Abstract
Pentoxifylline (PTX) has been shown to have beneficial effects on microcirculatory blood flow. In this study we evaluate the potential hemodynamic and metabolic benefits of PTX during hepatic ischemia. We also test the hypothesis that portal PTX infusion can minimize the I/R injury when compared to systemic infusion. Methods. Twenty-four dogs (18.1 ± 0.7 kg) were subjected to portal triad occlusion (PTO) for 45 min. The animals were assigned to 3 groups: CT (control, PTO, n = 8), PTX-syst (PTO + 25 mg/Kg of PTX IV, n = 8), and PTX-pv (PTO + 25 mg/Kg of PTX in the portal vein, n = 8). Animals were followed for 120 min. Systemic hemodynamics, gastrointestinal tract perfusion, oxygen-derived variables, and liver enzymes were evaluated throughout the experiment. Results. Animals treated with PTX presented significantly higher CO in the first hour after reperfusion, when compared to the CT (~3.7 vs. 2.1 L/min, P < 0.05). Alanine aminotransferase (ALT) was similar in the PTX groups two hours after reperfusion but significantly higher in the CT (227 vs. ~64 U/L, P < 0.05). Conclusion. PTX infusion was associated with hemodynamic benefits and was able to minimize liver injury during normothermic hepatic I/R. However, local PTX infusion was not associated with any significant advantage over systemic route.
Highlights
Despite technical advances in liver surgery in the last decades, the consequences of liver ischemia/reperfusion injury remain a major concern for surgeons
Portal triad occlusion promoted a slight reduction in MAP in all animals (Table 1)
This study confirms that intravenous systemic infusion of PTX is an effective strategy to prevent liver damage after normothermic I/R
Summary
Despite technical advances in liver surgery in the last decades, the consequences of liver ischemia/reperfusion injury remain a major concern for surgeons. Liver ischemia/reperfusion (I/R) injury is a complex cascade of events mediated by numerous inflammatory cells and molecular mediators, resulting in hepatocyte death and systemic inflammatory response. The degree of inflammatory response and organ dysfunction is dependent on duration of liver ischemia and underlying liver disease. In this setting, activation of hepatic macrophages plays an important role. Macrophages have been responsible for the release of various inflammatory mediators, including but not limited to tumor necrosis factor alpha (TNF-α). Several studies have shown that the inhibition of TNF-α production or its neutralization after isolated hepatic I/R decreases polymorphonuclear neutrophil infiltration with further reduction of the I/R injury [1,2,3]
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