Cold injury.

The pathophysiology of true frostbite reveals that the direct injury produced during the initial freeze process has a minor contribution to the global tissue damage. However, rapid rewarming to reverse the tissue crystallization has essentially been the lone frostbite intervention for almost half a century. The major pathologic process is the progressive microvascular thrombosis following reperfusion of the ischemic limb, with the cold-damaged endothelial cells playing a central role in the outcome of these frozen tissues. Newer interventions offer the opportunity to combat this process, and this article offers a scientific approach to frostbite injuries of the upper extremities.

[The role of lymphocyte-platelet adhesions, cytokines and endothelial dysfunction in pathogenesis of cold-induced lesions].

We studied the role of lymphocyte-platelet adhesion, IL-1beta, TNFalpha and endothelial dysfunction in pathogenesis of damage in local frostbites. Examination of 60 patients aged 17-50 years with frostbites of the second-forth degree has demonstrated that in patients with local frostbites the number of lymphocyte-platelet adhesions, circulating desquamated endothelial cells increases as well as the level of proinflammatory cytokines, while nitrites concentration decreases.

[Immune complex may play an important role in freezing injury of frostbite rats].

AIM: To explore the role of humoral immunity in the pathophysiological process of freezing injury and the possible immune interference in the preventation and treatment of frostbite. METHODS: Severe experimental freezing injury model was made in Wistar rats( n = 20). The concentration of three types of immunoglobulin (IgG, IgA and IgM), two types of complement components (C3 and C4), and circulating immune complex (CIC) were measured respectively before and at 4h, 1d, 3d, and 5d after frostbite. At the same time, the tissue immune complex (TIC) in skeletal muscle and the contents of the red blood cell immune complex (RBC-IC) were also observed and then was the red blood cell immune adherence activity (RCIA). RESULTS: Serum IgG concentration decreased rapidly to the lowest level at 4 h after frostbite IgA concentration dropped to the nadir on 1 day after freezing. Decreases of both immunoglobulins were maintained during the 5 days after frostbite. The fate of both C3 and C4 were the same as those immunoglobulins. Freezing had rather less effect on IgM level. CIC concentration in serum, expressed as the percent of prefreezing increased rapidly and to the zenith on the 3 days post-freezing. By immunofluorescence microscopy, thin continuous linear pattern (IgG) was demonstrated along the SM on the first day post-freezing. Granular and nodular deposits (IgG) appeared along the SM as the time proceeded after frostbite. RBC-IC contents, expressed as the erythrocyte IC rosette rate, increased significantly and to the zenith on the 3 d post-freezing, while RCIA depressed to the nadir at the same time. CONCLUSION: The freezing frostbite is an immune complex related disease which have not been reported by others before.

Role of neutrophil-endothelial cell adhesion in inflammatory disorders.

Polymorphonuclear leukocytes are armed with an impressive arsenal of bactericidal agents that allow these cells to play a vital role in host defense against invading pathogens. However, these same agents can produce extensive cellular damage in host tissues when leukocytes are activated during inflammatory conditions. Recognition of this fact, when coupled with the observation that leukocyte adhesion to post-capillary venules is a critical first step in the inflammatory process, has led to the development of the concept that inhibition of neutrophil-endothelial cell adhesion (NECA) may represent a novel therapeutic strategy for the prevention of leukocyte-dependent injury in inflammatory conditions. Indeed, pharmacological or immunologic inhibition of NECA reduces cellular injury, dysfunction, and necrosis induced by ischemia/reperfusion, circulatory shock and resuscitation, organ transplantation, cardiopulmonary bypass, frostbite, and thermal trauma. NECA also appears to play an important role in the pathobiology of airway inflammation and asthma, pulmonary oxygen toxicity, arthritis, bacterial meningitis, and cerebral malaria. The aim of this review is to summarize the evidence implicating NECA in the pathogenesis of these inflammatory conditions.

[The biochemical and immunological indices in the rehabilitation period of the victims of the accident on the Komsomolets atomic submarine]. / Biokhimicheskie i immunologicheskie pokazateli v reabilitatsionnom periode u postradavshikh v rezul'tate avarii atomnoi podvodnoi lodki "Komsomolets".

Biochemical and immunological indexes of peripheral blood were compiled in military sanatorium "Divnomorskoe" in seamen who have suffered from general supercooling in the result of "Komsomolets" atomic submarine breakdown. The patients had the symptoms of metabolic disturbance, immunodepression, a great concentration of proteins in acute phase and activity of MB-fraction of creatine phosphokinase. Immunodepression after the general supercooling was mainly conditioned by oppression of differentiation, metabolic changes and functional activity of T-lymphocytes. A course of immunocorrective therapy was employed using "thymogen"--synthetic peptide of thymus. In the process of rehabilitation there was a gradual functional recovery, normalization of metabolism and immunological indexes.

[Use of thymalin in the complex treatment of frostbite]. / Primenenie timalina v kompleksnom lechenii otmorozhenii.

The use of thymalin in the complex therapy of 19 patients with frostbites was shown by the authors to promote the stimulation of cell immunity, decrease the intensity of intravascular blood coagulation, to increase fibrinolysis, to improve the development of reparative processes in the wound and outcomes of autoplasty. It also decreased the percentage of infectious complications.

A rapid solid phase assay for the detection of circulating immune complexes.

A simplified process, which we have termed Enzyme Immune Complex Assay (EICATM) for the detection of circulating immune complexes (CICs), is described herein. The method utilizes readily available reagents, small quantities of serum, and can be performed quickly with a minimal amount of equipment. Serum from 38 normal controls, 98 burn patients, 36 frostbite injury patients, and 21 patients with elevated rheumatoid factor (RF) were tested for CICs in an immune function study. Elevated immune complex levels were found in the group of patients with frostbite injury, and in the group with elevated RF. Serum from thermally injured patients had slightly depressed yet normal CIC levels. The detection of elevated CICs by the EICATM method compared favorably with the more cumbersome Raji cell method, with the added advantage of simplicity, speed, and the ability to detect non-IgG immune complexes.

Complement in pemphigus vulgaris and other bullous dermatoses.

The behavior of the complement and of its components C4 and C3 has been studied in serum and in blister fluid both in patients with pemphigus vulgaris and other bullous dermatoses and in healthy subjects with experimentally induced blisters. The results are suggestive of local activation of the complement, in the blister fluid of patients with pemphigus vulgaris, pemphigus erythematosus and bullous pemphigoid according to the classical enzymatic sequence.