[The role of blood rheology and micro hemocirculation in development of generalized hypoxia in crush syndrome].
Crush syndrome (CS) is a type of traumatic pathology accompanied by intoxication of organism with a heavy and specific clinical course and high lethality. Numerous damages, the most significant of which are stress, shock, pain, violation of the neurohumoral system involving the mediators of the sympathic part of vegetative nervous system, and pathological condition in which the body as a whole (generalized hypoxia) or region of the body (tissue hypoxia) is deprived of adequate oxygen supply are common in CS. The aim of the research was to study factors, which determine tissue blood and oxygen supply and to detect the possible pathogenetic mechanisms of generalized hypoxia in decompressed tissues and organs in long CS. Systemic arterial pressure, blood supply of skeletal muscles and liver, mesenteric microcirculation, mechanical and chemical resistance of erythrocytes of rats in crash syndrome has been investigated with the use of electrotensometry, H+-clearance, telebiomicroscopy, ultrasound cytolysogram and photoelectrocolorimetry. The model of crush was created by compression of experimental animals' hip during 6 hours. The morphological study of brain tissue during different types of decompression has revealed a contraction of the vessels of the cerebral shell, hypoxia, and perivascular edema. It was stated that interrelated changes play significant role in development of generalized hypoxia of tissues; degree of disorders depend on duration of compression and decompression, reactivity of micro blood vessels; the fall of local hemocirculation in intact tissues and reduced resistance and deformability of erythrocytes takes place.
Pavliashvili
N
N
Tbilisi State Medical University, Department of pathophysiology.
Namoradze
M
M
Kipiani
V
V
Petriashvili
T
T
Kevlishili
O
O
D000818:Animals; D003444:Crush Syndrome / Q000097:blood* / Q000150:complications* / Q000503:physiopathology; D006461:Hemolysis; D000860:Hypoxia / Q000209:etiology* / Q000503:physiopathology; D008833:Microcirculation / Q000502:physiology*; D051381:Rats; D012212:Rheology