Abdominal aortic aneurysmectomy (AAA) results in thromboxane (Tx)A2 generation, a rise in mean pulmonary artery pressure (MPAP), leukopenia, and noncardiogenic pulmonary edema. This study tests whether mannitol, a hydroxyl radical scavenger, modifies these events. Patients received mannitol 0.2 g/kg (n = 14) or saline (n = 12) intravenously before infrarenal aortic clamping. With saline, 30 minutes after clamping, plasma TxB2 levels rose from 124 to 290 pg/mL (p < 0.01), and MPAP rose from 19 to 27 mmHg (p < 0.01). Aortic clamp release led to further increases in plasma TxB2 to 378 pg/mL (p < 0.01) and MPAP to 34 mmHg (p < 0.01). The white blood count (WBC) fell from 9800 to 4400/mm3 (p < 0.01). Four to eight hours after surgery, physiologic shunting (Q̇[sc]S[xsc]/Q̇[sc]T[xsc]) rose from 9% to 20% (p < 0.01) and peak inspiratory pressure (PIP) increased from 22 to 32 cmH2O (p < 0.01). Chest radiography demonstrated pulmonary edema while the pulmonary wedge pressure was 23 mmHg, excluding left ventricular failure. By 24 hours pulmonary edema resolved and the PIP and P(a)O2 returned to baseline. Mannitol treatment relative to saline, during and after aortic clamping reduced plasma TxB2 levels to 155 and 198 pg/mL, respectively (p < 0.01); MPAP to 21 and 26 mmHg (p < 0.01); minimized the decline in WBC to 5850/mm3 (p < 0.01), and the postoperative rise in Q̇[sc]S[xsv]/Q̇[sc]T[xsc] to 12%, and PIP to 28 cmH2O (both p < 0.01). Chest radiography showed no pulmonary edema. Finally in vitro studies documented that mannitol 1 to 10-4 M, but not dextrose, in a dose-dependent manner inhibited Tx synthesis by ADP-activated platelets. These data indicate that mannitol maintains pulmonary function after AAA by limiting ischemia-induced thromboxane synthesis.
|Original language||English (US)|
|Number of pages||6|
|Journal||Annals of Surgery|
|State||Published - 1989|
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