The Paradox of Pulmonary Vascular Resistance: Restoration of Pulmonary Capillary Recruitment as a Sine Qua Non for True Therapeutic Success in Pulmonary Arterial Hypertension

Figures

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  Figure 1. Schematic representation of increased functional capillary surface area (FCSA) during capillary recruitment, as cardiac output (CO) and thus pulmonary blood flow doubles. Individual capillary flow (Fcap) remains unchanged as more capillaries are recruited to accept the total blood flow. However, the surface area and the number of ectoenzyme sites available for substrate metabolism increases. Black symbols represent enzymatic sites, purple symbols represent blood cells, small black ovals represent unmetabolized substrate and small ovals represent metabolized substrate.

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  Figure 2. Functional capillary surface area normalized to body surface area (FCSA, mL/min/m2) in human lungs post acute vasodilator therapy, as compared to pulmonary artery pressure (PAP), cardiac output, and pulmonary vascular resistance (PVR) post vasodilator. The open circles represent “resistance” responders and the filled circles represent “pressure” responders. Data have been adapted from reference [32].

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  Figure 3. Functional capillary surface area normalized to body surface area (FCSA, mL/min/m2) in human lungs post acute vasodilator therapy, as compared to percent change in pulmonary vascular resistance (PVR) after administration of a vasodilator. The open circles represent “resistance” responders and the filled circles represent “pressure” responders. Data have been adapted from reference [32].

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  Figure 4. Schematic representation of the effects of pulmonary arterial hypertension (PAH) on pulmonary capillary surface area (CSA). Shown are the potential effect that vasodilator-type therapies (VASODILATOR), and therapies that would affect cellular proliferative obstruction (ANTIPROLIFERATIVE), would have on hemodynamics (PAP, pulmonary artery pressure; PVR, pulmonary vascular resistance) and CSA, at rest and upon exercise.