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. Sixteen pigs were randomly allocated to two groups of eight each. Their aorta 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 continuous infusion of Hartmann's solution 6.75 ml/kg/h throughout the experiment. The experimental group was given a potent specific PAF receptor antagonist 15 min before reperfusion (BB-882 1 mg/kg bolus followed by continuous infusion of 1 mg/ kg/h till the nd of the experiment). The control group was given vehicle instead. Reperfusion in the control group caused prolonged hypotension (mean arterial pressure (SEM): 29 (1) mm Hg, immediately after declamping, compared with 74 (3) at baseline), an increase in pulmonary vascular resistance (491.6 (51.5) dyn . 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 declamping, compared with 6.26 (0.6) mmol/l at baseline), and lactic acidemia (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 variables. PAF does not play a major role on cardiovascular dysfunction in postischemic shock in pigs.