Vasopressin deficiency and presser hypersensitivity in hemodynamically unstable organ donors

Background-Solid organ donors often develop hypotension due to vasodilation , and recently we observed that a variety of vasodilatory states are charac terized by vasopressin deficiency and hypersensitivity, Thus, we investigat ed the prevalence of vasopressin deficiency in hypotensive solid organ dono rs without clinical evidence of diabetes insipidus; we also investigated th e vasopressor effect of vasopressin replacement in hypotensive donors. Methods and Results-Fifty organ donors were evaluated for hemodynamic insta bility, (mean arterial pressure [MAP]less than or equal to 70 mm Hg despite the use of catecholamine vasopressors), and in those unstable donors who w ere not already receiving exogenous vasopressin, low-dose vasopressin was a dministered as a continuous infusion (0.04 to 0.1 U/min). MAP, catecholamin e requirements. serum vasopressin, and serum osmolality were obtained befor e and after vasopressin administration. Ten patients meeting the enrollment criteria received vasopressin and MAP increased from 72.7+/-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%). P lasma vasopressin levels (2.9+/-0.8 pg/mL) were low for the degree of hypot ension, Conclusions Hemodynamically unstable organ donors without clinically appare nt diabetes insipidus display a defect in the baroreflex-mediated secretion of vasopressin. In these patients, low-dose vasopressin significantly incr eases blood pressure with a presser response sufficient to reduce catechola mine administration.