6 Physiologic Modulation of Coronary Microvascular Permeability by Blood Components

Management of Hemophilia in France

Thrombosis and Haemostasis ◽

10.1055/s-0038-1647996 ◽

1976 ◽

Vol 35 (03) ◽

pp. 553-558 ◽

Cited By ~ 5

Author(s):

Jean-Pierre Allain

Keyword(s):

Home Care ◽

Replacement Therapy ◽

The Other ◽

Blood Components ◽

Careful Evaluation ◽

Viii And Ix ◽

Effective Use ◽

General Care

SummaryTwo important factors concerning the management of hemophilia in France are considered.The supply of factors VIII and IX for replacement therapy meets the current demand but as the demand increases with the development of self-infusion programs, the production will also have to increase. This can only be done through more effective use of all of the blood components and will require careful evaluation of the needs of each patient.Programs which teach self-infusion and the other aspects of home care are gradually allowing the hemophiliac and his family better understanding of the disease. These programs are developing slowly in France but must be expanded to improve the general care of all French hemophiliacs.

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Increased cardiac microvascular permeability and activation of cardiac endothelial nitric oxide synthase in high tidal volume ventilation-induced lung injury

Asian Biomedicine ◽

10.2478/abm-2010-0004 ◽

2010 ◽

Vol 4 (1) ◽

pp. 27-36

Author(s):

Ming-Jui Hung ◽

Ming-Yow Hung ◽

Wen-Jin Cherng ◽

Li-Fu Li

Keyword(s):

Nitric Oxide ◽

Nitric Oxide Synthase ◽

Lung Injury ◽

Tidal Volume ◽

Endothelial Nitric Oxide Synthase ◽

Microvascular Permeability ◽

Akt Phosphorylation ◽

Enos Phosphorylation ◽

Oxide Synthase ◽

Endothelial Nitric Oxide

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.

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