1. Endothelial Dysfunction Providing the Basis for the Treatment of Pulmonary Hypertension 
Timothy W. Higenbottam, MD, FCCP, Elizabeth A. Laude, PhD 
CHEST 
Volume 114, Issue 1, Pages 72S-79S (July 1998)
DOI: /chest.114.1_Supplement.72S
Copyright © 1998 The American College of Chest Physicians Terms and Conditions

2. Figure 1
Percentage survival of (top, A) those patients who had pulmonary vasodilation (measured as a fall in mean pulmonary artery pressure) with epoprostenol and (bottom, B) those patients who had no vasodilation with epoprostenol.
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Copyright © 1998 The American College of Chest Physicians Terms and Conditions

3. Figure 2
Comparison of effects on pulmonary (PVR) and systemic (SVR) vascular resistance of an infusion of PGI2 (0.5 mg in 250 mL) at rates of 4, 8, and 12 mL/h and inhalation of NO (40 ppm in air) with baseline (BL) values in eight patients with pulmonary hypertension. Means ± SEM are shown. Asterisk: p<0.05; double asterisk: p<0.01.
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Copyright © 1998 The American College of Chest Physicians Terms and Conditions

4. Figure 3
Regression of rate of production of NO against predicted KCO in primary pulmonary hypertension (closed circles) and control (open circles) groups.
CHEST  , 72S-79SDOI: ( /chest.114.1_Supplement.72S)
Copyright © 1998 The American College of Chest Physicians Terms and Conditions

5. Figure 4
Regulation of the effects of ET-1. ET = endothelin: ANP = atrial naturietic peptide.x
CHEST  , 72S-79SDOI: ( /chest.114.1_Supplement.72S)
Copyright © 1998 The American College of Chest Physicians Terms and Conditions