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Cardiovascular Research 1999 41(1):275-281; doi:10.1016/S0008-6363(98)00213-2
© 1999 by European Society of Cardiology
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Copyright © 1999, European Society of Cardiology

Analysis of endotoxin effects on the intact pulmonary circulation

Bernard Lambermont*, Philippe Kolh, Olivier Detry, Paul Gerard, Roland Marcelle and Vincent D'Orio

Hemodynamic Research Laboratory (Hemoliege), CHU Sart Tilman, University of Liege, 4000 Liege, Belgium

* Corresponding author. Address for correspondence: Intensive Care Unit (-2C), Department of Internal Medicine, CHU Sart Tilman (B35), University of Liege, 4000 Liege, Belgium. Tel.: +32-4-366-7111; fax: +32-4-366-7723.

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.

KEYWORDS Pig; Pulmonary circulation; Septic shock; Endotoxin; Models; Vascular resistance; Vascular compliance


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