Effects of arginine-vasopression on regional blood volume distribution in supine humans

Summary

In healthy humans, the increase in arterial blood pressure seen in patients with autonomic dysfunction in response to exogenous vasopressin (AVP) is abolished. We tested the hypothesis that redistribution of blood from the intra- to the extrathoracic vascular compartment might contribute to this buffer response. Regional distribution of^99mTc labeled autologous red cells was assessed in healthy supine volunteers (n=7) during arginine-vasopressin administration (1 ng·kg⁻¹ bolus i.v. followed by a 14-min infusion of 3 ng·kg⁻¹·min⁻¹), along with arterial and central venous pressures, and heart rate. Exogenous vasopressin increased plasma vasopressin concentration from 4.0±1.4 SEM to 91 pg·ml⁻¹±12. Thoracic counts increased slightly but significantly by 2.2%±0.9, while global abdominal counts remained unchanged. Most surprisingly, counts in the liver markedly increased (+8.1%±1.8, p=0.02), but significantly decreased in the spleen (−3.1%±1.4). Intestinal (−2.5%±2.4) and limb counts did not change significantly. Consistent with the increase in thoracic counts centralvenous pressure increased from 3.6 mm Hg±1 to 4.7±1 (p=0.02), while arterial pressure and heart rate did not change. All changes reversed towards baseline when vasopressin administration ceased. Thus, in humans with an intact autonomic system, vasopressin, at concentrations observed during hypotension, increases liver and, albeit to a small extent, also thoracic blood volume, but decreases splenic blood content. These results 1) are incompatible with the hypothesis that AVP induces a shift of blood from intra- to extrathoracic capacitance vessels, and 2) show that AVP increases rather than decreases central blood volume.