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Fig. 1 | Cardiovascular Diabetology

Fig. 1

From: Tissue inflammation and nitric oxide-mediated alterations in cardiovascular function are major determinants of endotoxin-induced insulin resistance

Fig. 1

Experimental Schematic. The impact of nitric oxide delivery (Group 1) in wild type (WT) mice and LPS (Group 2) administration in WT and iNOS knockout mice on insulin action (hyperinsulinemic-euglycemic clamp), and cardiovascular function (echocardiography and microspheres) (a) was assessed. Cohorts received either a nitric oxide donor (Group 1), LPS (2.0 mg/kg; Group 2), or saline. Design of hyperinsulinemic-euglycemic clamp protocol (Group 1 and 2, Panel b) in chronically catheterized (carotid artery and jugular vein) conscious mice. Droplets indicate blood sampling times (10 μL or 25 μL of whole blood for small and large, respectively). DG deoxyglucose, IV intravenous, KO whole-body iNOS knockout, LPS lipopolysaccharide, MAP mean arterial blood pressure, RBCs red blood cells, SNP sodium nitroprusside

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