Relationship Between Procalcitonin Values and Infection in Brain-Dead Organ Donors

Rangeard, O.; Audibert, G.; Perrier, Jean‐François; Loos-Ayav, Carole; Lalot, Jean-Marc; Agavriloaie, M.; Meistelman, Claude; Grégoire, Hélène; Mertès, Paul-Michel; Longrois, Dan

doi:10.1016/j.transproceed.2007.02.101

Cited by 5 publications

(1 citation statement)

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“…[30] Yet, a relationship of the above phenomenon to infection or systemic inflammatory changes in the brain-dead donor has not been established. [31] The higher levels of the brain-specific marker S-100b observed in our BD patients reflect the presence and the severity of cerebral damage, [32,33] but might also denote the major inflammatory impact of BD on peripheral organ dysfunction. [34–36]…”

Section: Discussionmentioning

confidence: 99%

Preclinical Pulmonary Capillary Endothelial Dysfunction is Present in Brain Dead Subjects

et al. 2013

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Pulmonary endothelium is a major metabolic organ affecting pulmonary and systemic vascular homeostasis. Brain death (BD)-induced physiologic and metabolic derangements in donors’ lungs, in the absence of overt lung pathology, may cause pulmonary dysfunction and compromise post-transplant graft function. To explore the impact of BD on pulmonary endothelium, we estimated pulmonary capillary endothelium-bound (PCEB)-angiotensin converting enzyme (ACE) activity, a direct and quantifiable index of pulmonary endothelial function, in eight brain-dead patients and ten brain-injured mechanically ventilated controls. No subject suffered from acute lung injury or any other overt lung pathology. Applying indicator-dilution type techniques, we measured single-pass transpulmonary percent metabolism (%M) and hydrolysis (v) of the synthetic, biologically inactive, and highly specific for ACE substrate 3H-benzoyl-Phe-Ala-Pro, under first order reaction conditions, and calculated lung functional capillary surface area (FCSA). Substrate %M (35 ± 6.8%) and v (0.49 ± 0.13) in BD patients were decreased as compared to controls (55.9 ± 4.9, P = 0.033 and 0.9 ± 0.15, P = 0.033, respectively), denoting decreased pulmonary endothelial enzyme activity at the capillary level; FCSA, a reflection of endothelial enzyme activity per vascular bed, was also decreased (BD patients: 1,563 ± 562 mL/min vs 4,235 ± 559 in controls; P = 0.003). We conclude that BD is associated with subtle pulmonary endothelial injury, expressed by decreased PCEB-ACE activity. The applied indicator-dilution type technique provides direct and quantifiable indices of pulmonary endothelial function at the bedside that may reveal the existence of preclinical lung pathology in potential lung donors.

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