Vasopressin deficiency and pressor hypersensitivity in hemodynamically unstable organ donors

Jonathan M. Chen, Suzanne Cullinane, Talia B. Spanier, John H. Artrip, Ranjit John, Niloo M. Edwards, Mehmet C. Oz, Donald W. Landry

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Abstract

Background - Solid organ donors often develop hypotension due to vasodilation, and recently we observed that a variety of vasodilatory states are characterized by vasopressin deficiency and hypersensitivity. Thus, we investigated the prevalence of vasopressin deficiency in hypotensive solid organ donors without clinical evidence of diabetes insipidus; we also investigated the vasopressor effect of vasopressin replacement in hypotensive donors. Methods and Results - Fifty organ donors were evaluated for hemodynamic instability, (mean arterial pressure [MAP]≤70 mm Hg despite the use of catecholamine vasopressors), and in those unstable donors who were not already receiving exogenous vasopressin, low-dose vasopressin was administered as a continuous infusion (0.04 to 0.1 U/min). MAP, catecholamine requirements, serum vasopressin, and serum osmolality were obtained before and after vasopressin administration. Ten patients meeting the enrollment criteria received vasopressin and MAP increased from 72.2±3.5 to 89.8±4.2 mm Hg, (P<0.05), allowing for complete discontinuation of catecholamine pressors in 4 (40%) patients and a decrement in pressor dose in 4 (40%). Plasma vasopressin levels (2.9±0.8 pg/mL) were low for the degree of hypotension. Conclusions - Hemodynamically unstable organ donors without clinically apparent diabetes insipidus display a defect in the baroreflex- mediated secretion of vasopressin. In these patients, low-dose vasopressin significantly increases blood pressure with a pressor response sufficient to reduce catecholamine administration.

Original languageEnglish (US)
Pages (from-to)II244-II246
JournalCirculation
Volume100
Issue number19 SUPPL.
DOIs
StatePublished - Nov 9 1999

Keywords

  • Blood pressure
  • Transplantation
  • Vasoconstriction

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