PURPOSE: The purpose of the study was to verify that the 81Rubidium/81mkrypton (81Rb/81mKr) method allows the quantitative measurement of myocardial perfusion. PRINCIPLE: The potassium analogous cation 81Rb is accumulated in the myocardium by the cell membrane-bound Na-K-ATPase. After accumulation an intracellular equilibrium establishes between 81Rb and its radioactive daughter nuclide 81mKr. The flow-sensitive method evaluates the disturbance of this equilibrium by perfusion which washes out the short-lived diffusable daughter nuclide 81mKr while the mother nuclide 81Rb remains cell-bound. METHODS: Isolated rabbit hearts were prepared in a modified Langendorff technique which allowed quantitative collection of the coronary sinus efflux. The myocardium was labeled with pure 81Rb by bolus injection into the aortic cannula. Spectroscopic measurements of 81Rb and 81mKr gamma radiation were performed using a germanium detector. Perfusion was varied in the range between 0 and 4 ml/min/g. The activity ratio 81Rb/81mKr was determined and compared with coronary sinus effusion. RESULTS: 81Rb/81mKr activity ratio was closely related (r = 0.98) to perfusion as described by the predicted equation Rb/Kr = (F/2.96 P) + 1. (Rb/Kr = activity ratio between 81Rb and 81mKr in the myocardium; F = myocardial perfusion (ml/min/g); P = partition coefficient (myocardium/perfusate) for Krypton gas). The constant P was found to be 1.14 +/- 0.06 (mean +/- SEM). No saturation of this ratio at high flow rates was observed. CONCLUSION: The activity ratio 81Rb/81mKr is a valid quantitative measure for myocardial perfusion in isolated hearts. The main limitation of the method before application in man is the correction of the different gamma ray tissue absorption of both nuclides.

Animals↗

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Spasms of the hepatic artery following percutaneous transluminal angioplasty and tolazoline administration in a liver transplant patient.

Vascular complications after liver transplantation include occlusion or stenosis near the sites of anastomosis in the hepatic artery, portal vein, and vena cava. Balloon angioplasty of these stenoses carries little risk and is a useful procedure for the treatment of these problems. Here we describe the case of a liver transplant patient who underwent balloon angioplasty for stenosis of the hepatic artery and who developed spasms of the hepatic artery which were aggravated following intraarterial administration of Tolazoline.

Angioplasty, Balloon↗

PubMedDate not supplied

Delayed clearance of HBsAG after transplantation for fulminant delta-hepatitis.

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Adult↗

PubMedDate not supplied

Computerized charting of case reports.

Follow-up schemas are used in the planning of care delivery for patients who had a larynx tumour resection. Because of the diversity of this population, the idea has arisen that control schemas should be tuned to individual patient histories in order to optimize care delivery. To arrive at refined guidelines, detailed analysis of 300 case reports is planned. In this context a patient case report tool PCRT has been developed to support the analysis of computerized case reports. PCRT is based on an existing patient case report language and can generate case report charts using a newly developed charting method implemented with internet-based technology. This paper presents the charting method and explains the charting algorithm.

Adult↗

PubMedDate not supplied

Incomplete resolution of basilar artery occlusion after intra-arterial thrombolysis: abciximab and heparin prevent early rethrombosis.

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Abciximab↗

PubMedDate not supplied

Alpha-1-antitrypsin deficiency and liver disease.

Alpha-1-antitrypsin deficiency is a common autosomal recessive disorder associated with premature development of emphysema, liver cirrhosis and hepatocellular carcinoma. This article reviews the existing literature on alpha-1-antitrypsin deficiency, with an emphasis on recent developments. A description of the protein, gene structure and function of alpha-1-antitrypsin as well as clinical aspects are presented. Treatment issues are addressed and a framework for the diagnostic workup and management of patients with alpha-1-antitrypsin deficiency and chronic liver disease is provided.

Carcinoma, Hepatocellular↗

PubMedDate not supplied

Hepatocellular transplantation into the lung in chronic liver failure following bile duct obstruction in the rat.

Injection of hepatocytes or cell-free supernatant into the lung was able to prevent death from surgically induced fulminant hepatic failure in the rat in over 90% and 53% of subjects, respectively. The aim of this study was to investigate whether this technique can be applied in chronic liver failure. Chronic liver failure was induced in Lewis rats by ligation and transection of the common bile duct, which led to cirrhosis after 3-5 wk in all animals. Four groups of animals were formed: group 1 (n = 5), normal rats, serving as control; group 2 (n = 15), cirrhotic rats, no further treatment; group 3 (n = 14), hepatocyte transplantation by injection of cell suspension transcutaneously into the right lung of cirrhotic animals four wk after bile duct ligation; group 4 (n = 17), injection of 1 mL cell-free supernatant intravenously at two-day intervals, starting 4 wk after ligation. Liver function tests, prothrombin time and serum protein levels were measured weekly before and every two days after transplantation. In group 2 all animals had died 56 (49-69) days after ligation. Survival in groups 3 and 4 was similar: all rats had died from liver failure 61 (51-72) and 60 (49-76) days following bile duct ligation. Survival rates and laboratory investigations showed no significant differences between treated and untreated cirrhotic animals. These data suggest that hepatocyte transplantation into the lung as well as supernatant injection do not have any significant effect on chronic hepatic failure, at least in the rat model.

Animals↗

PubMedDate not supplied

Activation of caspase-3 by interferon alpha causes interleukin-16 secretion but fails to modulate activation induced cell death.

Interferon alpha (IFN-alpha) is the mainstay in the treatment of chronic hepatitis C virus (HCV) infection. Interleukin-16 (IL-16) attracts CD4+ cells to sites of inflammation and plays a role in the interaction of dendritic cells, T cells and B cells. In this study, we show that IFN-alpha itself induces IL-16 secretion by peripheral blood lymphocytes (PBL) and enhances IL-16 secretion by anti-CD3 stimulated PBL. Pro-IL-16 is cleaved into its active form by caspase-3. IFN-alpha increases caspase-3 mRNA levels in activated T cells (ATC), as shown by Northern blot analysis, whereas IL-16 mRNA levels are not affected by IFN-alpha. IL-16 secretion into culture supernatants correlates tightly with intracellular caspase-3 activity in ATC. In our experiments addition of specific caspase inhibitors did not reduce the proportion of ATC undergoing Fas-mediated cell death, but completely blocked IFN-alpha-induced IL-16 secretion into culture supernatants. In conclusion, our results suggest that IFN-alpha activates caspase-3, thereby increasing secretion of IL-16, whereas IFN-alpha-enhanced Fas-mediated cell death in ATC is not caspase-dependent.

Antibodies↗

PubMedDate not supplied

Primary hepatic tuberculosis in homozygous alpha-1-antitrypsin deficiency.

The case of a young female patient with homozygous alpha-1-antitrypsin deficiency (Pi-ZZ) associated chronic liver disease, who developed primary hepatic tuberculosis shortly after delivery of a healthy baby girl is reported. These findings emphasize that this rare disease should be considered even in patients with precirrhotic liver disease, while pointing out that the genetically determined deficiency of protease inhibitor alpha-1-antitrypsin (AAT) predisposes to hepatic infection.

Adult↗

PubMedDate not supplied

Recurrent liver failure with severe rhabdomyolysis after liver transplantation for carbon tetrachloride intoxication.

Acute liver failure due to intoxication is a rare indication for liver transplantation which a usually has a good prognosis. We herein report the case of a young male, who underwent orthotopic liver transplantation for acute liver failure due to carbon tetrachloride intoxication. Apart from hepatic and renal failure, the patient also developed severe rhabdomyolysis, which has not thus far been described as a toxic effect of this chemical agent. Despite forced hyperventilation, which is known to be the most effective means of eliminating the specifically lipophylic agent, as well as excessive plasma exchange following intravenous administration of fat emulsions, liver failure recurred when blood carbon tetrachloride concentrations were already at non-toxic levels. Retransplantation of the liver together with a kidney was only temporarily successful, since the patient died due to aspergillus sepsis. Based on this experience, we would recommend that whenever possible in patients with carbon tetrachloride intoxication, liver transplant should be delayed until most of the toxic agent has been eliminated in order to prevent fatal graft damage.

Acute Kidney Injury↗