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No Evidence for Participation of Non-Adrenergic Non-Cholinergic Subtances in Brain Death-Related Hemodynamic Deterioration of the Feline Potential Heart Donor

GJ. Brandon Bravo Bruinsma, J.J. Bredee, T. J.C. Ruigrok, Van Echteld, J. H.H. Thijssen

Ann Transplant 2001; 6(4): 43-47

ID: 497839

Published: 2001-12-19


Objective: The onset of brain death (BD) is associated with a hyperdynamic cardiovascular response caused by the acute sympathetic release of catecholamines. This is followed by progressive hemodynamic deterioration which may preclude heart donation for transplantation. The mechanism of the hemodynamic collapse is not fully understood. Changes in plasma concentrations of non-adrenergic non-cholinergic (NANC) substances. neuropeptide-Y (NP-Y. a vasoconstrictor) and the vasodilators calcitonin gene-related peptide (CGRP) and substance P (SP). were studied in relation to BD-related hemodynamic alterations. Materials and Methods: Cats (6 BD and 6 controls (C» were studied for 6 h. Heart rat~ (HR) and mean arterial pressure (MAP) were monitored. BD was induced at t = 0 min. At t = -5, 15.60, 180 and 360 min. 5 ml arterial blood samples were taken. The plasma was collected and analyzed. The correlations between MAP and NANC levels were calculated. Results: In the BD cats a maximal and significant increase in HR and MAP was observed at t = 2 min. HR returned to basal levels at t = 20 min and remained at that level. However. MAPdeteriorated progressively to 53:t8 mmHg (p 0.00 I vs C) at / =360 min. NP-Yhad increased from 59.7:t2.5 to 110:t20.2 pmoVI (p 0.05 vsC) at t = 15 min, had returned to basal value at t =60 min and remained at that level. CGR Plevels were lower and SP levels did not change vs C but both showed a trend towards higher levels at t =360 min. The correlations between MAP and NP- Y, CGRP and SP appeared to be not significant. Conclusion: No evidence for participation of NANC substances could be demonstrated in brain death-related hemodynamic deterioration of the feline potential heart donor

Keywords: Brain Death, hemodynamic response, Neuropeptides



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