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Arteriolar vasoconstrictive response: comparing the effects of arginine vasopressin and norepinephrine

Barbara E Friesenecker1*, Amy G Tsai2, Judith Martini2, Hanno Ulmer3, Volker Wenzel4, Walter R Hasibeder5, Marcos Intaglietta2 and Martin W Dünser6

Author Affiliations

1 Division of General and Surgical Intensive Care Medicine, Department of Anesthesiology and Critical Care Medicine, Innsbruck Medical University, Innsbruck, Austria

2 Department of Bioengineering, University of California, San Diego, CA, USA

3 Institute of Biostatistics and Documentation, Medical University Innsbruck, Innsbruck, Austria

4 Division of Anesthesiology, Department of Anesthesiology and Critical Care Medicine, Innsbruck Medical University, Innsbruck, Austria

5 Department of Anesthesiology and Critical Care Medicine, Krankenhaus der Barmherzigen Schwestern, Ried im Innkreis, Austria

6 Department of Intensive Care Medicine, University Hospital of Bern, Bern, Switzerland

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Critical Care 2006, 10:R75  doi:10.1186/cc4922


See related commentary by Ertmer et al, http://ccforum.com/content/10/3/144

Published: 12 May 2006

Abstract

Introduction

This study was designed to examine differences in the arteriolar vasoconstrictive response between arginine vasopressin (AVP) and norepinephrine (NE) on the microcirculatory level in the hamster window chamber model in unanesthetized, normotonic hamsters using intravital microscopy. It is known from patients with advanced vasodilatory shock that AVP exerts strong additional vasoconstriction when incremental dosage increases of NE have no further effect on mean arterial blood pressure (MAP).

Methods

In a prospective controlled experimental study, eleven awake, male golden Syrian hamsters were instrumented with a viewing window inserted into the dorsal skinfold. NE (2 μg/kg/minute) and AVP (0.0001 IU/kg/minute, equivalent to 4 IU/h in a 70 kg patient) were continuously infused to achieve a similar increase in MAP. According to their position within the arteriolar network, arterioles were grouped into five types: A0 (branch off small artery) to A4 (branch off A3 arteriole).

Results

Reduction of arteriolar diameter (NE, -31 ± 12% versus AVP, -49 ± 7%; p = 0.002), cross sectional area (NE, -49 ± 17% versus AVP, -73 ± 7%; p = 0.002), and arteriolar blood flow (NE, -62 ± 13% versus AVP, -80 ± 6%; p = 0.004) in A0 arterioles was significantly more pronounced in AVP animals. There was no difference in red blood cell velocities in A0 arterioles between groups. The reduction of diameter, cross sectional area, red blood cell velocity, and arteriolar blood flow in A1 to A4 arterioles was comparable in AVP and NE animals.

Conclusion

Within the microvascular network, AVP exerted significantly stronger vasoconstriction on large A0 arterioles than NE under physiological conditions. This observation may partly explain why AVP is such a potent vasopressor hormone and can increase systemic vascular resistance even in advanced vasodilatory shock unresponsive to increases in standard catecholamine therapy.