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Sepsis ve İnflamasyon Mediatörleri

Sepsis and inflammatory mediators

Journal Name:

  • İnönü Üniversitesi Tıp Fakültesi Dergisi

Publication Year:

  • 1996

Key Words:

Keywords (Original Language):

Author NameUniversity of AuthorFaculty of Author
Abstract (2. Language): 
Septicemia and septic shock are dramatic clinical syndromes which result from acute invasion of the bloodstream by certain microorganisms or their toxic products. The clinical manifestations of septicemia and septic shock are the result of an interplay between microbial products and host mediator systems. Sepsis provokes a neuroendocrine and inflammatory response to promote survival. A variety of host mediators have been implicated in the pathogenesis of septic shock including active metabolites of the complement, kinin, and coagulation systems as well as factors released from stimulated cells, particularly, the cytokines. From the standpoint of vascular perfusion and organ function a vicious circle is established that results in altered blood flow in the microcirculation and progressive injury to the capillary endothelium and tissue. Now, all of the cytokines are not identified thus far, TNFcc appears to be the most potent mediator the pathophsiology of the sepsis syndrome. In addition, other many inflammatory mediators have been identified as inflammatoy factors in sepsis. It is also likely that in the near future we will be able to take advantage of the recent developments in molecular biology and a better understanding of the pathogenesis of the septic process. [Journal of Turgut Özal Medical Center 1996;3(4):374-381]
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Abstract (Original Language): 
Sepsis ve septik şok; bazı mikroorganizmaların veya bu organizmaların toksik ürünlerinin akut olarak kan dolaşımı ile yay ılımı sonucunda gelişen dramatik bir klinik tablodur. Bu tablonun klinik bulguları mikroorganizma ve ürünleri ile konakçının medyatör sistemleri arasındaki mücadelenin bir sonucudur. Sepsis konakçının nöroendokrin, immün ve inflamatuar sistemlerini uyarır ve bu cevabın şiddeti de klinik seyri belirler. Septik şokun patogenezini; konakçı mediatörlerinin bir bölümü; kompleman, kinin, koagülasyon sistemlerinin aktif metabolitleri ve özellikle sitokinler oluşturur. Kapiller endoteldeki ve dokudaki sürekli zedelenme, mikrosirkülasyondaki kan akımı değişikliği, vasküler perfüzyonun durumu ve organ fonksiyonlarındaki kısır döngüyü belirler. Günümüzde sitokinlerin tamamı ayrıştır ilam am ıştır, ancak TNF anın sepsis sendromu patofizyoloj"isinde en potent mediator olduğu açıktır. Ayrıca diğer pekçok inflamatuar mediatörün de sepsiste rol aldığı tespit edilmiştir. Muhtemelen yakın bir gelecekte mole kül er biyolojideki yeni gelişmeler sonucunda septik sürecin patogenezini daha iyi anlayabileceğiz. Bu da yeni tedavi yaklaşımları oluşturmamızı sağlayacaktır. [Turgut Özal Tıp Merkezi Dergisi 1996;3(4):374-381]
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  • 4
374-381
  • Turkish

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