gms | German Medical Science

28. Wissenschaftlicher Kongress der Deutschen Hochdruckliga

24. bis 27.11.2004, Hannover

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Clonidin senkt den Blutdruck durch Vasodilatation und Senkung des Herzminutenvolumens

Meeting Abstract (Hypertonie 2004)

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  • presenting/speaker J. Nürnberger - Universitätsklinikum Essen, Klinik für Nieren- und Hochdruckkrankheiten
  • presenting/speaker A. Opazo Saez - Universitätsklinikum Essen, Klinik für Nieren- und Hochdruckkrankheiten
  • presenting/speaker A. Mitchell - Universitätsklinikum Essen, Klinik für Nieren- und Hochdruckkrankheiten
  • presenting/speaker R. Schäfers - Universitätsklinikum Essen, Klinik für Nieren- und Hochdruckkrankheiten
  • presenting/speaker T. Philipp - Universitätsklinikum Essen, Klinik für Nieren- und Hochdruckkrankheiten

Hypertonie 2004. 28. Wissenschaftlicher Kongress der Deutschen Hochdruckliga. Hannover, 24.-27.11.2004. Düsseldorf, Köln: German Medical Science; 2005. Doc04hochP72

The electronic version of this article is the complete one and can be found online at: http://www.egms.de/en/meetings/hoch2004/04hoch072.shtml

Published: August 10, 2005

© 2005 Nürnberger et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.en). You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.

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Aim: Clonidine is a classical sympatholytic drug that is widely used for the treatment of hypertension. The aim of this study was to determine the hemodynamic response to Clonidine under physiological conditions and to test the hypothesis that Clonidine would reduce cardiac output and blood pressure resulting in an increase in total peripheral resistance.

Methods: Clonidine's hemodynamic effect was evaluated in 28 young, healthy subjects after a single i. v. dose of 1 µg x kg-1. Impedance cardiography, systolic time intervals and pulse wave analysis were used to characterize myocardial and vascular function.

Results: Clonidine lowered blood pressure, heart rate, left ventricular ejection time, and pulse wave velocity and increased pre-ejection period. Stroke volume and cardiac output decreased gradually over the investigation time of 240 min. Central systolic blood pressure (SBP) was lowered to a larger extent than peripheral SBP. Total peripheral resistance was characterized by an immediate fall of short duration followed by a continuous rise above baseline after 120 min.

Conclusions: Clonidine's blood pressure lowering effect is mediated by both an immediate decrease in vascular resistance and a prolonged decrease in cardiac output, and Clonidine lowers central SBP more than peripheral SBP.