Baroreceptor dysfunction induced by nitric oxide synthase inhibition in humans
Lukas E. Spieker, MDa,
Roberto Corti, MDa,
Christian Binggeli, MDa,
Thomas F. Lüscher, MD, FACC, FRCP, FESCa and
Georg Noll, MD, FESCa
a Department of Cardiology, University Hospital, Zürich, Switzerland
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Figure 1 Relative changes of central venous pressure (CVP), systolic blood pressure, muscle sympathetic nerve activity (MSA, bursts per minute and volts per minute) and heart rate during lower body negative pressure. Central venous pressure similarly decreased in both drugs (*p < 0.05 vs. baseline, intergroup differences NS). Also, there was no difference in systolic blood pressure, which remained constant during lower body negative pressure in both drugs. During infusion of L-NMMA (1 mg/kg/min), heart rate failed to increase in response to decreased central venous pressure. This was in contrast to phenylephrine (100 µg/min), where heart rate increased ( p < 0.05 vs. phenylephrine; *p < 0.01 by repeated-measures analysis of variance). Open circles = control; black circles = L-NMMA; black boxes = phenylephrine.
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Figure 2 Hemodynamics and muscle sympathetic nervous activity (MSA) at similar levels of systemic arterial (sBP) and central venous (CVP) blood pressure after infusion of L-NMMA (1 mg/kg/min), and phenylephrine (PE, 100 µg/min) in combination with lower body negative pressure (LBNP –30 mm Hg). Stroke volume index (SVI) was significantly lower during L-NMMA infusion than during phenylephrine, whereas systemic vascular resistance (SVR) was significantly higher. No significant difference in sympathetic nerve activity between L-NMMA and phenylephrine could be observed (*p < 0.05).
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