MODERN ASPECTS OF CCHF PATHOGENESIS

Vestnik ◽  
2021 ◽  
pp. 228-231
Author(s):  
Ф.А. Бердалиева ◽  
Г.Н. Абуова ◽  
Т.В. Полукчи ◽  
Д.С. Алиев ◽  
С.П. Ауезханов
Keyword(s):  
Inflammatory Response ◽  
Multiple Organ Failure ◽  
Organ Failure ◽  
Causal Relationship ◽  
Vascular System ◽  
Multiple Organ ◽  
High Potential ◽  
Target Cells ◽  
Present Stage ◽  
Relationship Of

На современном этапе в вопросах причинно-следственной связи патофизиологических, иммунологических, биохимических и других процессов, обуславливающих механизм возникновения и течения ККГЛ определены основные векторы: повреждение вирусом клеток - мишеней ( эндотелий сосудистой системы в органах и тканях, моноцитарные макрофаги, гепатоциты и др.); высокий потенциал вируса к репликации; стремительная вирусемия; развертывание локального и генерализованного иммуновоспалительного ответа; нарушение гемостаза и гемодинамики; развитие ДВС синдрома; синдрома полиорганной недостаточности. At the present stage, the main vectors have been identified in the causal relationship of pathophysiological, immunological, biochemical and other processes that determine the mechanism of the occurrence and course of CCGL: damage to target cells by the virus ( endothelium of the vascular system in organs and tissues, monocytic macrophages, hepatocytes, etc.); high potential of the virus for replication; rapid viremia; deployment of a local and generalized immuno-inflammatory response; violation of hemostasis and hemodynamics; development of DIC syndrome; multiple organ failure.

Possible role of increased oxidant stress in multiple organ failure after systemic inflammatory response syndrome

2003 ◽  
Vol 31 (4) ◽  
pp. 1048-1052 ◽  
Author(s):  
Takeshi Motoyama ◽  
Kazufumi Okamoto ◽  
Ichirou Kukita ◽  
Masamichi Hamaguchi ◽  
Yoshihiro Kinoshita ◽  
...  
Keyword(s):  
Systemic Inflammatory Response Syndrome ◽  
Inflammatory Response ◽  
Multiple Organ Failure ◽  
Organ Failure ◽  
Oxidant Stress ◽  
Multiple Organ ◽  
Systemic Inflammatory Response

The Injured Child Is Resistant to Multiple Organ Failure: A Different Inflammatory Response?

2002 ◽  
Vol 53 (6) ◽  
pp. 1058-1063 ◽  
Author(s):  
Casey M. Calkins ◽  
Denis D. Bensard ◽  
Ernest E. Moore ◽  
Robert C. McIntyre ◽  
Christopher C. Silliman ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Multiple Organ Failure ◽  
Organ Failure ◽  
Multiple Organ ◽  
Injured Child

scholarly journals Infective Endocarditis: Inflammatory Response, Genetic Susceptibility, Oxidative Stress, and Multiple Organ Failure

2019 ◽  
Author(s):  
Pedro Eduardo Alvarado Rubio MD ◽  
Roberto Brugada Molina MD ◽  
Pedro Eduardo Alvarado Ávila MD ◽  
Alejandro González Mora MD ◽  
Cesar Augusto González López MD
Keyword(s):  
Oxidative Stress ◽  
Infective Endocarditis ◽  
Inflammatory Response ◽  
Multiple Organ Failure ◽  
Genetic Susceptibility ◽  
Organ Failure ◽  
Multiple Organ

Intestinal preconditioning prevents inflammatory response by modulating heme oxygenase-1 expression in endotoxic shock model

2007 ◽  
Vol 293 (6) ◽  
pp. G1308-G1314 ◽  
Author(s):  
Fabienne Tamion ◽  
Vincent Richard ◽  
Sylvanie Renet ◽  
Christian Thuillez
Keyword(s):  
Inflammatory Response ◽  
Multiple Organ Failure ◽  
Organ Failure ◽  
Heme Oxygenase ◽  
Ischemia Reperfusion ◽  
Multiple Organ ◽  
Intestinal Injury ◽  
Heme Oxygenase 1 ◽  
Zinc Protoporphyrin ◽  
Lps Challenge

Gut mucosal injury observed during ischemia-reperfusion is believed to trigger a systemic inflammatory response leading to multiple organ failure. It should be interesting to demonstrate this relationship between gut and multiple organ failure in a sepsis model. Intestinal preconditioning (PC) can be used as a tool to assess the effect of intestinal ischemia in inflammatory response after LPS challenge. The aim of this study was to investigate the protective effect of PC against LPS-induced systemic inflammatory and intestinal heme oxygenase-1 (HO-1) expression. ES was performed with LPS (10 mg/kg iv) with or without PC, which was done before LPS. Rats were first subjected to sham surgery or PC with four cycles of 1 min ischemia and 4 min of reperfusion 24 h before LPS challenge or saline administration. PC significantly reduced fluid requirements, lung edema, intestinal lactate production, and intestinal injury. Inflammatory mRNA expressions for intestine and lung ICAM and TNF were significantly reduced after PC, and these effects were significantly abolished by zinc-protoporphyrin (a specific HO-1 activity inhibitor) and mimicked by bilirubin administration. Intestinal PC selectively increased HO-1 mRNA expression in intestine, but we have observed no expression in lungs. These findings demonstrate that intestinal injury is a important event for inflammatory response and multiple organ injury after LPS challenge. Intestinal HO-1 expression attenuates LPS-induced multiple organ failure by modulating intestine injury and its consequences on inflammatory response. Identification of the exact mechanisms responsible for intestine HO-1 induction may lead to the development of new pharmacological interventions.

Posttraumatic Inflammatory Response, Secondary Operations, and Late Multiple Organ Failure

1996 ◽  
Vol 40 (4) ◽  
pp. 624-631 ◽  
Author(s):  
Christian Waydhas ◽  
Dieter Nast-Kolb ◽  
Arnold Trupka ◽  
Ralph Zettl ◽  
Margit Kick ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Multiple Organ Failure ◽  
Organ Failure ◽  
Multiple Organ ◽  
Secondary Operations
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