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Effects of isoproterenol on distribution of perfusion in embolized dog lungs.

In 19 mechanically venilated, anesthetized dogs, autologous venous thrombi were formed in the inferior vena cava and subsequently released. Serial perfusion lung scintigrams revealed the postembolic distribution of pulmonary blood flow before, during, and after the infusion of isoproterenol at 2.2 micrograms/min. Isoproterenol failed to restore perfusion to embolically occluded regions. When reperfusion occurred it was attributable to clot resolution. Gas exchange and hemodynamic measurements obtained in seven thromboembolized animals showed no scan evidence of reperfusion during the isoproterenol infusion. After embolization, cardiac output increased from 1.7 to 2.6 liter/min (p less than 0.05), and PvO2 from 38.0 to 45.3 mm Hg (p less than 0.05). Shunt fraction remained unchanged. The postembolic infusion of isoproterenol was associated with a further increase in cardiac output to 3.6 liter/min (p less than 0.01), an elevation in PvO2 to 50.7 mm Hg, along with a decrease in pulmonary vascular resistance from the postembolic mean of 448 to 246 dynes.sec.cm-5 (p less than 0.05). Perfusion defects following acute pulmonary thromboembolization are not altered by the infusion of the potent pulmonary vasodilator, isoproterenol. Infusion of this drug following thromboembolization may have potential therapeutic benefit by reducing pulmonary vascular resistance, increasing cardiac output, and elevating the mixed-venous oxygen tension.