Hochschulschrift:
Dissertation, Mathematisch-Naturwissenschaftliche Fakultät der Universität Greifswald, 2023
Anmerkungen:
Literaturverzeichnis: Seite 26-35. - Literaturangaben
Text deutsch, Publikationen englisch
Beschreibung:
Mukoadhäsion, Gastrointestinaler Transit, Schluckbare Sensoren, Film
In the setting of septic shock, vasopressin is administered alongside catecholamines for circulatory stabilization. Animal models have revealed that selective AVPR1a stimulation surpasses non-specific AVPR stimulation by vasopressin in terms of both outcome and hemodynamics. However, the roles of vasopressin receptors and the molecular mechanisms associated with capillary leakage remain largely unexplored. Stimulation of AVPR2 by Desmopressin has been observed to result in the release of von Willebrand Factor (vWF) from Weibel-Palade-Bodies in vivo. These bodies also contain Ang-2, elevated in the blood of septic patients, correlating with inflammatory markers such as CRP and TNF-alpha, as demonstrated for other Weibel-Palade-Body components, including P-selectin. This prompts the question of vasopressin's influence on the release of capillary destabilizing mediators and, consequently, the development of capillary leakage. The aim of this study was to develop a cell culture model to investigate AVPR1a and AVPR2 agonists and antagonists regarding their release of vWF, Ang-1, Ang-2, and P-selectin and to analyze their impact on capillary leakage in vivo. HUVEC, HDMEC, and HPMEC, primary endothelial microvascular cells, were examined for the expression of AVPR1a, AVPR2, and vWF using immunofluorescence, Western-Blot, FACS, and rtPCR. Verification of AVPR2 stimulation leading to vWF release from Weibel-Palade-Bodies in this model was pivotal. To achieve this, a protocol was ...