Dose-response to inhaled aerosolized prostacyclin for hypoxemia due to ARDS

Citation
Pv. Van Heerden et al., Dose-response to inhaled aerosolized prostacyclin for hypoxemia due to ARDS, CHEST, 117(3), 2000, pp. 819-827
Citations number
36
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
CHEST
ISSN journal
0012-3692 → ACNP
Volume
117
Issue
3
Year of publication
2000
Pages
819 - 827
Database
ISI
SICI code
0012-3692(200003)117:3<819:DTIAPF>2.0.ZU;2-O
Abstract
Study objectives: This study was carried out to determine the efficacy of a nd dose-response relationships to inhaled aerosolized prostacyclin (LAP), w hen used as a selective pulmonary vasodilator (SPV) in patients with severe hypoxemia due to ARDS. Design: Unblinded, interventional, prospective clinical study. Setting: A general ICU in a university-affiliated, tertiary referral center . Patients: Nine adult patients with severe ARDS (lung injury score, greater than or equal to 2.5). Interventions: All patients received IAP over the dose range 0 to 50 ng/kg/ min, The IAP was delivered via a jet nebulizer placed in the ventilator cir cuit. Dose increments were 10 ng/kg/min every 30 min. Measurements and results: Cardiovascular parameters (cardiac index and mean pulmonary and systemic pressures), indexes of oxygenation (Pao(2)/fraction of inspired oxygen [FIO2] ratio and alveolar-arterial oxygen partial press ure difference [P(A-a)O-2] and shunt fraction were measured or calculated a t each dose interval, as were platelet aggregation and systemic levels of p rostacyclin metabolite (6-keto prostaglandin F1 alpha). A generalized linea r regression model was used to determine a dose effect of MP on these param eters, The Wilcoxon rank sum test for related measures was used to compare the effects of various doses of LAP, IAP acted as an SPV, with a statistica lly significant dose-related improvement in Pao(2)/FIO2 ratio (p = 0.003) a nd P(A-a)O-2 (p = 0.01). Systemic prostacyclin metabolite levels increased significantly in response to delivered LAP (p = 0.001). There was no signif icant dose effect on systemic or pulmonary arterial pressures, or on platel et function, as determined by platelet aggregation in response to challenge with adenosine diphosphate. Conclusions: LAP is an efficacious SPV, with marked dose-related improvemen t in oxygenation and with no demonstrable effect on systemic arterial press ures over die dose range 0 to 50 ng/kg/min. Despite significant systemic le vels of prostacyclin metabolite, there was no demonstrable platelet functio n defect.