Effect of NO synthase inhibition on cardiovascular and pulmonary dysfunction in a porcine short-term model of endotoxic shock
| Autor: | Silvia Mazzola, S. Radice, M.G. Clement, Sabah N. A. Hussain, Claudio L. Lafortuna, Mariangela Albertini |
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| Rok vydání: | 2002 |
| Předmět: |
Lipopolysaccharides
Cardiac output Time Factors Central Venous Pressure Lipopolysaccharide Swine Clinical Biochemistry Hemodynamics Blood Pressure Pharmacology Cardiovascular System Guanidines chemistry.chemical_compound Oxygen Consumption Heart Rate Escherichia coli medicine Animals Cardiac Output Enzyme Inhibitors Respiratory system biology Respiration Cell Biology Shock Septic Nitric oxide synthase Disease Models Animal NG-Nitroarginine Methyl Ester medicine.anatomical_structure Blood pressure chemistry Anesthesia Circulatory system Vascular resistance biology.protein Vascular Resistance Nitric Oxide Synthase |
| Zdroj: | Prostaglandins, Leukotrienes and Essential Fatty Acids. 67:365-372 |
| ISSN: | 0952-3278 |
| Popis: | In a porcine model of endotoxic shock, we evaluated the circulatory and respiratory effects of NO synthase (NOS) blockade. Twenty anaesthetised pigs were divided into three groups and studied for 240 min after induction of endotoxic shock with lipopolysaccharides of Escherichia coli (LPS). After 180 min of endotoxic shock, one group ( n = 6) received aminoguanidine, another group ( n = 6) received N G -nitro-L -arginine methyl ester (L -NAME) and a third group ( n = 8) received only LPS. A sham group ( n = 3) was also studied. LPS decreased systemic arterial pressure and cardiac output (CO) and increased mean pulmonary arterial pressure (MPAP), pulmonary vascular resistance (PVR) and heart rate. Significant changes were also observed in compliance (−18.4%) and resistance (+33.6%) of the respiratory system. Aminoguanidine did not modify LPS-dependent effects, while, after L -NAME, a significant increase in MPAP, PVR and SVR and a decrease in CO were observed. In conclusion, aminoguanidine does not play a significant cardiocirculatory and pulmonary role in the short-term dysfunction of endotoxic shock, while L -NAME has a detrimental effect on haemodynamics, suggesting a protective role of constitutive NO production at vascular level during the early stages of endotoxaemia. |
| Databáze: | OpenAIRE |
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