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Structural Functional Manifestations of Crush-Syndrome

#G-808


Morphology and Pathogenesis of the Microcirculatory Systemic Damage under Crush-Syndrome

Tech Area / Field

  • MED-OTH/Other/Medicine

Status
3 Approved without Funding

Registration date
26.09.2001

Leading Institute
Georgian Academy of Sciences / A. Natishvili Institute of Experimental Morphology, Georgia, Tbilisi

Collaborators

  • Universitat Munster / Klinik and Poliklinik fur Thorax-, Herz- und Gefabchirurgie, Germany, Münster

Project summary

The main goal of the proposed work is to investigate structural functional manifestations of Crush –syndrome, in particular the systemic damage of the microcirculatory bed, to reveal general changes due to hypovolemia, hyperfunction and local ones, of organospecific (kidneys, liver, lungs).
Crush-syndrome is a compound symptomocomplex observed both in peacetime and during war. In mass catastrophes (earthquake, explosions, destructions) it causes a wide spectrum effects of “shock” factors on the organism providing blood circulation centralization during compression, a development of homodynamic disturbances at microcirculation level, suppression of macrophagal and immune systems.
Our proceeding studies revealed a complex of changes, especially vessel spasms, kidneys and liver failures having a special pathogenic significance [3]. But the basis of destructive and autotoxic processes in compression and especially in decompression periods is formed by not only hypoxia but also by the destructive effect of catecholamines on cellular membranes, thus increasing in microcirculation disturbances.
The role of monocytes, macrophages and lymphocytes when damaging kidney, liver and lungs parenchyma has not been studied.
What is the interdepence of microcirculation vessel changes with the “shock toxin” effect – histamine, especially in decompression, the gravest period of Crush-syndrome? How do microcirculation vessels interact with “shock toxin” – histamine?
First of all the course of the postcompression depends on the solution of this question and hence the decision and choice of the most advisable preventive measures and methods of treatment.
How and through which structural moduluses is the inflammatory reaction manifested in Crush-syndrome? The classical examinations revealed a structural insuffiency of inflammatory infiltrate cells in detritus resorbtion.
The data of these studies show a long presence of necrosis foci in parenchyma of damaged organs and muscles; cell apoptosis is quite possible [4]. Can we activate fibroblastic reactions; prevent the development of secondary circulatory hypoxia and ishemic process generalization? These questions will be also studied in the supposed research.


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