Viktig bilde av hva som går galt i kapillærene ved skade, betennelse, o.l. Selv om vi har angiogenese så produseres det helt feil når andre ting ikke stemmer.
Når sympaticus nervesystemet aktiveres lukkes kapillærene så blodet størmmer i de større årene. Mindre oksygen fraktes til vevet.
Studie som nevner svært mye interessant om blodsirkulasjon, tensegritet og om bindevev. Den er rettet mot en spesifikk metode for spontan bevegelse, men har mye interessante teamer som gjelder andre bodyworkmetoder også.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3242644/
«Vascular research especially made a jump forward with the Nobel Prize awarded to Furchgott, Ignarro and Murad for having discovered the endogenous production of nitric oxide (NO). »
«Mesenchyme differentiates and generates every type of connective tissue and many organs in adults(3) including bone, muscle, and the middle layer of the skin, excepting nervous tissue and the digestive track(7).»
«In this study, one can notice that they are totally or partially at the origin of vascular endothelium and mesothelium (peritoneum, pleura, pericardium)(6). And this vascular endothelium is the origin of blood, which is also considered as specialized connective tissue(6).»
Forskjellen mellom arterier og kapillærer:
«Capillaries have the function of distributing blood in the body, bringing about an exchange between blood and tissues. Structurally, arteries carry and separate blood and tissues.»
«Fascia is a very sensitive tissue that detects any kind of stress — physical, emotional or psycho-social. It reacts by contracting and imprisoning the organs it covers, thus impairing their physiological functions. Furthermore, the tightening of their connective parts induces a perceptible disturbance in mobility and rhythm of these organs.»
«ECs respond to increased blood flow by causing relaxation of the surrounding VSMCs. VSMC relaxation in response to flow occurs over seconds to minutes and if high flow persists, remodeling of the artery wall enlarges the lumen over time in a period of weeks to months(36). Decreased flow induces vessel narrowing(37), and extreme low flow may lead to complete vessel regression, which involves apoptosis of the ECs(38).»
«The human body seems to be made of the only and same tissue which is functionally differentiated: there are only tissue connections, simply a histological continuum without any clear separation between the skin and hypodermis, the vessels, the aponeurosis, and the muscles(46). So connective tissue, its cells, MEC, and fibers are an obvious link in this construction.»
«The theory of tensegrity emerged from the interests of architects (from Richard Buckminster Fuller to Rene Motro) and biologists (Donald Ingber(47)), and their meeting point of connection with our discussion can be found in these definitions: “a type of prestressed structural network, composed of opposing tension and compression elements that self-stabilizes its shape through establishment of a mechanical force balance”, and “tensegrity is used to stabilize the shape of living cells, tissue and organs, as well as our whole bodies”(4). Hence, the use of this architectural system for structural organization provides a mechanism to physically integrate part and whole(4).»
«Arteries have a special relation with fascias. Connective tissue is present in the three tunics of the artery. Adventitia is a typical sheathing fascia, which becomes tense in reaction to stress. Media is an association of muscle and connective tissue reacting to local mechanical variations (i.e. blood pressure) or general influence (i.e. stress) by tensing and/or by contracting. Intima, whose endothelium can be assimilated to a very big autocrine/paracrine formation(48)reacting mainly to the influence of blood qualities (i.e. type of flow, components), lies on a connective layer underlining endothelium.»
Om bindevevets struktur, mye om mechanoreceptors i bindevevet (golgi, ruffini og pacini spesielt), pluss den nevner «dynamic ligaments» som en del av bindevevet inni og igjennom muskler.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3091473/
«The discrimination between so-called joint receptors and muscle receptors is an artificial distinction when function is considered. Mechanoreceptors, also the so-called muscle receptors, are arranged in the context of force circumstances-that is, of the architecture of muscle and connective tissue rather than of the classical anatomic structures such as muscle, capsules, and ligaments. »
«The receptors for proprioception are concentrated in those areas where tensile stresses are conveyed over the elbow joint. Structures cannot be divided into either joint receptors or muscle receptors when muscular and collagenous connective tissue structures function in series to maintain joint integrity and stability. In vivo, those connective tissue structures are strained during movements of the skeletal parts, those movements in turn being induced and led by tension in muscular tissue. In principle, because of the architecture, receptors can also be stimulated by changes in muscle tension without skeletal movement, or by skeletal movement without change in muscle tension. »
«A mutual relationship exists between structure (and function) of the mechanoreceptors and the architecture of the muscular and regular dense connective tissue. Both are instrumental in the coding of proprioceptive information to the central nervous system.»
«Schleip mentions the fascia as «the dense irregular connective tissue that surrounds and connects every muscle, even the tiniest myofibril, and every single organ of the body forming continuity throughout the body.»(
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Destroy user interface control2,
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Destroy user interface control3) In this way, fascia is considered an important integrative element in human posture and movement organization (locomotor apparatus) and is often referred to as the «organ of form.»(
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Destroy user interface control4) »
«The primary connective tissue of the body is the embryonic mesoderm. The mesoderm represents the matrix and environment within which the organs and structures of the body have been differentiated and therefore are embedded.»
«The principal function of mesoderm as «inner tissue» is «mediating» in the sense of «connecting» (binding) and «disconnecting» (shaping space). »
«Regular dense connective tissue structures such as ligaments convey (transmit) those forces «passively.»»
«Connective tissue and fasciae are richly innervated. Fascial layers may thus play an important role in proprioception and nociception. Considerations such as «architecture versus anatomy (topography),»mutatis mutandis may also apply for the spatial organization of mechanoreceptors, the morphologic substrate for proprioception. »
«Mechanoreceptors are in fact free nerve endings (FNEs), whether or not equipped with specialized end organs. The main stimulus for such receptors is deformation. Variation exists as to the microarchitecture of the ending.»
«Mechanoreceptors associated with muscles, including the muscle auxiliary structures such as tendons, are usually classified(14–
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The mechanoreceptors typically associated with joints are these:
«Those nerve fibers are involved in the afferent pathway of proprioceptive information from the transitional areas between the connective tissue layers and the muscle fascicles organized in series with them [shown schematically in Fig. 7(a)]. This also seems to represent a more ligamentous or articular «pattern of innervation» compared with the related nerve fascicles running on the «outside» of the innervated structure. This is actually a typical capsular or articular pattern [see Fig. 7(a)]. »
«An in series unit of muscular tissue/RDCT layer/skeletal element equipped with mechanosensitive substrate at the transitional areas between the various tissue components constitutes the basic unit of the spatial organization of the substrate of proprioception. Such a unit may occur as a muscle fraction in series with a muscle compartment wall that is shared with the muscular tissue of an adjacent muscle. It may also appear as a muscle compartment wall with muscle fascicles inserting unilaterally and with afferent nerve fibers reaching the related mechanoreceptors from the outer side. This was introduced earlier as the typical «dynamic ligament» (dynament-see Fig. 10, pattern 4).»
«The conclusion is that, in vivo, the activity of a mechanoreceptor is defined not only by its functional properties, but also by its architectural environment. If Abrahams, Richmond, and Bakker(
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Destroy user interface control34) state that the topography of mechanoreceptors provides a «subtle comparative function in the process of sensory coding of muscle events,» they raise the important issue of the spatial distribution of receptors in the process of proprioception. To this should be added the notion that the architecture of the muscular and connective tissue and consequent receptor distribution plays a significant role in the coding of the proprioceptive information that is provided.»
Om slump test for å finne ut av nevropatisk smerte eller betennelse.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2565641/
«While non-neural structures such as subcutaneous connective tissues, skin, blood vessels, and fascia may also be placed under increasing loads during neural tissue testing, Coppieters et al demonstrated that successive stages of the Slump Test did not alter the perception of experimentally induced muscle pain (i.e., non-neural pain). This finding provides some validation for use of the Slump Test in the examination of neural structures.»
«The procedure was divided into four stages:
«All responses were located in the back or neck for the 29.8% of subjects who experienced a sensory response during SS, but for the subsequent three stages of the test, the vast majority of responses were located in the thigh, knee, or calf (Table 1)»
«A positive Slump Test implicates neural tissue as the source of symptoms. As found in this study, responses other than the presenting symptoms may simply be an artefact of the test, typical of the normal response in asymptomatic subjects; such responses must not be assumed to indicate a positive Slump Test. Bilateral comparison is advocated in interpreting this test.»
Om triggerpunkter og hvordan muskelspenninger gir oksygenmangel som så fører til melkesyreopphopning. Nevner også at capillærer trekker seg sammen. En annen studie som det refereres til viser bilder og grafer av hvordan dette skjer; økt blodoppsamling pga trange kapillære vener der blodet strømmer ut fra triggerpunktet.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3440564/#__ffn_sectitle
«Since the capillary blood pressure ranges from approximately 35 mm Hg at the beginning (arterial side) to 15 mm Hg at the end of the capillary beds (venous side), the capillary blood flow is temporarily obstructed during muscle contractions. The blood flow recovers immediately with relaxation, which is consistent with its normal physiological mechanism. In dynamic rhythmic contractions, intramuscular blood flow is enhanced by this contraction-relaxation rhythm, also known as the muscular pump. During sustained muscle contractions, however, muscle metabolism is highly dependent upon oxygen and glucose, which are in short supply.»
«Since oxygen and glucose are required for the synthesis of adenosine triphosphate (ATP), which provides the energy needed for muscle contractions, sustained contractions may cause a local energy crisis due to the lack of oxygen. To guarantee an adequate supply of ATP, the muscle can switch within a few seconds to anaerobic glycolysis. »
«Under anaerobic circumstances, however, most of the pyruvic acid produced during glycolysis is converted into lactic acid, thereby increasing the intramuscular acidity (pH). Most of the lactic acid diffuses out of the muscle into the bloodstream; post-exercise lactic acid is washed out within 30 minutes after exercise. Unfortunately, when the capillary circulation is restricted, as in sustained low-level contractions, this process comes to a standstill.»
«Small increases of the H+ concentration, as seen with inflammation, heavy muscle work, and ischemia, are sufficient to excite muscle group IV endings, contributing to mechanical hyperalgesia and central sensitization (15).»
«They identified 2 contributing factors, namely an increase in the volume of the vascular compartment, and an increased outflow resistance. Increased outflow resistance could be due to muscle contractures at the TrP that compress the capillary or venous bed. Sustained low-level contractions are common in the workplace where many occupations rely on prolonged postures, as seen in musicians, supermarket cashiers, computer operators, hairdressers, and dentists, among others.» Bilder ref til denne studies: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3493167/
«Hägg suggested that the continuous activity of these motor units in sustained contractions causes overuse muscle fiber damage, especially to the Type I fibers during low-level activities, which he summarized in his Cinderella hypothesis21. It is conceivable that in sustained low-level contractions and in dynamic repetitive contractions, ischemia, hypoxia and insufficient ATP synthesis in type I motor unit fibers are responsible for increasing acidity, Ca2+ accumulation, and subsequently sarcomere contracture. Furthermore, starting with the sarcomere (super-) contraction, the intramuscular perfusion slows down and ischemia and hypoxia will occur. This may lead to the release of several sensitizing substances causing peripheral sensitization15,22.»
«A key factor is the local ischemia, which leads to a lowered pH and a subsequent release of several inflammatory mediators in muscle tissue. Hocking proposed an interesting counterargument, which deserves further exploration. Whether overuse mechanisms are the crucial initiating factor or persistent nociceptive input remains a point of debate and further study.»
Forklaring på hva Hocking mener:
«Rather than looking at overuse mechanisms, Hocking maintains that persistent nociceptive input causes the formation of TrPs through central sensitization of the C-fiber nociceptive withdrawal reflex and plateau depolarization of withdrawal agonist alpha-motor neurons and compensatory reticulospinal motor facilitation of antigravity muscles and plateau depolarization of withdrawal antagonist alpha-motor neurons (33). «
Om hva nevropati og skader på nerver gjør, og hvordan neurodynamiske øvelser øker blodsirkulasjon internt i nerven. Nevner også hvordan skader, lav blodsirkulasjon og betennelser skaper sammensmeltninger i bindevevet mellom nerver og omliggende vev (muskler, skjelett, bindevev) som gjør at nervene ikke glir og dermed kan gi oss begrenset bevegelighet.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3172954/
«These disorders include compression syndromes or other neuromuscular conditions that may be accompanied by neuropathic pain. Damaged nerves exhibit predictable pathophysiological responses including impaired nerve mobility, increased mechanosensitivity, impaired nerve conduction, nerve tissue ischemia, axonal transport inhibition, and intraneural edema.
The following popper user interface control may not be accessible. Tab to the next button to revert the control to an accessible version. Impaired nerve mobility and increased mechanosensitivity provide the basis for existing studies of neurodynamic techniques. »
«Impaired nerve mobility and mechanosensitivity can be clinically assessed by measuring changes in joint range of motion, pain reproduction, or change of symptoms following neurodynamic mobilization.
«Intraneural edema is a common response to nerve injury, and is intimately involved in the proliferation of damage to nerve structure and function.
The following popper user interface control may not be accessible. Tab to the next button to revert the control to an accessible version. Edema is found in peripheral nerves that have been subject to trauma such as compression,excessive tension events, or vibration. Even mild injury may result in epineurial edema, but compression that is prolonged or of great magnitude leads to a breach of the diffusion barriers created by both the perineurium and microvasculature, resulting in endoneurial edema. The absence of lymphatic vessels in the endoneurium limits drainage of this edema, thereby creating a ‘mini-compartment syndrome’ within the nerve. »
«This ‘mini-compartment syndrome’, due to the increase in endoneurial pressure, subsequently leads to fibrosis and adhesions, impairing intrafascicular gliding. This loss of intrafascicular gliding creates an internal stretch lesion (Fig. 1). »
«The results showed significant mobilization effects in that there was increased fluid dispersion within the tibial nerve after the intervention. »
…de brukte bare kadavere i denne studien.
«The results showed significant mobilization effects in that there was increased fluid dispersion within the tibial nerve after the intervention. Because the tibial nerve was dissected free of all adjacent tissue and eliminated any external interfaces, the response to the mobilization appeared to be due to intraneural mechanics.»
Bevegelsene «pumper» internt i nerven og øker blodgjennomstreømning.
«During the mobilization technique, the tibial nerve alternately elongated and shortened which may have provided a temporary increase in intraneural pressure followed by a period of relaxation. Although speculative, it appears that this repetitive or ‘pumping’ action may have created a flushing of the dye and an alteration of the intraneural pressure as the intraneural fluid was dispersed.»
«In the early stages of stretch injury or compression, the ability to prevent or at least reduce edema may prevent or slow the inhibition of blood flow, thus preventing the sequelae leading to impaired axonal transport, demyelination, loss of elasticity due to fibrosis or adhesions, and ultimately to alteration in nerve structure and function. «
Viktig studie om nevropatier og body sway, men svært vanskelig å kopiere tekst fra.
Ett par studier om Merkel celler som reagerer på vibrasjon med lav frekvens (5-30 Hz) som sier mange ting om deres funksjon. Den sier bl.a. at de utløser glutamate, som er et nevropeptid relatert til smertetilstander. Men den utløser også andre nevrotransmittere som nedregulerer andre sanse-nevroner. Pluss at den innerverer eptielceller.
http://m.pnas.org/content/101/40/14503.full
«These data indicate that Merkel cells are poised to release glutamate and neuropeptides.»
«Because the question of whether Merkel cells are sensory cells is unresolved, other functions have been proposed. For example, Merkel cells may play a passive role in touch by efficiently transmitting force to mechanosensitive afferents (12). Alternatively, they may release neuromodulators to regulate the sensitivity of mechanoreceptive neurons (20). Merkel cells have also been proposed to influence the development or innervation of epithelia (ref. 21, but see ref. 22).»
«Together, these data demonstrate that Merkel cells are excitable cells and designate glutamate and CCK8 as candidate neurotransmitters at synapses between Merkel cells and sensory afferents in vivo. Our conclusion that Merkel cells function as excitable cells is strengthened by the abundance of neuronal transcription factors that we found to be enriched in Merkel cells (Table 1).»
«How might neurotransmitter release be stimulated from Merkel cells? Merkel cells may be mechanoreceptive cells that are directly activated by touch. Alternatively, Merkel cells may receive input from active afferent terminals. The latter conjecture is bolstered by reports of reciprocal connections in Merkel cell-neurite complexes (11).»
Nevner forholdet mellom eksperter og ikke-eksperters vurdering av menneskekroppen.
http://www.sherman.edu/research/archives/Jclub/Hestbeck_Lebouf_critical%20review.pdf
«This reviews shows that when comparing students with clinicians (eg, Harvey [1991] and Jensen [1993]), the students consistently did best. When comparing “experts” (ie, Rhudy [1990]) with ordinary clinicians, the experts did not produce better results than ordinary clinicians and in some cases produced worse results. This may occur because the clinician develops idiosyncratic standards for the procedure.»
Viktig studie om mekanismen bak hvordan hypoxi gir arrvev (adhesions) i kroppen. Relatert til hyperventilering vil lite CO2 gir hypoxi og sammen med trange blodkar vil de utsatte stedene i kroppen utvikle arrvev mellom muskler og nerver. Nevner hvordan antioksidanter er viktig for å unngå arrvev, spesielt etter operasjoner. Og motsatt, at oksidanter kan skape arrvev fra friskt vev. Nevner også hvordan nitratreaksjoner er med å skaper arrvev, så mulig at CO2 bidrar med å dempe nitratreaksjonene og dermed dempe dannelsen av arrvev. Den viser også at det kan være mulig å få arrvev celler om til å bli normale celler.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2574925/
«Adhesion fibroblasts exhibit higher TGF-β1 and type I collagen expression as compared to normal peritoneal broblasts. Furthermore, exposure of normal peritoneal fibroblasts to hypoxia results in an irreversible increase in TGF-β1 and type I collagen. We postulated that the mechanism by which hypoxia induced the adhesion phenotype is through the production of superoxide either directly or through the formation of peroxynitrite. »
«Hypoxia treatment resulted in a time-dependent increase in TGF-β1 and type I collagen mRNA levels in both normal peritoneal and adhesion fibroblasts.»
«In contrast, treatment with SOD, to scavenge endogenous superoxide, resulted in a decrease in TGF-β1 and type I collagen expression in adhesion fibroblasts to levels seen in normal peritoneal fibroblasts; no effect on the expression of these molecules was seen in normal peritoneal fibroblasts. »
«In conclusion, hypoxia, through the production of superoxide, causes normal peritoneal fibroblasts to acquire the adhesion phenotype. Scavenging superoxide, even in the presence of hypoxia, prevented the development of the adhesion phenotype. These findings further support the central role of free radicals in the development of adhesions.»
«Postoperative adhesions are a significant source of impaired organ functioning, decreased fertility, bowel obstruction, difficult reoperation, and possibly pain (1,2)
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«The processes that result in either normal peritoneal tissue repair or the development of adhesions include the migration, proliferation, and/or differentiation of several cell types, among them inflammatory, immune, mesothelial, and fibroblast cells (3)
«Hypoxia, resulting from tissue injury, has been suggested to play an important role in wound healing, and may therefore be a critical factor in the development of postoperative adhesions (4,7)
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Destroy user interface contrHypoxia is known to trigger the expression of TGF-β1, which consequently increases the expression of extracellular matrix proteins, including type I collagen (4)
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Destroy user interface contr«Type I collagen synthesis has been shown to be crucially dependent on the availability of molecular oxygen in tissue culture, animal, and human wound healing experiments (8,9)
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Destroy user interface controlMoreover, exposure of normal peritoneal fibroblasts to hypoxia irreversibly induces TGF-β1 and type I collagen to levels seen in adhesion fibroblasts (4,10)
«Additionally, hypoxia is known to acutely promote superoxide (O2.−) generation from disparate intracellular sources that include xanthine dehydrogenase oxidase (11), mitochondrial electron transport chain (12), and NAD[P]H oxidase (13).
In biological systems, superoxide dismutase (SOD) protects against the deleterious actions of this radical by catalyzing its dismutation to hydrogen peroxide plus oxygen, (14) Whereas SOD breaks down O2.−, xanthine oxidase synthesizes O2.−. Xanthine oxidase appears to be one of the major superoxide-producing enzymes (14)«
«Scavenging superoxide restores both TGF-β1 and type I collagen mRNA levels in adhesion fibroblasts to levels observed in normal peritoneal fibroblasts»
«Normal peritoneal and adhesion fibroblasts treated with super-oxide dismutase, a O2.− scavenging enzyme, exhibited a dose–response decrease (0, 5, 10, 15, and 20 units/ml) in TGF-β1 and type I collagen mRNA levels in adhesion fibroblasts while not effecting normal peritoneal fibroblasts (Figs. 3A and B).»
«Scavenging superoxide during hypoxia exposure protects against the development of the adhesion phenotype»
«Peroxynitrite treatment increased the adhesion phenotype markers, TGF-β1 and type I collagen»
«Adhesion fibroblasts are myofibroblasts, defined as transiently activated fibroblasts exhibiting features intermediate between those of smooth muscle cells and fibroblasts, including the expression of α-SM actin (29,21) and a depleted antioxidant system (22). In normal wound healing, as the wound resolves, the cellularity decreases and the myofibroblasts disappear by apoptosis (23). However, in several pathological cases, including fibrosis, myofibroblastic differentiation persists and causes excessive scarring (24,25).»
«This is further supported by the fact that when O2.− was scavenged, there was in a significant decrease in TGF-β1 and type I collagen in adhesion fibroblasts to levels seen in normal peritoneal fibroblasts. »
«Reactive oxygen species (ROS) are involved in TGF-β-stimulated collagen production in murine embryo fibroblasts (NIH3T3), and the effect of glutathione depletion on TGF-β-stimulated collagen production may be mediated by facilitating ROS signaling (37).»
«Reactive oxygen and nitrogen intermediates control the synthesis of cytokines and growth factors in several in vitro models (40). For instance, they modulate the expression and/or release of monocyte chemoattractant protein-1 (41,42), tumor necrosis factor-α, interleukin (IL)-1 (43,44), IL-8 (45,46), platelet-derived growth factor (47,48), and TGF-β1 (49). «
«Adhesion fibroblasts exhibited a significantly lower level of nitric oxide (NO) and higher protein nitration as compared to normal peritoneal fibroblasts, although there was no difference in the iNOS expression level between the two cell lines (17,50,51). This strongly indicates that adhesion fibroblasts use NO to form ONOO−, and consequently their basal ONOO− levels are higher than normal peritoneal fibroblasts. «
«Thus, treatment with SOD might affect the homeostasis of myofibroblasts by inducing cell death or the phenotypic reversion of myofibroblasts into normal fibroblasts. »
«Our results clearly indicate that hypoxia generated O2.− is a key player in the formation of the adhesion phenotype. This became evident when normal peritoneal fibroblasts were treated with SOD under hypoxic conditions and no change in adhesion markers was seen.»
«In this model, hypoxia-generated O2.− exerts its effect directly by enhancing the expression of TGF-β1, which consequently leads to elevated levels of type I collagen, a hallmark of the adhesion phenotype.»
Verkstedet Bodywork & Breathing System 