Hemodynamic aspects of the pulmonary circulation during retrograde perfusion.
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Biomedical subjects
Publications and source records attributed to J A Awad.
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Surgically explanted vascular grafts, including 47 autografts, 14 allografts, 103 chemically processed human umbilical vein (HUV) grafts, and 406 polytetrafluoroethylene (PTFE) grafts, were studied histopathologically. Autografts, HUV, and PTFE grafts were implanted mostly in the femoropopliteal position, whereas allografts were used as a blood access for hemodialysis. The main cause for explantation in autografts (53.6%), HUV (74.8%), and PTFE (61.3%) was thrombosis, whereas allograft failure was usually related to aneurysmal degeneration (72.7%). The infection rates of HUV (20.9%) and PTFE (25%) grafts were higher than those of autografts (4.8%) and allografts (9.1%). Furthermore, bacterial colonization occurred more frequently in HUV (63.9%) and PTFE (64.7%) than in autografts (6.7%) and allografts (0%). Leukocyte infiltration was detected mostly in HUV (39.4%) and PTFE (27%) explants. Autografts and allografts both showed a 7.1% rate of lipid uptake, whereas lipid retention was observed in 84.9% of HUV and 79.8% of PTFE grafts. These results suggest that biologic vascular grafts are to be used preferentially in small diameter arterial reconstruction because of their resistance to bacterial colonization and lipid uptake.
Newborns suffering from severe respiratory difficulties and not responding to conventional methods have been successfully treated by extracorporeal circulation with a membrane oxygenator (ECMO). However, the technique needs a highly specialized staff, excellent laboratory support, and continuous surveillance of the procedure to prevent complications. In a series of experiments on newborn and preterm lambs, we have investigated a relatively simpler technique of respiratory support that involves a pumpless arteriovenous bypass by cannulating both umbilical arteries and the umbilical vein. A highly efficient microporous membrane oxygenator (MO) with very low resistance was selected. This type of perfusion that mimics the placental circulation, besides providing an additional amount of oxygen to the blood, has proven to be very effective for CO2 extraction. Before its application in humans, however, improvements in the catheters to be inserted in the umbilical vessels, some modifications in the design of the MO, and improvements in the blood compatibility of all foreign surfaces in contact with blood are needed.
In spite of extensive searching for clues to the pathogenesis of the hepatorenal syndrome (HRS), its cause remains an enigma. The renal dysfunction in HRS has been attributed to intense but reversible renal vasoconstriction. This has engendered the hypothesis that the renal vasoconstriction is caused by a circulating factor. Patients with HRS exhibit chronic endotoxemia and may have tissue hypoxia, an environment conducive for the formation of free radicals. Recently, we discovered a series of novel prostaglandin (PG) F2-like compounds, termed F2-isoprostanes, that are produced in vivo as products of free radical catalyzed lipid peroxidation independent of the cyclooxygenase enzyme. One of these compounds, 8-epi-PGF2 alpha, has been found to be an extremely potent renal vasoconstrictor. Therefore, we quantified levels of these prostanoids in patients with HRS and compared them to various control groups. Plasma levels of these compounds were markedly elevated only in patients with HRS (113 +/- 30 pg/ml) (p < 0.01) compared to normal controls (19 +/- 7 pg/ml), patients with compensated liver disease (20 +/- 4 pg/ml), patients with decompensated liver disease (22 +/- 4 pg/ml), and patients with chronic renal failure (23 +/- 4 pg/ml). The increased levels of these compounds are unlikely the result of reduced hepatic and renal clearance of the compounds since levels are not markedly increased in patients with either decompensated liver disease or chronic renal failure alone. Whether F2-isoprostanes are the elusive mediators responsible for the renal vasoconstriction in HRS remains to be established. However, these findings do suggest that oxidant injury may be a fundamental abnormality involved in the pathogenesis of HRS.