Macromolecular basis of globular protein exclusion and of swelling pressure in loose connective tissue (Umbilical cord)

Meyer, F. A.

doi:10.1016/0304-4165(83)90242-8

Cited by 94 publications

(63 citation statements)

References 29 publications

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“…15 The chemistry of these barrier properties has been studied experimentally. 16,17 These studies support the idea that the tissue of the hyalinization reaction may provide limited protection of the delicate inner ear structures from potentially toxic substances produced by otosclerotic bone tissues with a high turnover rate. A review of publications concerning the association of otosclerotic endosteal involvement and sensorineural hearing loss reveals contradictory concepts regarding the pathophysiologic characteristics of the disease process.…”

Section: Discussionsupporting

confidence: 67%

Analysis of the Hyalinization Reaction in Otosclerosis

Nelson

Hinojosa

2014

JAMA Otolaryngol Head Neck Surg

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O tosclerosis is a disease of abnormal bone remodeling, which is unique in that it occurs only in the otic capsule of the human temporal bone. Large foci of otosclerosis may penetrate the endosteal layer of the cochlea, resulting in direct contact of otosclerotic bone with the softtissue structures of the inner ear. We have previously reported variable amounts of cochlear element degeneration with otosclerotic endosteal penetration, 1 and in that earlier study, the cochlear elements, including the hair cells, ganglion cells, and stria vascularis, were evaluated quantitatively. A reduction in the population of cochlear elements was not related to the extent and location of otosclerotic endosteal involvement, and a reduction in sensorineural thresholds was observed in some, but not all cases. These observations suggest that factors that limit the effect of otosclerotic endosteal involvement on the cochlear elements may be present. Reports on the association between endosteal involvement of the otic capsule with otosclerosis and sensorineural hearing loss have been summarized in a review of the literature. 1As early as 1899, Siebenmann 2 speculated that the diffusion of toxic substances from otosclerotic bone into the inner ear fluids resulted in hearing loss. Evidence now supports this concept. Hydrolytic enzymes produced by otosclerotic bone have been identified in perilymph and appear to be a factor leading to the degeneration of cochlear sensorineural elements and sensorineural hearing loss. 3,4 In addition, cytokines released by otosclerotic bone have been suggested as a potential source of spiral ligament dysfunction resulting in a loss of cochlear fluid and ion homeostasis. 5Histologic changes occurring in the cochlear soft tissues at the site of otosclerotic endosteal penetration have been descriptively referred to as a hyalinization reaction. [6][7][8] In hematoxylineosin stained temporal bone sections, the hyalinized tissue appears pink in color and is characterized by decreased cellularity IMPORTANCE Otosclerotic bone has been observed to penetrate the endosteal layer of the cochlea, resulting in direct contact with the soft-tissue structures of the inner ear. Sensorineural hearing loss has been observed in some, but not all, of these cases. The development of histologic changes occurring in the cochlear soft tissues at the site of otosclerotic endosteal penetration has been descriptively referred to as a hyalinization reaction. The role of the hyalinization reaction in the development of hearing loss is unknown.OBJECTIVE To evaluate the composition of these hyalinized soft tissues using immunostaining techniques. DESIGN, SETTING, AND PARTICIPANTSRetrospective review in a human temporal bone histopathology research laboratory of 3 specimens from patients with endosteal otosclerotic involvement.INTERVENTIONS Evaluation of human temporal bone pathology findings. MAIN OUTCOMES AND MEASURESHuman temporal bone sections with endosteal otosclerotic involvement were studied using immunostaining techniques to ide...

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Section: Discussionsupporting

confidence: 67%

Analysis of the Hyalinization Reaction in Otosclerosis

Nelson

Hinojosa

2014

JAMA Otolaryngol Head Neck Surg

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“…495.1 o connective tissue cells to the connective tissue fibres. The tissue is then allowed to expand due to its content of glycosaminoglycans and hyaluronan (Meyer, 1983). This expansion of the tissue without simultaneous addition of fluid will create an increased negativity of Pif.…”

Section: Discussionmentioning

confidence: 99%

“…The finding that blockade of fl1-integrins results in a lowering of Pif has been explained as follows. The tendency of loose connective tissues to swell (Meyer, 1983) is normally balanced by connective tissue cells exerting a tension on ECM fibres, which thereby restrain the swelling glycosaminoglycanhyaluronan gel. According to this concept, a perturbation or blockade of the /,J-integrin function will cause the tissue to expand until a new balance is achieved between the expanding hyaluronan, the restraining fibre network(s) and the negative Pif.…”

mentioning

confidence: 99%

A novel physiological function for platelet‐derived growth factor‐BB in rat dermis.

Rodt

Åhlén

Berg

et al. 1996

The Journal of Physiology

119

102

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1. The present experiments describe a role for platelet-derived growth factor-BB and cellular adhesion receptors towards extracellular matrix molecules (/1-integrins) in control of interstitial fluid pressure (Pif). and decreased to -2-50 + 0 35 mmHg (P < 0 05) and -3-88 + 1P45 mmHg (P < 0 05) at anti-a2/11 concentrations of 0-56 and 1P12 mg ml-', respectively.4. The effect of anti-a0231 was abolished when platelet-derived growth factor-BB (PDGF-BB) (200 ng ml-') was injected together with anti-ca2/1. 5. The time-and dose-responses of PDGF-BB to counteract increased negativity of Pif were studied further using dextran anaphylaxis as an experimental model inducing increased negativity of Pif in skin. Control Pif averaged -0 33 + 0A43 mmHg and fell to -4-10 + 1P47 mmHg within 10 min after dextran (P < 0-01). Subsequent subdermal injection of PDGF-BB at 200 ng ml-' normalized Pif in 10-20 min which became -1-37 + 1-23 mmHg (P < 0'01 versus dextran, P > 0.05 versus control). PDGF-BB had little or no effect at 50 ng ml-. PDGF-AA and basic fibroblast growth factor had no effect on Pif.6. The in vivo function reported for PDGF-BB has not been described previously and provides further evidence for active participation of connective tissue cells in control of Pif by altering tension on extracellular matrix structures.During the initial stage of several acute inflammatory reactions, loose connective tissues will 'actively' enhance transcapillary fluid flux and oedema formation in skin and airways, since an increased negativity of interstitial fluid pressure (Pif) from -1 to between -5 and -10 inmHg will provide an increased driving pressure for fluid filtration

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“…An ex vivo parallel to the negative interstitial pressure is the tendency of an excised tissue to swell or imbibe fluid when soaked in a saline solution (66,291 (493). As pointed out previously (25,493), P if is of interest for several reasons, since it is one of the determinants of capillary fluid filtration, is a likely determinant of initial lymph formation, and is a necessary parameter for estimating interstitial compliance.…”

Section: Definitionsmentioning

confidence: 99%

Interstitial Fluid and Lymph Formation and Transport: Physiological Regulation and Roles in Inflammation and Cancer

Wiig

Swartz²

2012

Physiological Reviews

563

574

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The interstitium describes the fluid, proteins, solutes, and the extracellular matrix (ECM) that comprise the cellular microenvironment in tissues. Its alterations are fundamental to changes in cell function in inflammation, pathogenesis, and cancer. Interstitial fluid (IF) is created by transcapillary filtration and cleared by lymphatic vessels. Herein we discuss the biophysical, biomechanical, and functional implications of IF in normal and pathological tissue states from both fluid balance and cell function perspectives. We also discuss analysis methods to access IF, which enables quantification of the cellular microenvironment; such methods have demonstrated, for example, that there can be dramatic gradients from tissue to plasma during inflammation and that tumor IF is hypoxic and acidic compared with subcutaneous IF and plasma. Accumulated recent data show that IF and its convection through the interstitium and delivery to the lymph nodes have many and diverse biological effects, including in ECM reorganization, cell migration, and capillary morphogenesis as well as in immunity and peripheral tolerance. This review integrates the biophysical, biomechanical, and biological aspects of interstitial and lymph fluid and its transport in tissue physiology, pathophysiology, and immune regulation.

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Macromolecular basis of globular protein exclusion and of swelling pressure in loose connective tissue (Umbilical cord)

Cited by 94 publications

References 29 publications

Analysis of the Hyalinization Reaction in Otosclerosis

Analysis of the Hyalinization Reaction in Otosclerosis

A novel physiological function for platelet‐derived growth factor‐BB in rat dermis.

Interstitial Fluid and Lymph Formation and Transport: Physiological Regulation and Roles in Inflammation and Cancer

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