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Ann Thorac Surg 2001;71:1756
© 2001 The Society of Thoracic Surgeons
a Department of Cardiothoracic Surgery, University of Texas Medical Branch, 301 University Blvd, Route 0528, Galveston, TX 77555-0528, USA
e-mail: slick{at}utmb.edu
To the Editor
Given Dr Clark’s premises, Occam’s (therapeutic) razor favors pentoxifylline. The notion that a single injection of a drug—and one so common and safe as pentoxifylline (better known in its oral form as a rheologic "lubricant" for red blood cells in claudicators)—will ameliorate lung injury is enticing.
However, upon revisiting Dr Clark’s group’s papers, controlled reperfusion did not get its fair due. In their model of controlled reperfusion [1], they controlled the main pulmonary arteries with snares, with the end point being transplant lung mean pulmonary artery pressure of 20 mm Hg, which is hardly below normal. Flow was pulsatile, generated by the right heart, and not controlled. There was no concomitant substrate enhancement or leukocyte filtration. Not surprisingly, they found that the pentoxifylline group performed better than their "controlled reperfusion" group. In their second study [2], this time with a pulseless circuit, pentoxifylline and leuko-depleted blood groups performed similarly, but at a mean perfusion pressure of 25 mm Hg. In our series, on the other hand, the lung was perfused with a pulseless circuit at a very limited flow (around 200 mL/min), which generally led to pressures of 10 to 13 mm Hg. Only when the catheter migrated distally into a lobar or segmental artery did the pressure rise to 20 mm Hg, but then fell immediately upon repositioning. Also, we used both substrate enhancement and white cell filtration. In both studies, nothing comparable with controlled reperfusion as we performed it (pulseless flow at 200 mL/min, pressure well below 20 mm Hg, substrate enhanced, leuko-depleted) was tested head-to-head with pentoxifylline.
The larger point is that reperfusion injury occurs on many fronts, by many mechanisms. The list of interventions shown to lessen reperfusion injury in lungs is long, and some are potentially complementary. Controlled reperfusion as described in our article directly addresses the mechanisms of white cell number and shear, substrate enhancement, pressure, and flow. It also allows direct delivery (without systemic circulatory effects) of any other antireperfusion injury agent of one’s choosing. As such, we consider it not a fixed treatment, but a beginning: a delivery vehicle, with cargo that has yet to be optimized.
References
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