HALOTHANE-INDUCED INTRAHEPATIC PORTOVENOUS SHUNTING REDUCES HEPATIC MICROVASCULAR SINUSOIDAL PERFUSION DURING CONTRAST ANGIOGRAPHIC PROCEDURES

PURPOSE: Reduced intrahepatic perfusion that occurs during contrast an giography performed after administration of halothane anesthesia is th ought to result from halothane-induced systemic hemodynamic alteration s, such as reduced splanchnic blood flow, rather than intrahepatic mic rovascular alterations. The authors postulate that intrinsic hepatic e ffects caused by inhalational anesthetic agents rather than contrast m aterials, further reduce liver perfusion. MATERIALS AND METHODS: With use of dynamic video microscopy, intrahepatic microvascular flow rates and patterns, hepatic cord/sinusoidal diameters, portal venous pressu re changes, and quantitative and qualitative Kupffer cell phagocytic a ctivity were continuously recorded in isolated perfused rat Livers bef ore and during exposure to 1.5% halothane in O-2/CO2, with and without the addition of iothalamate meglumine. RESULTS: Exposure of livers to halothane resulted in intrahepatic portovenous shunting secondary to obstruction to sinusoidal outflow, diminished sinusoidal perfusion, an d a mean elevation in terminal portal venous pressure of 12.8 mm Hg. K upffer cell phagocytic activity was reduced even when normalized for f low within sinusoids. None of these changes were attributed to use of contrast material. CONCLUSIONS: Alterations in hepatic blood flow duri ng exposure to halothane result, in part, from increased intrinsic hep atic vascular resistance, sinusoidal outflow obstruction, and portoven ous shunting, and not only from systemic hemodynamic changes. Iothalam ate meglumine produced no microvascular alterations.