Chest
Clinical Investigations: VascularLisinopril Attenuates Acute Hypoxic Pulmonary Vasoconstriction in Humans
Section snippets
Subjects
Ten healthy male volunteers, age (mean ± SEM) 27.2 ± 2.1 years (range, 20 to 37 years) were studied. Prior to inclusion, subjects were required to have no abnormality on clinical history or examination, and 12-lead ECG, echocardiogram, biochemical screening, and hematologic indexes were also normal. In addition, spot urinary sodium level was required to be more than 100 mmol/L and no medications were permitted during and for 1 month before the study. Informed written consent to the study
Pulmonary Hemodynamics
There was no significant difference in MPAP at baseline (ie, at T1) between the two study days: lisinopril, 9.2 ± 0.9 mm Hg, vs placebo, 8.6 ± 1.3 mm Hg (Fig 1, top). Likewise, TPR at T1 was similar on both study days: lisinopril, 121 ± 12 dyne·s·cm−5, vs placebo, 122 ± 22 dyne·s·cm−5 (Fig 1, bottom). Hypoxemia caused a significant (p<0.001) increase in MPAP on both study days, although MPAP at T2 was significantly (p<0.005) lower after lisinopril pretreatment (22.6± 1.0 mm Hg) compared with
DISCUSSION
In the present study, we have shown that acute HPV is significantly attenuated by lisinopril in normal humans. We believe this to be directly related to the suppressed plasma levels of ANG II rather than due to a nonspecific vasodilatory action.
It is also important to note that lisinopril pretreatment had no confounding effects on baseline pulmonary or systemic hemodynamic parameters prior to inducing hypoxemia. In the absence of an activated RAS, lisinopril, as would be expected, did not
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This research program was supported by a grant from the Scottish Hospital Endowments Research Trust.
revision accepted July 29.