ISCHEMIA AND REPERFUSION INJURY - PREVENTION OF PULMONARY-HYPERTENSION AND LEUKOSEQUESTRATION FOLLOWING LOWER-LIMB ISCHEMIA

Ischemia is a common clinical event with potentially serious consequen ces. The major part of tissue damage occurs upon reperfusion and is me diated by activated neutrophils. Ischemia reperfusion injury is manife sted by oedema and increased microvascular permeability. This study te sted cardiopulmonary functions following 2 h of lower limb ischemia. A nesthetized dogs were randomized into three groups: nonischemic sham d ogs (n = 4), ischemic control dogs (n = 8) and ischemic dogs pretreate d with prostaglandin (PG)E(1) (n = 8). In control animals, mean pulmon ary artery pressure (mPAP) increased 1 min after declamping from 13.37 +/- 2.61 mmHg to 16.88 +/- 3.68 mm Hg (P < 0.05). Pulmonary microvasc ular pressure (Pmv) increased within 1 minute of reperfusion from 7.71 +/- 1.87 mm Hg to 10.54 +/- 3.71 mm Hg (P < 0.05). These changes are consistent with increased lung microvascular permeability. White blood cell count fell slightly but not significantly and lung histology sho wed leukosequestration in alveoli of 171 +/- 22 polymorphonuclear leuk ocyte (PMN)/10 high powered fields (HPF) in the ischemic control group compared with 121 +/- 56 PMN/10 HPF in the sham group (P < 0.05). Sys temic arterial pressure, cardiac output, central venous pressure and p ulmonary artery wedge pressure were unaffected. In animals pretreated with PGE(1), mPAP and Pmv were unchanged during reperfusion. Lung hist ologic findings appeared normal and leukosequestration was not observe d. PMN counts in alveoli showed 95 +/- 26 PMN/10 HPF, lower than in is chemic control animals (P < 0.05). These data indicate that lower limb ischemia during reperfusion leads to pulmonary hypertension and leuko sequestration. PGE(1) infusion is effective in limiting ischemia reper fusion injury.