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Newer Review of the Traction Procedure's Ability to Treat Gastroparesis

Posted by screeb , 09 April 2012 · 404 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
Background: A study found that the long-term consumption of caffeine can induce ventriculomegaly. In the caffeine-treated rats with ventriculomegaly, there was increased production of CSF , associated with the increased expression of Na(+), K(+)ATPase and increased cerebral blood flow (CBF). In contrast, acute treatment with caffeine decreased the production of CSF, suggesting ‘effect inversion’ associated with caffeine, which was mediated by increased expression of the A1 adenosine receptor, in the chroid plexus (CP) of rats chronically treated with caffeine. Adenonosine receptor signaling can regulate the production of CSF by controlling the expression of Na(+), K(+) ATPase and CBF, decreased by caffeine, causing decreased CSF production into ventricles. ANP titers in human CSF have previously been shown to increase proportionally to increments in ICP (intra-cranial pressure). Therefore, caffeine decreases CSF production via decreased ICP at the CPs. The above system is directly proportional to AQP1 (aquaporin 1) system expressed at the CP. AQP is activated by an endogenous receptor guanylate cyclase for atrial natriuretic peptide (ANP). AQP1 Current activation decreases the normal basal-to-apical fluid transport equivalent to decreased CSF-pressure. The cGMP (cyclic Guanosine monophosphate)-gated conductance has properties of permeability to Na+, K+ , and dependence on cGMP. Thus , AQP1 can function as both a water channel and a gated ion channel. To maintain CSF-pressure equilibrium, when the Na+, K+ ATPase system increased, (to decrease CSF-pressure), the ANP system must be decreased by receptor internalization, but is at an excess before its elimination. The excess ANP is a ligand for NPR-A (ANP receptors) receptors via ICP through the central canal to the Fourth ventricle, causing cGMP increasing fluid out.
Stimulation of aquaporin-mediated fluid transport by cyclic GMP with ANP (stimulating the natriuretic signaling pathway) , would induce a net apical-to-basal transport of fluid. NPR-C neutralizes ANP by receptor internalization at the basal lamina of the CP, thus slowing down CSF production. The distribution of NPR-A in eel was examined . The immunoreactive neurons in the glossopharyngeal-vagal motor complex were observed via auto-radiography.
The projections of primary afferents from rostral cervical segments to the brainstem and the spinal cord of the rat were investigated by using anterograde transport techniques. Lateral collaterals projected mainly to the lateral spinal lamina V. Results from transganglionic staining indicated the lateral collaterals were contributed to by suboccipital proprioceptive fibers. The spinothalamic tract (STT) arises primarily from cells in lamina I of the dorsal horn, from lamina V cells and respond only to noxious mechanical stimuli. STT cells of lamina V tend to respond to both innocuous and noxious stimuli. Using anterograde transport , it was found that there is a substantial projection of the dorsal STT to the posterior nuclei (Po). There is increased activity in the primary somatosensory cortex (SI) a major projection target of Po that plays an important role in processing sensory-discriminative aspects of pain. STT axons passed through Po thalamus en route to VP, (I.E. the Po is caudal to the primary somatosensory nuclei,--in the ventral posterior thalamus). The Po thalamus palys a qualitiatvely different role in pain sensation from the VP. Although the role of SI in nociceptive processing is controversial, several lines of evidence support the notion the SI is a key component of the cortical network that is responsible for pain perception. With regard for the specific role SI may play in pain processing, electrphysiological studies in animals and human functional neuroimaging studies have found that SI encodes stimulus intensity.
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.
Mesenteric veins are more sensitive than arteries to the constrictor effects of sympathetic nerve stimulation. Norepinephrine induced constriction from concentration-response curves were left-shifted in veins compared to arteries.
The equation of momentum conservation together with the constitutive relation for a Newtonian fluid yield the famous Navier-Stokes equations, which are the principal conditions to be satisfied by a fluid as it flows. The fluid flow patterns in laminar flow are also called potential flow, because its linear velocity is the gradient of some function called the velocity potential. Potential flow is represented by the Laplace equation. The vascular system was analyzed as being analogous to an electrical transmission line where various influences on BP wre described in quantitative terms via the Navier-Stokes equation, for the transmitted wave’s homodynamic character. This was an exact analogy to an electrical transmission line where pressure is analogous to voltage, flow is analogous to current, and the hydraulic parameters of resistance ®, inductance (L), and capacitance © are analogous to their electrical equivalents. It is interesting to note that the transmission co-efficient across the pre-capillary sphincter plexus increases to greater than 1, which would produce an increase in blood pressure at the venous system inlet,( see references).
A key part of the theory involves adrenal sympathetic nerves and epinephrine secretion as the result of the use of a cervical traction apparatus. This causes vasodilation of the mesenteric veins that project to the hepatic portal vein. Inhalation compresses the splanchnic-hepatic arteries causing an inveresly proportional decrease in portal vein pressure. The increased pressure at the hepatic arterioles projects to the hepatic veinules via an increased transmission coeffecient at the sinusoids. The reference for this last concept was written by my father. Other concepts involve an Abdominal Circulaory Pump which applies the math of the "vascular waterfall," and to show the concept in another light, there is an inverse-Winkesel explaining how the systolic pulse, propagates the venous wave. In other words, the nitty-gritty of the equations hasn't been performed in this paper, but can be obtained from the formulas in the references.

The present conception of the arterial and the venous system in an extension of the hydraulic pressure reservoir model to a dynamic model in which arterial and venous Winkessel pressures vary during the cardiac cycle in precise proportion to the volumes that they contain. During diastole, the arterial reservoir discharges and the venous reservoir charges; during systole, the arterial reservoir charges and the venous reservoir discharges. The term “Windkessel” is used to describe the change in pressure associated with the dynamic variation in reservoir volume.
The venous system behaves as waves propagating on a time-varying reservoir, the venous Windkessel, which is the exact analog of the author’s study of the arterial Winkessel, but with reversed functionality. The exponential rise of P(IVC)—inferior vena cava pressure—is due to the charging of the venous reservoir by blood flowing into it from the arterial system. The pressure associated with waves is the excess pressure—P (ex), which is the difference between the observed pressure P (IVC), and the reservoir pressure P (Wk).
The approach incorporates a three element Windkessel, the impedance-analysis approach. The venous Windkessel is is an upside-down version of the arterial Windkessel. The fact that the mean arterial Windkessel pressure is entirely consistent with blood flowing through a large-artery resistance. Instantaneous flow out of the arterial Windkessel is proportional to the difference between P Wk-a and P-a, so the difference between mean PWK-a and P-a should govern Winkessel outflow during the cycle. The same is true of the venous system. The fact that mean IVC pressure is measurably lower than mean venous winkessel pressure is consistent with blood flowing through a large-vein resistance. Also, according to the theory given above, instantaneous flow into the venous Windkessel is proportional to the divergence between P-v and P WK-v, and so the difference between mean P-v and P-wk-v should govern venous windkessel inflow during the cycle. Finally, the resistance between the arterial and venous Windkessels should be a function of the difference between P-a and P-v. The fraction of total systemic venous resistance accounted for by the microcirculatory resistance may vary widely from ~40% (e.g. methoxamine) to ~15% (e.g. sodium nitroprusside).
The splanchnic circulation receives 25% of cardiac output, and splanchnic flow would be expected to rise. Blood in the splanchnic vasculature can be transferred to the systemic circulation. Blood shifts in normal subjects by measuring changes in body volume by whole body pletysmography, during contractions of the diaphragm and abdominal muscles were quantified. Because both breathing with gas expansion or compression resulted in rapid emptying from the liver followed by slower flow from non-hepatic viscera, splanchnic flow fell and rose, where splanchnic emptying shifted up to 650 ml of blood. With emptying, the increased hepatic vein flow increases the blood pressure at its entry into the inferior vena cava and abolishes the pressure gradient producing flow between the femoral vein and the IVC.
Blood in the splanchnic vasculature can be transferred out by step increases in abdominal pressure (inhalation) (Pab), resulting in rapid emptying presumably from the liver followed by slower flow from non-hepatic viscera. Splanchnic emptying shifted up to 650 ml blood. With emptying, the increased hepatic vein flow increases the blood pressure at its entry into the IVC and abolishes the pressure gradient producing flow between the IVC, inferior to the hepatic vein and the IVC superior to it. Compression of the IVC results in a vascular waterfall, where the pressure driving flow out of the splanchnic vasculature into the IVC is Pmc (mean circulatory pressure), whereas at the downstream end it is Picv-Pab. It is important to remember that Pmc-Pab is the elastic recoil pressure of the splanchnic vasculature. When P-ab increases and blood flows out of the splanchnic bed, the elastic recoil pressure both decrease. Nevertheless as long as Pivc>Pab, flow is proportional to Pmc-Pivc. Epinephrine increased the contribution of the splanchnic venous blood flow. These results indicate that venous blood flow increase in the splanchnic vessels largely determined the formation of changes in the IVC blood flow in response the catecholamines, causing RAP (right atrial pressure) and ANP release from cardiac tissue.
NPR-A and NPR-B have the membrane-bound particulate guanylate cyclase (pGC), which can catalyze the formation of cGMP from GTP, (guanosine tri-phosphate). NPRs are distributed in gastric smooth muscle layers. Studies have confirmed that ANP-synthesizing cells exist in different regions of the gastric mucosa in rats, therefore, ANP can be considered an endogenous natriuretic peptide of gastric mucosa.
Tetrahydrobioperin (BH 4), an essential co-factor for NOS is intracellularly produced from GTP via GTP-cyclohydrolase I and acts as a redox switch in the oxygenase domain of NOS. Reduced levels of BH4 impair the production of NO and lead to increased superoxide radical production. BH4 deficiency has been associated with diabetic complications including gastroparesis. Decreased availability of BH4 and nNOS (neuronal nitric oxide synthase) uncoupling which results in impaired nitrergic relaxation and thus gastroparesis.
Conclusion-- The CNS is projected to by muscle spindle afferents of the sub-occipital region of the neck (activated by a cervical traction apparatus). This triggers a dual input to the Po along with SP (substance pain)-Lamina I projections from the colonic-extrinsic primary afferent nerves. The increased pain intensity encoding produced by caffeine consumption leads to an epinephrine secretion that causes an increase in venous pressure across the capillary plexus that in an “Abdominal Circulatory Pump” fashion, causes a splanchnic recoil that is discharged during the vascular waterfall created between the femoral vein and IVC. I can feel a side sensation that corresponds to splanchnic vascular filling, and an upper-central (spinal area) back pain at the end of inhalation that corresponds to the liver draining through the hepatic veins. This venous pulse goes to the right atrium causing RAP (right atrial pressure) which produces ANP that is not in the brain’s CSF. This ANP goes systemic, hitting the gastric blood supply and increasing BH4 and nNOS causing pyloric relaxation and gastric emptying.


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