The aim of this study was to determine whether mitochondrial nitric oxide (NO) synthase (NOS) is involved in septic shock myocardial depression. The cecal ligation and puncture (CLP) method was used to induce septic shock. There was a significant depression of hemodynamic parameters recorded in the septic shock stage. After using nonselective NOS inhibitor N-nitro-L-arginine methyl ester (L-NAME), inducible NOS inhibitor aminoguanidine (AMG), and neuronal NOS inhibitor 7-nitroindazole (7-NI), depression of the parameters was partly attenuated. Nitric oxide production in isolated cardiac mitochondria increased obviously in the CLPYseptic shock stage, L-NAME and 7-NI both decreased NO production significantly. Nitrite/nitrate (NOx-) production in the septic shock stage was much greater than those in the corresponding sham groups, and NOx- production in the cytosol by inducible NOS was greater. Treatment with AMG suppressed NOx- production in the cytosol by iNOS, whereas treatment with 7-NI decreased NOx- production in the mitochondria. Mitochondrial NOS expression increased significantly in the septic shock stage, and its overexpression was attenuated using 7-NI. There was no significant decrease in the mitochondrial permeability transition pore measurement in the CLPYseptic shock group, whereas a significant decrease was observed in those treated with L-NAME or 7-NI. These results indicate that overexpression of mitochondrial NOS is involved in myocardial depression.
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出版当年[2011]版:
大类|3 区医学
小类|2 区外科3 区危重病医学3 区血液学3 区外周血管病
最新[2025]版:
大类|3 区医学
小类|3 区血液学3 区外周血管病3 区外科4 区危重病医学
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出版当年[2010]版:
Q1PERIPHERAL VASCULAR DISEASEQ1SURGERYQ2HEMATOLOGYQ2CRITICAL CARE MEDICINE
最新[2023]版:
Q1SURGERYQ2CRITICAL CARE MEDICINEQ2HEMATOLOGYQ2PERIPHERAL VASCULAR DISEASE