‘gliotransmitters.” NTS astrocytes activate NTS neurons via glutamate gliotransmission, and NTS astrocytes are activated directly by glutamatergic inputs from vagal afferents.

Stimulation of astrocytic AMPA receptors (AMPAR—a subunit of NMDA, GluR1), induced activation of NTS astrocytes. The NTS uses AMPAR signaling to increase astrocytic [Ca2+]I to produce a rapid response to induce gliotransmitter release that is time-locked to bursts of local vagal afferent input. This could be rapid glial amplification or attenuation of vago-vagal reflex sensitivity.

Treatment--Caffeine causes INS release which ends up stimulating the DMV (collector), via increased INS overcoming INS resistance. The explanation of the Traction device's function is that it stretches the neck and activates the adrenal glands. Adrenaline stimulates vagal afferents (the emitter). Traction must be used after caffeine is digested, to turn on electricity to the amplifier circuit that is set up via INS at IRS-2(Insulin Receptor Substrate -2) receptors, connecting the NTS with the DMV synaptically.
The gastric emptying of coffee (caffeine) causes insulin (INS) exocytosis. Caffeine is a ryanodine receptor agonist and has recently been shown to increase luminal [Ca(2+)]I at beta cells, causing INS release. INS enhances transient receptor potential vanilloid type 1 (TRPV1) mediated currents. The expression of TRPV1 in the DMV is present as well as TRPV1 receptors at liver-related preautonomic neurons, suggesting that insulin and TRPV1 actions may affect liver-related preautonomic neurons. The TRPV1 agonist capsaicin robustly enhanced glutamate release onto DMV neurons by acting at preterminal receptors, and induced TRPV1 receptor trafficking to the terminal membrane of the DMV. TRPV1 is a glutamate channel across the axon terminal/receptor synapse. The DMV integrates peripheral and central signals and sends efferent output to the gastrointestinal system and stomach.
Another effect of caffeine’s INS production is that INS suppresses lipolysis and by dampening SNS outflow to adipose tissue, INS reduces hepatic glucose production. The reduction in hyperglycemia after digestion of caffeine, but before Traction, decreases blood sugar by 15 mG/dL (n=9 for S.D.). INS also blunts the response of glucose-excited neurons in the ventrolateral-ventromedial hypothalamic nucleus to decreased glucose. The continued decrease in lypolysis, sustains the hypoglycemia and decreases epinephrine production.
In general, in central nervous system adrenal sympathetic efferent nerve activity and catecholamine secretion increase in response to noxious somatic stimulation. To determine whether noxious movements of the mechanoreceptor-rich deep tissues of the neck modulate the sympathetic outflow to the adrenal glands, a computer driven small animal manipulator was used to impose ramp and hold rotational displacements of the 2nd vertebra while recording multi-unit activity from sympathetic nerves innervations the adrenal gland. The data suggest that noxious stimuli may modulate sympathetic outflow.
There is catecholamine-induced activation of vagal afferent pathways (in regulation of sympathoadrenal system activity—a negative feedback loop). This turns on glutamate inflow (cathode) to the NTS (control grid), and produces vagal efferent outflow (the collector) to the stomach. In nNOS(-/-) mice, (with decreased apoE), vagal efferent stimulation paradoxically increase pyloric motility. The connections described here are a reverse engineering analysis of how the Traction procedure works.

Motoyasu et al., “Rapid gastric emptying, rather than delayed gastric emptying, , might provoke functional dyspepsia.” J Gastro and Hepat, 2011;26 : 75-78.
Falken et al., “Actions of prolonged ghrelin infusion on gastrointestinal transit and glucose homeostasis in humans.” Neurogastroenterol Motil, 2010; 22(6), e192-200.
Espiritu et al., “Hyperglycemia and advanced glycosylation end products suppress adipocyte apoE expression: implications for adipocyte triglyceride metabolism.” Am J Physiol Endocrinol Metab, 2010; 299(4): e615-23.
Ravella K, Yang H, Gangula P, “Impairment of gastric nitrergic and NRF2 system in Apolipoprotein E Knockout Mice,” 2-3- 2012, Dig Dis Sci; epub ahead of print.
Sivarao DV, Mashimo H, Goyal RK, “Pyloric sphincter dysfunction in nNOS-/- and W/Wv mutant mice: animal models of gastroparesis and duodenogastric reflux,” Gastroenterol, 2008; 135(4): 1258-66.
Dockray, Graham J., ‘Cholecystokinin,” Current Opinion in Endocrinology, Diabetes, and Obesity, 2012; 19(1):8-12.
McDougal DH, Herrman GE, Rogers RC, “Vagal afferent stimulation activates astrocytes in the nucleus of the solitary tract via AMPA receptors: evidence of an atypical neural-glial interaction in the brainstem,” J Neurosci, 2011;31(39): 14037-45.
Bolton P, Budgell B, Kimpton A, “Influence of innocuous cervical vertebral movement on the efferent innervations of the adrenal gland in the rat.” Auton Neurosci, 2006;124: 103-11.
Choi et al., “Ca-induced Ca release from internal stores in INS-1 rat insulinoma cells,” Korean J Physiol Pharmacol, 2011; 15(1): 53-9.
Zsombok A et al., “Functional plasticity of central TRPV1 receptors in brainstem dorsal vagal complex circuits of streptozotocin-treated hyperglycemic mice,” J Neurosci, 2011; 31(39): 14024-31.
Scherer et al, “Brain insulin controle adipose tissue lypolysis and lipogenesis.” Cell Metab, 2011; 13(2): 183- 194.
Mravec B, “Role of catecholamine-induced activation of vagal afferent pathways in regulation of sympathoadrenal system activity: negative feedback loop of stress response.” Endocrine Regulations, 2011; 45:37-41.






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