Reference : Analysis of Endotoxin Effects on the Intact Pulmonary Circulation
Scientific journals : Article
Human health sciences : Cardiovascular & respiratory systems
Analysis of Endotoxin Effects on the Intact Pulmonary Circulation
Lambermont, Bernard mailto [Centre Hospitalier Universitaire de Liège - CHU > > Frais communs médecine >]
Kolh, Philippe mailto [Université de Liège - ULg > Département des sciences biomédicales et précliniques > Service de biochimie et de physiologie humaines, normale et pathologique > > >]
Detry, Olivier mailto [Centre Hospitalier Universitaire de Liège - CHU > > Chirurgie abdominale- endocrinienne et de transplantation >]
Gérard, Paul mailto [Université de Liège - ULg > Département de mathématique > Statistique (aspects expérimentaux) >]
Marcelle, Roland [Université de Liège - ULg > > Relations académiques et scientifiques (Médecine) >]
D'Orio, Vincenzo mailto [Université de Liège - ULg > Département des sciences cliniques > Médecine d'urgence - bioch. et phys. hum. normales et path.]
Cardiovascular Research
Yes (verified by ORBi)
[en] OBJECTIVE: The mechanism of sustained alterations in pulmonary hemodynamics during endotoxin shock remains unclear. To gain more detailed knowledge we used the four-element windkessel model as a descriptor of the pulmonary circuit. METHODS: Consecutive changes in characteristic resistance (R1), vascular compliance (C), input resistance (R2) and inductance (L) were continuously assessed following injection of endotoxin in 6 anaesthetised pigs, and were compared with the corresponding values measured in a similar group of sham-operated animals. RESULTS: Endotoxin challenge resulted in a biphasic pulmonary artery pressure response. Blood flow decreased progressively from 2.8 +/- 0.2 l/min to 2 +/- 0.2 l/min. Ohmic pulmonary vascular resistance (PVR) increased gradually from 0.2 +/- 0.04 to 0.76 +/- 0.1 mm Hg s ml-1. The early increase in PAP (from 14 +/- 2 to 27 +/- 4 mm Hg) was mediated by changes in both R1 (from 0.04 +/- 0.01 to 0.06 +/- 0.01 mm Hg s ml-1) and R2 (from 0.16 +/- 0.04 to 0.61 +/- 0.2 mm Hg s ml-1). These responses, in turn, altered the proximal vascular compliance. A subsequent increase in PAP (from 27 +/- 2 to 32 +/- 3 mm Hg) paralleled the specific decline in distal pulmonary vasculature compliance from 0.84 +/- 0.1 to 0.65 +/- 0.1 ml/mmHg. Analysis of the time course of PVR did not allow us to distinguish between vasoconstriction and stiffening of the vascular tree as mechanisms accounting for PAP changes. CONCLUSIONS: Endotoxemia leads to pulmonary hypertension, which is a result of constriction of proximal pulmonary arteries during the early phase, whereas the late phase is characterised by a decline in distal pulmonary vasculature compliance.

File(s) associated to this reference

Fulltext file(s):

Restricted access
Lambermont_41_1_275_1999.pdfPublisher postprint176.27 kBRequest copy
Open access
Lambermont_Cardiovasc Res_1999_41_275.pdfAuthor postprint129.45 kBView/Open

Bookmark and Share SFX Query

All documents in ORBi are protected by a user license.