Simulation in surgery is becoming an important component of surgical education. Training on bench top models has been demonstrated to improve technical skills. The objective of our project was to create a vascular surgery simulation model. The simulation model consists of a platform, artificial blood reservoir, artificial blood, inflow and outflow limbs, electric motor, battery, pulse generator, and cryopreserved vessel. Three different vascular surgery simulation stations were created: carotid endarterectomy with shunting and patch angioplasty, arterial bypass, and arteriovenous graft formation. A scientific study involving surgical residents will need to be undertaken to determine whether this simulator has intermodal transferability.
Prostaglandin (PG) E1 administered intravenously has been used for the treatment of primary nonfunction of hepatic allografts and fulminant hepatic failure. It has been proposed that this therapy may improve hepatic blood flow via the vasodilating properties of PGE1. However, PGE1 undergoes extensive metabolic inactivation by the lung and the concentration of PGE1 reaching the liver during intravenous administration has not been determined. Thus, we measured plasma PGE1 concentrations in patients with hepatic dysfunction being treated with PGE1 and in a swine model of PGE1 infusion. We also determined the hemodynamic effects of PGE1 infusion in swine. Blood was sampled from the pulmonary artery, carotid artery, portal vein, and hepatic vein in swine infused with PGE1 (range, 0.67-4.9 microg/kg/hr) demonstrating: (1) a pulmonary extraction ratio of PGE1 of 0.78 +/- 0.12, (2) a splanchnic extraction ratio of PGE1 of 0.54 +/- 0.23, and (3) levels of PGE1 in the systemic circulation of = 78 pg/ml, even at the highest infusion rates. Despite significant increases in body temperature and pulse rate, hepatic hemodynamics were not affected by the PGE1 infusions in healthy swine. Seven patients receiving intravenous PGE1 for hepatic dysfunction (0.11-1.30 microg/kg/hr) had a pulmonary extraction ratio of 0.69 +/- 0.17. Systemic arterial concentrations of PGE1 were = 62 pg/ml. These results suggest that due to clearance of PGE2 in the pulmonary and splanchnic circulations, current clinical protocols for intravenous administration of PGE1 are not likely to affect perihepatic hemodynamics.
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