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To study the value of indexes of endothelial cell function in experimentally induced pulmonary microvascular injury, lung damage was produced in anesthetized dogs by intravenous injection of oleic acid (OA; n = 6), alpha-naphthylthiourea (ANTU; n = 5), or phorbol myristate acetate (PMA; n = 6). Angiotensin-converting enzyme (ACE) activity in serum and simultaneous measurements of serotonin (SER) and propranolol (PROP) pulmonary extraction along with several physiologic parameters were determined and compared with those obtained in a control group (n = 5) before and then at 2-h intervals for 8 h after administration of the toxic agent. ACE activity in serum showed a sustained and significant increase in the PMA and OA groups throughout the whole study period, whereas it decreased significantly at 4 h in the ANTU group. SER pulmonary uptake decreased significantly, but slightly, only in the PMA group at 8 h (-5%). At 6 and 8 h respectively, PROP extraction dropped significantly in the PMA (-11 and -13%) and OA (-13 and -19%) groups. This decrease in PROP extraction was likely to result from physiologic changes due to the development of pulmonary edema as suggested by the correlation between the changes in amine uptake and those affecting pulmonary artery pressure and total static respiratory compliance. The lack of effects on SER uptake by the lungs under these experimental conditions indicate that dissociation exists between metabolic dysfunction of pulmonary endothelial cells and fluid leakage.

Left lower lobe-to-total blood flow ratio (Ql/QT) was measured with electromagnetic flow probes in anesthetized open-chest dogs. There was a 66% reduction in Ql/QT during lobar collapse, a 53% reduction during lobar ventilation hypoxia with pulmonary venous PO2 and PCO2 equal to mixed venous tensions, and a 45% reduction during a similar degree of ventilation hypoxia but with normal end-tidal PCO2. We concluded that the reduction in blood flow during lobar collapse is due predominantly to hypoxic vasoconstriction, but that this mechanism is augmented by the raised PCO2 and mechanical factors present during collapse.

Dopamine increases blood flow to a hypoxic left lower lobe in dogs. To elucidate possible mechanisms, left lower lobe collapse was induced in anesthetized dogs, and lobar (QLLL) and total (QT) pulmonary blood flow was measured by electromagnetic flow probes. Dopamine infusion increased mean pulmonary arterial pressure (Ppa), QT, and QLLL. However, the increase in QLLL was double that produced by a similar increase in Ppa without increase in QT (inflation of a Swan-Ganz balloon in right pulmonary artery) or by a similar increase in QT with smaller increase in Ppa (opening of arteriovenous fistulas). QLLL/QT was not changed by opening arteriovenous fistulas, but was increased by Swan-Ganz balloon inflation, and by infusion of dopamine. It is concluded that the increase in QLLL/QT produced by dopamine was due to a decrease in hypoxic vasoconstriction in the lobe secondary to an increase in mixed venous PO2 and to vasoconstriction in the oxygenated lung.

Venovenous perfusion has been conducted in 12 healthy dogs to examine carbon dioxide (CO2) transfer and haemocompatibility over 9 h during total extracorporeal CO2 removal using a microporous polypropylene membrane lung with secondary flows in the blood channel. The anaesthetized animals were maintained normocapnic by including CO2 in the inspired gases. The CO2 removal was achieved using 0.631 m2 of active membrane, at a pulsatile Reynolds number of 50, and a CO2 extraction from blood of 17.8 ml (STP) dl-1. Gas exchange remained constant during the perfusions. Several aspects of our results suggest that the haemocompatibility of a system of the kind used here is at least as favourable as that of a steady flow device using a continuous silicone rubber membrane of equivalent gas transfer capability.

Hypoxic pulmonary vasoconstriction was induced in the left lower lobe of fifteen dogs by ventilating the lobe with 7% O2 or by absorption collapse, and the distribution of flow between the lobe and the remainder of the lung was measured with electromagnetic flow probes. The lobar to total blood flow ratio was reduced by lobar ventilation hypoxia and decreased further during lobar collapse. In seven dogs, an infusion of 20 micrograms kg-1 min-1 of dopamine produced an increase in total blood flow, an increase in pulmonary artery pressure (P less than 0.01), and an increase in lobar to total flow ratio (P less than 0.05) during both hypoxic states. There was a significant fall in arterial PO2 (P less than 0.01) during ventilation hypoxia. Similar changes in total and lobar to total flow ratio (P less than 0.01) were observed in eight dogs given 20 micrograms kg-1 min-1 of dobutamine, but there were no changes in pulmonary artery pressure. The greater increase in total flow (+ 111%) resulted in a marked increase in mixed venous PO2 and no significant changes in arterial PO2 in this group of dogs. It is concluded that both drugs produce an increase in lobar to total blood flow ratio and shunt fraction, but that the mechanisms causing the redistribution of flow may differ.