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Terlipressin in Septic Shock: When and How Much?

  • C. Ertmer
  • A. Morelli
  • M. Westphal
Conference paper

Abstract

Septic shock is the prototype of distributive shock characterized by arteriolar and venous vasodilation and pronounced vascular leakage, resulting in tissue edema, low systemic vascular resistance (SVR) and a subsequent fall in mean arterial pressure (MAP) [1]. Multiple mechanisms are involved in the pathogenesis of the vasodilatation noticed in septic shock. Excessive nitric oxide (NO) formation subsequent to upregulation of inducible NO synthase (iNOS) and increased activity of the neuronal NOS isoform (nNOS) represents a major contributor to vasodilation, basically mediated by interaction with the cyclic guanosine monophosphate (cGMP) pathway [1]. In addition, there is increasing evidence that adenosine triphosphate (ATP)-sensitive potassium (K+ ATP) channels are critically involved in the regulation of arterial vascular smooth muscle tone, as well as in the pathophysiology of catecholamine tachyphylaxis in the presence of systemic inflammation and shock states [1, 2]. Further mechanisms include adrenoceptor desensitization and downregulation due to high circulating levels of catecholamines [3, 4]. Last but not least, vasopressin deficiency has been considered as a causative factor in the pathogenesis of vasodilation in septic shock [1, 5].

Keywords

Septic Shock Mean Arterial Pressure Systemic Vascular Resistance Arginine Vasopressin Septic Shock Patient 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer Science + Business Media Inc. 2008

Authors and Affiliations

  • C. Ertmer
    • 1
  • A. Morelli
    • 2
  • M. Westphal
    • 1
  1. 1.Department of Anesthesiology and Intensive CareUniversity HospitalMuensterGermany
  2. 2.Department of Anesthesiology and Intensive CareUniversity of Rome “La Sapienza”RomeItaly

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