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PubMed1994

Changes in pulmonary circulation during the early postoperative period following single lung transplantation.

This study examines the pulmonary hemodynamics during reimplantation and rejection following unilateral lung transplantation in dogs. Nineteen mongrel dogs were divided into three groups according to the method of treatment used: group 1 (n = 6) underwent modified autotransplantation of the left lung; group 2 (n = 6), allotransplantation without immunosuppression; and group 3 (n = 7), allotransplantation with immunosuppression. The pulmonary arterial blood flow and ventilation scores, assessed by chest X-rays, were measured for 2 weeks postoperatively. Pulmonary blood flow to the transplanted lung decreased slightly in group 1, whereas in group 2, it decreased sharply from the 3rd postoperative day (POD) and was almost completely absent by the 14th POD. In group 3, it decreased by 28% on the 1st POD but recovered gradually to 37% by the 14th POD. Ventilation scores were the same among the three groups on the 1st POD but in group 2, they decreased rapidly from the 3rd POD. This change correlated well with that of the pulmonary arterial (PA) flow, although the ventilation score changed after the PA flow did. In conclusion, rejection was reflected earlier and more distinctly by the changes in PA flow than by chest X-rays.

Animals↗
PubMed1984

Differential response of the pulmonary circulation to prostaglandins E2 and F2 alpha in the presence of unilateral alveolar hypoxia.

Pulmonary hemodynamic responses to several prostaglandins (PGs) are augmented by hypoxia. To test whether responses to vasoconstrictor PGs would be enhanced in hypoxic areas of the lung, resulting in redistribution of blood flow to well-oxygenated areas, the effects of PGE2 and PGF2 alpha were evaluated in anesthetized dogs with divided ventilation, one lung being ventilated with 100% N2 and the other with 100% O2. Thermal dilution techniques coupled with electromagnetic flow measurements permitted estimates of blood flow to each lung. After indomethacin (5 mg/kg i.v.), PGE2 at 0.01, 0.025 and 0.10 micrograms/kg/min i.v. produced significant increases in flow to the O2-ventilated lung at each dose. In addition, PGE2 increased total pulmonary blood flow, but only at the two larger doses. Concomitantly, systemic arterial PO2 increased from 104 +/- 21 to 138 +/- 26 mm Hg (P less than .001). Identical results were obtained when meclofenamate (5 mg/kg i.v.) was used to block PG synthesis. PGF2 alpha increased total pulmonary blood flow (P less than .01) only at the largest dose (0.10 micrograms/kg/min), but did not redistribute flow or increase PO2. Atrial pacing increased total pulmonary blood flow (P less than .001) and flow to both O2 (P less than .001)- and N2 (P less than .05)-ventilated lungs with no change in PO2. We conclude that PGE2 redistributes pulmonary blood flow to well-oxygenated alveoli through mechanisms not related solely to its vasoconstrictor properties or to its capacity to increase cardiac output.

Animals↗