Key result
BQ-123 decreased pulmonary vascular resistance by 26% and systemic vascular resistance by 21% during normoxia (P<0.05), but did not alter the pulmonary vasoconstrictive response to acute hypoxia.
Why the study?
Does BQ-123 alter resting pulmonary vascular tone and hypoxic pulmonary vasoconstriction in healthy volunteers?
Does BQ-123 alter resting pulmonary vascular tone and hypoxic pulmonary vasoconstriction in healthy volunteers?
Endothelin contributes to basal pulmonary and systemic vascular tone during normoxia but does not mediate acute hypoxic pulmonary vasoconstriction in humans.
Answers are grounded in this paper and cite their sources.
Endothelin contributes to basal vascular tone in healthy humans; leaves open its role in hypoxic pulmonary vasoconstriction during disease.
The contribution of endothelin to resting pulmonary vascular tone and hypoxic pulmonary vasoconstriction in humans is unknown. We studied the hemodynamic effects of BQ-123, an endothelin type A receptor antagonist, on healthy volunteers exposed to normoxia and hypoxia. Hemodynamics were measured at room air and after 15 min of exposure to hypoxia (arterial PO(2) 99.8 +/- 1.8 and 49.4 +/- 0.4 mmHg, respectively). Measurements were then repeated in the presence of BQ-123. BQ-123 decreased pulmonary vascular resistance (PVR) 26% and systemic vascular resistance (SVR) 21%, whereas it increased cardiac output (CO) 22% (all P < 0.05). Hypoxia raised CO 28% and PVR 95%, whereas it reduced SVR 23% (all P < 0.01). During BQ-123 infusion, hypoxia increased CO 29% and PVR 97% and decreased SVR 22% (all P < 0.01). The pulmonary vasoconstrictive response to hypoxia was similar in the absence and presence of BQ-123 [P = not significant (NS)]. In vehicle-treated control subjects, hypoxic pulmonary vasoconstriction did not change with repeated exposure to hypoxia (P = NS). Endothelin contributes to basal pulmonary and systemic vascular tone during normoxia, but does not mediate the additional pulmonary vasoconstriction induced by acute hypoxia.
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Johnson et al. (2002) studied Healthy volunteers. BQ-123 vs. Vehicle-treated control / absence of BQ-123 was evaluated on Hemodynamic effects including pulmonary vascular resistance (PVR), systemic vascular resistance (SVR), and cardiac output (CO) (p=<0.05). BQ-123 decreased pulmonary vascular resistance by 26% and systemic vascular resistance by 21% during normoxia (P<0.05), but did not alter the pulmonary vasoconstrictive response to acute hypoxia.
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