Pharmacological factors that may affect hypoxic pulmonary vasoconstriction (HPV)

Pulmonary vasodilatory drugsPulmonary vasoconstrictive drugs
Soluble guanylate cyclase (sGC) activators, PDE5 inhibitors: decreased V/Q matching/oxygenation in COPD-PH but not in fibrosis patients or healthy volunteers [35–37].Catecholamines with positive inotropic effects and systemic vasoconstriction (α1 receptor stimulation): norepinephrine, phenylephrine, enhance HPV; epinephrine can dose-dependent inhibit HPV due to effects on β2-receptors [38].
NO donors: i.v. application did not impair V/Q matching in healthy volunteers [39] but oxygenation in ARDS patients [40]; inhaled NO can improve V/Q matching [41, 42] (see text).Nitrous oxide: the effects on HPV are unclear; it may increase basal PAP [38].
Prostacyclins and prostacyclin analogs: i.v. application decreased oxygenation and increased shunting in ARDS patients [43]; inhaled iloprost can improve V/Q matching in ARDS [42] (see text).Vasopressin: systemic vasoconstriction, suggested to decrease the PVR/SVR ratio in low doses [44].
Endothelin receptor antagonists: decreased oxygenation in COPD patients [45].
Calcium channel inhibitors: s.l. nifedipine may attenuate V/Q matching in hypoxic or COPD lungs [39, 46, 47]; i.v. diltiazem decreased V/Q matching in ARDS patients [48].
ACE inhibitors/ATII receptor blockers: vasodilatory in volunteers with an activated renin–angiotensin system [49]; lisinopril [50] and losartan [51] decreased HPV in healthy volunteers.
Vasodilators with positive inotropic effects and systemic vasodilation:
dobutamine (β2-adrenergic) inhibits HPV [38], milrinone (PDE3 inhibitor) [52]; inhaled β2-agonists may affect V/Q matching, primarily in asthmatics [53].
Other drugs decreasing HPVDrugs specifically enhancing HPV
Volatile anaesthetics (e.g. halothane, isoflurane and sevoflurane): inhibit HPV and impair oxygenation to varying degrees during one-lung ventilation [38, 54].Almitrine: at low doses, enhances HPV via an unknown mechanism, at least partially via Ca2+-dependent K+ channels [55] (see text).
Acetazolamide (uncertain mechanism, unrelated to carbonic anhydrase) [56].

ACE: angiotensin converting enzyme; ARDS: acute respiratory distress syndrome; ATII: angiotensin II; COPD: chronic obstructive pulmonary disease; NO: nitric oxide; PAP: pulmonary artery pressure; PDE: phosphodiesterase; PH: pulmonary hypertension; PVR: pulmonary vascular resistance; SVR: systemic vascular resistance; V/Q: ventilation/perfusion.