Modulation of Pulmonary Vascular Resistance and Edema Formation by Short-Term Infusion of a 10% Fish Oil Emulsion

1993 ◽  
Vol 20 (6) ◽  
pp. 291-300 ◽  
Author(s):  
T. Koch ◽  
H.P. Duncker ◽  
A. Klein ◽  
E. Schlotzer ◽  
B.M. Peskar ◽  
...  
Keyword(s):  
Fish Oil ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Short Term ◽  
Edema Formation ◽  
Oil Emulsion

Alteration of n-3 fatty acid composition in lung tissue after short-term infusion of fish oil emulsion attenuates inflammatory vascular reaction

1996 ◽  
Vol 24 (11) ◽  
pp. 1893-1902 ◽  
Author(s):  
Irmingard Breil ◽  
Thea Koch ◽  
Axel Heller ◽  
Ewald Schlotzer ◽  
Adolf Grunert ◽  
...  
Keyword(s):  
Fatty Acid Composition ◽  
Fatty Acid ◽  
Fish Oil ◽  
Acid Composition ◽  
Lung Tissue ◽  
Short Term ◽  
Oil Emulsion ◽  
Vascular Reaction

Intravenous lipid composition affects hypoxic pulmonary vasoconstriction in the newborn piglet

2001 ◽  
Vol 79 (7) ◽  
pp. 594-600 ◽  
Author(s):  
Keith J Barrington ◽  
George Chan ◽  
John E. Van Aerde
Keyword(s):  
Pulmonary Hypertension ◽  
Cardiac Output ◽  
Fatty Acid ◽  
Parenteral Nutrition ◽  
Fish Oil ◽  
Total Parenteral Nutrition ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Plasma Levels ◽  
Lipid Emulsion

To examine the effects of altering the fatty acid (FA) composition of intravenous (IV) lipid emulsions on pulmonary vascular resistance (PVR) and thromboxane production, we studied three groups of newborn piglets after three days of either sow's milk (milk), or total parenteral nutrition (TPN) with either iv soy bean oil (SBO, 52% n-6 and 8% n-3 FA) or fish oil (FO, 5% n-6 and 51% n-3 FA) emulsions. At baseline, and during hypoxia at 20 min and 2 h, cardiac output (Q) was measured, PVR calculated and plasma levels of a prostacyclin metabolite (6-keto-PgF1α) and thromboxane B2 (TxB2) were measured. Fatty acid composition of the lung phospholipids was analyzed. There was an exaggerated increase in PVR and decrease in Q during prolonged hypoxia in the TPN-SBO group as compared with the other two groups. There was no difference in PVR and Q between the milk and TPN-FO groups. FA of lung phospholipids reflected the high dietary level of long chain n-3 FA in the TPN-FO group. However, no differences in plasma levels of 6-keto-PgF1α or TxB2 were found. Intravenous emulsions made from SBO reduced cardiac output and increased pulmonary vascular resistance in the hypoxic newborn piglet, whereas iv FO emulsions did not. When subjects with pulmonary hypertension are receiving TPN iv SBO may be detrimental; iv FO may be beneficial, giving similar responses as in a milk-fed subject.Key words: total parenteral nutrition, fish oil, pulmonary hypertension, lipid emulsion, fatty acids.Key words: total parenteral nutrition, fish oil, pulmonary hypertension, lipid emulsion, fatty acids.

Effect of endotoxin pretreatment on the pulmonary vascular response to hypoxia in O2-exposed lambs

1988 ◽  
Vol 65 (4) ◽  
pp. 1586-1591 ◽  
Author(s):  
T. A. Hazinski ◽  
K. A. Kennedy ◽  
M. L. France
Keyword(s):  
Respiratory Failure ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Pressor Response ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Oxidant Stress ◽  
Lung Edema ◽  
Vascular Response ◽  
Edema Formation ◽  
Constrictor Response

We recently reported that endotoxin infusion before O2 exposure significantly reduced or delayed the onset of pulmonary edema formation and respiratory failure by reducing the oxidant stress of O2 exposure. Despite these beneficial effects of endotoxin treatment, lung microvascular permeability eventually increased, but postmortem lung water content was less than expected. Prolonged O2 breathing blunts or abolishes the pulmonary constrictor response to alveolar hypoxia in some species, and it is possible that the loss of this response could contribute further to edema formation. To determine whether the reduction in lung edema observed in endotoxin-treated, O2-exposed lambs was linked to the preservation of hypoxic pulmonary vasoconstriction (HPV), we measured pulmonary vascular resistance before and after 8 min of isocarbic hypoxia (inspired O2 fraction 0.12) during each day of O2 exposure. In six control lambs, the pressor response to hypoxia was abolished after 72 h in O2, and the lambs developed respiratory failure shortly thereafter. In six endotoxin-treated lambs, HPV was preserved for as long as 144 h of O2 exposure. In two control O2-exposed lambs in whom HPV was abolished, the infusion of either angiotensin or prostaglandin H2 analogue increased pulmonary vascular resistance by greater than 75%. We conclude that in lambs 1) hyperoxia abolishes the pulmonary vascular response to hypoxia, 2) endotoxin pretreatment reduces acute O2-induced lung injury and preserves the pulmonary constrictor response to hypoxia, and 3) the loss of HPV during O2 exposure may be the result of oxidant-mediated injury to the hypoxia response itself and not the result of diffuse damage to the vasoconstrictor effector mechanism.

Pulmonary Vascular Versus Right Ventricular Function Changes During Targeted Therapies of Pulmonary Hypertension – An Argument for Upfront Combination Therapy?

2012 ◽  
Vol 8 (3) ◽  
pp. 209
Author(s):  
Wouter Jacobs ◽  
Anton Vonk-Noordegraaf ◽  
◽  
Keyword(s):  
Combination Therapy ◽  
Right Ventricle ◽  
Right Ventricular ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Meta Analysis ◽  
Right Heart Failure ◽  
Functional Class ◽  
Pulmonary Vasculature ◽  
The Right

Pulmonary arterial hypertension is a progressive disease of the pulmonary vasculature, ultimately leading to right heart failure and death. Current treatment is aimed at targeting three different pathways: the prostacyclin, endothelin and nitric oxide pathways. These therapies improve functional class, increase exercise capacity and improve haemodynamics. In addition, data from a meta-analysis provide compelling evidence of improved survival. Despite these treatments, the outcome is still grim and the cause of death is inevitable – right ventricular failure. One explanation for this paradox of haemodynamic benefit and still worse outcome is that the right ventricle does not benefit from a modest reduction in pulmonary vascular resistance. This article describes the physiological concepts that might underlie this paradox. Based on these concepts, we argue that not only a significant reduction in pulmonary vascular resistance, but also a significant reduction in pulmonary artery pressure is required to save the right ventricle. Haemodynamic data from clinical trials hold the promise that these haemodynamic requirements might be met if upfront combination therapy is used.

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