ROLE OF PLATELET-ACTIVATING-FACTOR ON CARDIOVASCULAR DYSFUNCTION IN POSTISCHEMIC SHOCK IN PIGS

This study aimed at evaluating the role of platelet-activating factor (PAF) on cardiovascular dysfunction in postischemic shock in pigs. Six teen pigs were randomly allocated to two groups of eight each. Their a orta was clamped above the celiac axis for 45 min and then declamped. The animals were studied for 2 h after declamping. They were given a c ontinuous infusion of Hartmann's solution 6.75 ml/kg/h throughout the experiment. The experimental group was given a potent specific PAF rec eptor antagonist 15 min before reperfusion (BB-882 1 mg/kg bolus follo wed by continuous infusion of 1 mg/ kg/h till the nd of the experiment ). The control group was given vehicle instead. Reperfusion in the con trol group caused prolonged hypotension (mean arterial pressure (SEM): 29 (1) mm Hg, immediately after declamping, compared with 74 (3) at b aseline), an increase in pulmonary vascular resistance (491.6 (51.5) d yn . s . cm(-5), 2 h after declamping, compared with 274.2 (19.4) dyn . s . cm(-5) at baseline), a reduction in cardiac output (1.75 (0. 15) liters/min, 2 h after declamping, compared with 2.8 (0.21) liters/min at baseline), hyperglycemia (13.7 (0.8) mmol/l, immediately after dec lamping, compared with 6.26 (0.6) mmol/l at baseline), and lactic acid emia (11.28 (0.5) mmol/l, immediately after declamping, compared with 4.55 (0.67) mmol/l at baseline). BB-882 did not improve any of these v ariables. PAF does not play a major role on cardiovascular dysfunction in postischemic shock in pigs.