Apnea causes microvascular perfusion maldistribution in isolated rat lungs.

Abstract

Obstructive sleep apnea is associated with significant cardiovascular disease, yet little is known about the effects of OSA on pulmonary microvascular perfusion. In a recent report, we showed that pulmonary microvascular perfusion was significantly mal‐distributed in anesthetized, spontaneously breathing rats exposed to five episodes of obstructive apnea. We quantified microvascular perfusion by analyzing trapping patterns of 4 μm diameter fluorescent latex particles infused into the pulmonary circulation after the last episode. We could not determine if the perfusion maldistribution was due to the effects of large subatmospheric intrapleural pressures during apnea, or to precapillary OSA hypoxic vasoconstriction. To address this, we repeated these studies using isolated, buffer‐perfused rat lungs (P pulm art, 10 cm H2O) ventilated in a chamber (−5 to −15 cm H2O, 25 breaths/min; P trachea = 0). We simulated apnea by clamping the trachea and cycling the chamber pressures between −25 and −35 cm H2O for five breaths. After five apnea episodes, we infused 4 μm diam. fluorescent latex particles into the pulmonary artery. The number of particles recovered from the venous effluent was 74% greater in nonapneic isolated lungs compared to apneic lungs (P ≤ 0.05). Apneic lungs also had perfusion maldistributions that were 73% greater than those without apnea (P ≤ 0.05). We conclude that simulated apnea in isolated, perfused rat lungs produces significantly greater particle trapping and microvascular perfusion maldistribution than in nonapneic isolated lungs. We believe these effects are due to the large, negative intrapleural pressures produced during apnea, and are not due to hypoxia.