BACKGROUND/AIMS: The aim of this study was to determine the pharmacodynamics of cisplatin following three different treatment procedures for intrahepatic arterial infusion therapy for hepatocellular carcinoma (HCC). METHODS: We divided 13 HCC patients into the following three groups: group A, lone injection of cisplatin (n=3); group B, combined injection of cisplatin and lipiodol, with embolization using small gelatin cubes (GCs) (n=5); and group C, injection of suspended lipiodol with cisplatin powder, with embolization using small GCs (n=5). In each group, the free cisplatin concentration in the hepatic vein was measured at 0, 5, 10, and 30 minutes. RESULTS: The mean free cisplatin concentrations were as follows. For group A, the mean was 48.58 microg/mL at 0 minute, 7.31 microg/mL at 5 minutes, 5.70 microg/mL at 10 minutes, and 7.15 microg/mL at 30 minutes. For the same time points, for group B, the concentrations were 8.66, 4.23, 3.22, and 1.65 microg/mL, respectively, and for group C, the concentrations were 4.81, 2.61, 2.52, and 1.75 microg/mL, respectively. The mean area under the curve (AUC)0-infinity for the free cisplatin concentration was 7.80 in group A, 2.48 in group B, and 2.27 in group C. The AUC0-infinity for the free cisplatin concentration gradually decreased, from group A to group C. CONCLUSIONS: These results indicate that the combination of lipiodol and small GCs may be useful for delaying cisplatin drainage from the liver.
Carcinoma, Hepatocellular ; Cisplatin ; Drainage ; Drug Delivery Systems ; Ethiodized Oil ; Gelatin ; Hepatic Veins ; Humans ; Liver ; Pilot Projects

Between January 1980 and September 1993, 7(8.4%) of 83 patients with aortic dissection had coincident atherosclerotic true aneurysms of thoracic and/or abdominal aorta or had undergone operation of true aortic aneurysms. There was no difference in the segments of aortic dissection; 4 of 50 patinets classified as DeBakey III and 3 of 33 patients classified as DeBakey I or II, whereas the site of atherosclerotic true aneurysms was more often in the abdominal aorta than in the thoracic aorta. Five patients had undergone surgery for or had the abdominal aortic aneurysms and 2 patients had thoracic aortic aneurysms. In 2 patients who had previously undergone abdominal aortic aneurysmectomy, the dissected aorta ruptured soon after the onset of dissection. In the patients in whom the true aneurysm and the aortic dissection involve the same segments surgical treatment would be extended and complex.

The purpose of this study was to examine the responses of cerebral blood flow and metabolism to changes in arterial carbon dioxide tension during moderate hypothermic cardiopulmonary bypass in patients with cerebrovascular disease undergoing open heart surgery. Computed tomography scan (CT) and single photon emission computed tomography (SPECT) were performed preoperatively for 17 patients. The patients were categorized according to their CT and SPECT findings. Ten patients were included in the normal group, 7 patients were included in the CVD group. Blood flow velocity in the middle cerebral artery (MCAv) was measured by means of transcranial Doppler ultrasonography at two different arterial carbon dioxide tensions (at a high PaCO₂ of 45-50mmHg, at a low PaCO₂ of 30-35mmHg, uncorrected for body temperature) during moderate steady-state hypothermic cardiopulmonary bypass. Simultaneously cerebral oxygen consumption was estimated by relating the arteriovenous oxygen content difference to flow velocity (D-CMRO₂). MCAv and D-CMRO₂ were expressed as percentages of the values determined at 30 minutes before cardiopulmonary bypass. In the normal group, a PaCO₂ of 47.4±2.5mmHg (mean±SD) was associated with an MCAv of 99.4±17.8% and a D-CMRO₂ of 53.4±25.5%, while a PaCO₂ of 33.7±1.3mmHg was associated with an MCAv of 64.3±18.1% and a D-CMRO₂ of 53.5±26.2%. In the CVD group, a PaCO₂ of 49.1±4.2mmHg was associated with an MCAv of 81.4±22.3% and a D-CMRO₂ of 34.0±19.4%, while a PaCO₂ of 33.6±1.3mmHg was associated with an MCAv of 54.7±23.8% and a D-CMRO₂ of 49.0±19.4%. We conclude that in patients with cerebrovascular disease cerebral blood flow is changed in response to changes in arterial dioxide tension during moderate hypothermic cardiopulmonary bypass, however a high PaCO₂ depresses cerebral oxygen consumption because hypercarbia may cause potentially harmful redistribution of regional cerebral blood flow away from marginally-perfused to otherwise well-perfused areas.