The control of interstitial fluid volume and pressure and the mechanism of edema formation

The control of interstitial fluid volume and pressure and the mechanism of edema formation

THE CONTROL OF INTERSTITIAL FLUID VOLUME AND PRESSURE AND THE MECHANISM OF EDEMA FORMATION R. K. Reed Department of Physiology, University of Bergen, ...

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THE CONTROL OF INTERSTITIAL FLUID VOLUME AND PRESSURE AND THE MECHANISM OF EDEMA FORMATION R. K. Reed Department of Physiology, University of Bergen, Norway

AUTOMATIC INJECTOR FOR EMERGENCY INTRODUCTION OF ANTI-SHOCK MEDICINES V.N.Yelsky,G.K.Krivobok, G.A. Krivobok,A.G.Antonov, N.N. Bondarenko, V.I. Zacharov State Medical University Named After M. Gorkey, Donetsk, Ukraine

Interstitial fluid pressure (Pif) is one of the pressures governing transcapillary exchange and is also considered the filling pressure for the lymphatics. Traditionally Pif is considered a passive controller of interstitial fluid volume (IFV) since increased capillary filtration will raise IFV and thereby Pif which in turn acts to limit further filtration. Contrary to this normal role of Pif, we have observed that in a series of acute inflammatory reactions, Pif becomes more negative concomitant with edema formation, i.e. Pif becomes an “active” driving force for edema formation. Following bum injury Pif decreases from -1 to -150 mmllg. Mast cell degranulation, neurogenic inflammation, anaphylaxis, PGEl and PG12 cause Pif to decrease from -1 to between -5 and -10 mmHg, raising net capillary filtration pressure by lo-20 times from 0.5-l mmHg. The increased negativity of Pif is induced by perturbation of the cellular matrix receptors towards extracellular matrix components, the Dl-integrins The increased negativity of Pif is attenuated by platelet derived-growth factor (PDGF), lD-myo-inositol-1,2,6-trisphosphate and PGF2a. Thus, the interstitial matrix is an active participant in control of transcapillary exchange and edema formation.

Is developed small-sized automatic injector, intended for use on a body in extreme conditions, where the occurrence of explosion or tire is possible and is complicated itself and mutual aid working whose - or without help and irrespective of condition consciousness suffering. Injector contains a mobile gofer elastic ampoule with a needle, the mechanism connected with the gauge, sensitive to change of temperature and pressure, holding the mechanism in the cocked condition and atmospheric pressure, working for want of increase, or temperature of an environment of the above installed significance. Injector is placed incapsules, fixed on a zone under clothes, that provides it contact to a body. Ampoules with a needle are intended for unitary use, other elements are designed on repeated use. Use of gauges sensitive to other extreme factors expands a range use injector in medicine of accidents.

(R.K. Reed et al. News Physiol. Sci. 12: 42, 1997)

048 AUTOIMMUNE DISEASES IN ANIMAL MODELS AND HUMAN PATIENTS Noel R. Rose Department of Pathology and Department of Molecular Microbiologv and Immunology, The Johns Hopkins Medical institutions, Baltimore, MD, USA

MECHANISMS OF MAJOR DISEASE PROCESSES, FROM MOLECULES TO MAN Chair: Dr. Jan W. Guzek, Lo& Poland and George G. Somjen, Durham, North Carolina, USA Three review lectures sponsored by the Commission on Teaching of the International Society for Pathophysiology, designed for teachers and researchers of pathophysiology, with the purpose of reviewing and updating three major topics: the mechanisms of (1) oedema formation, (2) autoimmune disease, and (3) hypoxic and hyperoxic tissue damage.

The autoimmune diseases represent a major medical and public health problem. In the United States, for example, approximately 10 million cases of the 24 most prominent autoimmune diseases occurred in 1996. The evidence for an autoimmune disease in humans may be direct, indirect or circumstantial. The examples of direct evidence are relatively rare because it is based on instances in which the disease is transferred from a patient to a normal individual by antibody or T cells. For most autoimmune diseases we rely on indirect evidence derived from animal models. Sometimes the disease can be reproduced by immunizing a susceptible animal with the candidate antigen. In other cases, an equivalent, spontaneous disease has been found in animals. Recently, genetic manipulation of mice has been successful in reproducing several human diseases. Finally, circumstantial evidence may provide tentative evidence of an autoimmune etiology of a human disease. Such evidence includes familial clustering and HLA association. As the lists of autoimmune diseases grow, we are learning more valuable lessons about the fundamental basis of normal self-tolerance and opening new opportunities for specific therapies.

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