BACKGROUND AND METHODS: It is hypothesized that pentoxifylline may be beneficial during shock states by improving tissue oxygenation. To test this hypothesis, we examined the effect of pentoxifylline on hemodynamics, oxygen delivery (DO2), and tissue metabolism during severe hemorrhagic shock. We conducted a placebo-controlled, randomized trial using anesthetized, mechanically ventilated dogs in hemorrhagic shock maintained at a mean arterial pressure of 45 to 50 mm Hg. Six animals were treated with a 10-mg/kg bolus of iv pentoxifylline followed by a continuous infusion at 5 mg/kg.hr. The controls consisted of six animals treated with saline. RESULTS: There were no significant differences between the groups before treatment. During 150 mins of posttreatment, repeated measurements of the control and pentoxifylline groups showed no significant differences in heart rate (HR), cardiac output, systemic and pulmonary vascular resistances, DO2, or blood lactate concentration (repeated-measures analysis of variance). CONCLUSIONS: In this acute, nonresuscitated, canine hemorrhagic shock model, pentoxifylline did not act as a vasodilator, or have any significant effect on HR, cardiac output, oxygen transport, or lactic acidosis.
BACKGROUND AND METHODS: It is hypothesized that pentoxifylline may be beneficial during shock states by improving tissue oxygenation. To test this hypothesis, we examined the effect of pentoxifylline on hemodynamics, oxygen delivery (DO2), and tissue metabolism during severe hemorrhagic shock. We conducted a placebo-controlled, randomized trial using anesthetized, mechanically ventilated dogs in hemorrhagic shock maintained at a mean arterial pressure of 45 to 50 mm Hg. Six animals were treated with a 10-mg/kg bolus of iv pentoxifylline followed by a continuous infusion at 5 mg/kg.hr. The controls consisted of six animals treated with saline. RESULTS: There were no significant differences between the groups before treatment. During 150 mins of posttreatment, repeated measurements of the control and pentoxifylline groups showed no significant differences in heart rate (HR), cardiac output, systemic and pulmonary vascular resistances, DO2, or blood lactate concentration (repeated-measures analysis of variance). CONCLUSIONS: In this acute, nonresuscitated, caninehemorrhagic shock model, pentoxifylline did not act as a vasodilator, or have any significant effect on HR, cardiac output, oxygen transport, or lactic acidosis.