Inflammation-induced vasoconstrictorhyporeactivity is caused by oxidative stress
Johannes Pleiner, MD*,
Friedrich Mittermayer, MD*,
Georg Schaller, MD*,
Claudia Marsik, MD*,
Raymond J. MacAllister, MD, FRCP and
Michael Wolzt, MD*,*
* Department of Clinical Pharmacology, University of Vienna, Vienna, Austria
Centre for Clinical Pharmacology and Therapeutics, Department of Medicine, University College London, London, United Kingdom
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Figure 1 Forearm blood flow (FBF) dose–response curves to norepinephrine (NE, upper panel), angiotensin II (ANG II, middle panel), and vasopressin (VP, lower panel) at baseline and after administration of LPS (closed symbols) or placebo (open symbols). The response to vasoconstrictors was attenuated after LPS. The FBF ratio (intervention vs. control arm, baseline defined as 100%) is expressed as mean ± SEM. n = 9; *p < 0.05 between groups, repeated measures ANOVA and Bonferroni corrected t tests.
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Figure 2 Vasoconstriction to norepinephrine at baseline (open symbols) and 4 h after LPS, with co-infusion of placebo (closed symbols, upper panel) or vitamin C (closed symbols, lower panel) on two different study days. The FBF ratio (intervention vs. control arm, baseline defined as 100%) is expressed as mean ± SEM. n = 8; *p < 0.05 between groups, repeated measures ANOVA and Bonferroni corrected t tests.
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Figure 3 Vasoconstriction to angiotensin II at baseline (open symbols) and 4 h after LPS, with co-infusion of placebo (closed symbols, upper panel) or vitamin C (closed symbols, lower panel) on two different study days. The FBF ratio (intervention vs. control arm, baseline defined as 100%) is expressed as mean ± SEM. n = 8; *p < 0.05 between groups, ANOVA and Bonferroni corrected t tests.
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