Serotonin and Microvascular Permeability

Author(s):  
F. De Clerck ◽  
R. S. Reneman

2010 ◽  
Vol 4 (1) ◽  
pp. 27-36
Author(s):  
Ming-Jui Hung ◽  
Ming-Yow Hung ◽  
Wen-Jin Cherng ◽  
Li-Fu Li

Abstract Background: Positive pressure ventilation with large tidal volumes has been shown to cause lung injury via the serine/threonine kinase-protein kinase B (Akt) and endothelial nitric oxide synthase (eNOS)-pathways. However, the effects of high tidal volume (VT) ventilation on the heart are unclear. Objectives: Evaluate the effect of VT ventilation on the cardiac vascular permeability and intracellular Akt and eNOS signaling pathway. Methods: C57BL/6 and Akt knock-out (heterozygotes, +/−) mice were exposed to high VT (30 mL/kg) mechanical ventilation with room air for one and/or five hours. Results: High VT ventilation increased cardiac microvascular permeability and eNOS phosphorylation in a timedependent manner. Serum cardiac troponin I was increased after one hour of high VT ventilation. Cardiac Akt phosphorylation was accentuated after one hour and attenuated after five hours of high VT ventilation. Pharmacological inhibition of Akt with LY294002 and high VT ventilation of Akt+/− mice attenuated cardiac Akt phosphorylation, but not eNOS phosphorylation. Conclusion: High VT ventilation increased cardiac myocardial injury, microvascular permeability, and eNOS phosphorylation. Involvement of cardiac Akt in high VT ventilation was transient.





2001 ◽  
Vol 90 (1) ◽  
pp. 261-268 ◽  
Author(s):  
Leonardo C. Clavijo ◽  
Mary B. Carter ◽  
Paul J. Matheson ◽  
Mark A. Wilson ◽  
William B. Wead ◽  
...  

In vivo pulmonary arterial catheterization was used to determine the mechanism by which platelet-activating factor (PAF) produces pulmonary edema in rats. PAF induces pulmonary edema by increasing pulmonary microvascular permeability (PMP) without changing the pulmonary pressure gradient. Rats were cannulated for measurement of pulmonary arterial pressure (Ppa) and mean arterial pressure. PMP was determined by using either in vivo fluorescent videomicroscopy or the ex vivo Evans blue dye technique. WEB 2086 was administered intravenously (IV) to antagonize specific PAF effects. Three experiments were performed: 1) IV PAF, 2) topical PAF, and 3) Escherichia coli bacteremia. IV PAF induced systemic hypotension with a decrease in Ppa. PMP increased after IV PAF in a dose-related manner. Topical PAF increased PMP but decreased Ppa only at high doses. Both PMP (88 ± 5%) and Ppa (50 ± 3%) increased during E. coli bacteremia. PAF-receptor blockade prevents changes in Ppa and PMP after both topical PAF and E. coli bacteremia. PAF, which has been shown to mediate pulmonary edema in prior studies, appears to act in the lung by primarily increasing microvascular permeability. The presence of PAF might be prerequisite for pulmonary vascular constriction during gram-negative bacteremia.





2004 ◽  
Vol 494 (2-3) ◽  
pp. 241-249 ◽  
Author(s):  
Gabriela Cavriani ◽  
Ricardo Martins Oliveira-Filho ◽  
Aryene Góes Trezena ◽  
Zilma Lúcia da Silva ◽  
Helori Vanni Domingos ◽  
...  


1989 ◽  
Vol 17 (12) ◽  
pp. 1306-1309 ◽  
Author(s):  
BASHIR A. ZIKRIA ◽  
CHIVUKULA SUBBARAO ◽  
MEHMET C. OZ ◽  
SCOTT T. SHIH ◽  
PAUL F. MCLEOD ◽  
...  




1987 ◽  
Vol 136 (1) ◽  
pp. 134-141 ◽  
Author(s):  
Kenneth E. Burhop ◽  
William M. Selig ◽  
Donald A. Beeler ◽  
Asrar B. Malik


Shock ◽  
2002 ◽  
Vol 18 (1) ◽  
pp. 75-81 ◽  
Author(s):  
Carl I. Schulman ◽  
Joseph K. Wright ◽  
Fiemu Nwariaku ◽  
George Sarosi ◽  
Richard H. Turnage


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