Clinical significance of increased tricuspid valve incompetence following implantation of ventricular leads.

Purpose: Cardiac rhythm management devices (CRMD) require a ventricular lead to be placed across the tricuspid valve. Tricuspid regurgitation (TR) is an under-recognized clinical complication of lead implantation and its clinical significance is unknown. We studied the incidence of hospitalizations for congestive heart failure (CHF) exacerbation among patients with worsening TR after ventricular lead implantation.

Liver hyperthermia and oxidative stress: role of iron and aldehyde production.

Hyperthermia has been used to treat cancer in the liver. However, significant hepatotoxicity occurs at a therapeutic temperature of 42-43 degrees C. We have proposed that heat toxicity is the result of oxidative stress from superoxide generation with resultant lipid peroxidation.

Genetic alterations of microsatellites on chromosome 18 in human breast carcinoma.

Allelic alterations of chromosome 18 microsatellites were determined using normal and tumor DNA pairs from 29 patients with infiltrating ductal carcinoma of the breast. Loss of heterozygosity was detected in 62% (18 of 29 patients) of the tumors at one or more of these microsatellites. Eight of the 18 patients exhibited deletions in the region at 18q21.

Total pelvic exenteration. A 50-year experience at the Ellis Fischel Cancer Center.

Objective: To review a 50-year experience with total pelvic exenteration for treatment of advanced pelvic cancer.

Design: Retrospective study with 100% follow-up.

Setting: Cancer hospital.

Involvement of xanthine oxidase in oxidative stress and iron release during hyperthermic rat liver perfusion.

The hepatotoxic effects of hyperthermia have been proposed to be related to lipid peroxidation as a consequence of oxidative stress. This can result from exposure of the cell to "radical oxygen" species such as the superoxide and hydrogen peroxide generated by the activity of the oxidase form (type O) of xanthine oxidase (XO), which is converted to that form by perfusion of the liver at hyperthermic temperatures. These radical species are not reactive enough in themselves to cause cell damage but require the presence of a catalyst such as low molecular weight chelated iron.

Oxidative stress as a precursor to the irreversible hepatocellular injury caused by hyperthermia.

Heat-induced hepatotoxicity accompanying hyperthermic liver perfusion was studied in the isolated, haemoglobin-free perfused rat liver. Trypan blue uptake, a sensitive indicator of cell death, was used to examine the relationship between the efflux of oxidized glutathione (oxidative stress), the appearance of cytosolic enzymes in the perfusate and cell death. Livers were perfused at 37, 42, 42.

Lipid peroxidation caused by hyperthermic perfusion of rat liver.

The data presented support the premise that hyperthermia-induced hepatocellular injury is the end result of lipid peroxidation. Evidence for lipid peroxidation is the formation of diene conjugates and the decrease in microsomal P450 and glucose-6-phosphatase activity during hyperthermic liver perfusion.

Hyperthermic liver toxicity: a role for oxidative stress.

Rat livers were perfused at 37 degrees C, 41 degrees C, 42 degrees C, 42.5 degrees C, and 43 degrees C for 2 hr. Among perfusate constituents analyzed were urea, total amino acids, N-acetyl-beta-glucosaminidase (NAG), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), malonaldehyde (MDA), glutathione (GSH), oxidized glutathione (GSSG), allantoin, potassium, phosphate, and glucose.

Effects of hyperthermia on xanthine oxidase activity and glutathione levels in the perfused rat liver.

The hepatotoxic effects of hyperthermic liver perfusion were investigated in male Fischer 344 rat livers. Perfusions were carried out at 37, 41, 42, 42.5, and 43 degrees C for 2 hr.

Hyperthermic liver perfusion and release of lysosomal enzymes.

Perfused rat liver was used to study the relationship between the hepatotoxic effects of hyperthermia and the effects of heat on lysosomes. Livers from fed rats were perfused for 180 min at 37-43 degrees C. Release of lysosomal enzymes into the perfusate during perfusion and lysosomal fragility at the end of perfusion were determined.

Nitrogen metabolism and lipid peroxidation during hyperthermic perfusion of human livers with cancer.

Isolation-perfusion was used as a means of heating human livers with cancer. Perfusion was at 42-42.5 degrees C for 4 h.

Tumoricidal effects and patient survival after hyperthermic liver perfusion.

Hyperthermic liver perfusion for four hours at 42.0 degrees C to 42.5 degrees C was used as the sole modality of therapy for cancer confined to the liver in eight patients.

Alterations in biochemical functions during hyperthermic isolation-perfusion of the human liver.

Hyperthermia (42-42.5 degrees) was applied to the liver of eight patients with cancer in the liver by a technique of isolation-perfusion. Hepatic functional integrity was assessed during perfusion through measurement of multiple perfusate constituents.

Interrelationships and metabolic effects of fatty acids in the perfused rat liver at hyperthermic temperatures.

Livers of fasted rats were perfused for 70 min at 37 degrees-43 degrees C in the presence or absence of acetate, octanoate or palmitate. Hepatic biosynthetic capacity was assessed by measuring rates of gluconeogenesis, ureogenesis, ketogenesis and O2 consumption. In the presence of each fatty acid, gluconeogenesis, ureogenesis and oxygen consumption were maintained at 37 degrees and 42 degrees C.

Canine liver isolation-perfusion at normo- and hyperthermic temperatures with perfluorochemical emulsion (Fluosol-43).

A perfluorocarbon emulsion, Fluosol-43, was used as a blood substitute for oxygen transport during isolation-perfusion of the dog liver at 37 and 43 degrees C. Preservation of hepatic functional integrity was assessed through analysis of perfusate constituents and animal survival after perfusion. Flow to the liver during perfusion was greater than 1 ml/min/g with one-third of total flow provided through the hepatic artery and two-thirds through the protal vein.

A technique for isolated hyperthermic liver perfusion.

Hyperthermia, either alone or combined with chemotherapy, has been shown to be effective in treating cancer. Because some investigators believe that regional hyperthermia may be more effective than whole body hyperthermia, we developed a technique to heat only the liver to 42-43 degrees for 4 hr. The procedure was adapted from a previously described animal model and was performed in four humans.

Azathioprine induction of lymphomas and squamous cell carcinomas in rats.

The carcinogenicity of azathioprine was evaluated in weaning female noninbred Sprague-Dawley rats by feeding it in the diet. Due to toxicity, the dose had to be changed during the course of the experiments and ranged from 0.015 to 0.

A technique for isolation perfusion of the canine liver with survival.

A technique of isolation perfusion of the canine liver was developed as a model for treating cancer limited to the liver. Preservation of hepatic functional integrity was dependent on maintenance of near physiologic conditions for the perfusion. Flow to the liver, 1 ml/min/g, was provided by gravity to the portal vein at two thirds total flow, and by pump to the hepatic artery at one third total flow.

Effect of palmitate or lipid emulsion on nitrogen metabolism during hyperthermic perfusion of rat liver.

Livers of fasted rats were perfused for one hour at 37 degrees or 42 degrees. Endogenous hepatic ureogenesis was increased twofold at 42 degrees and the release of endogenous ninhydrin-reactive amino nitrogen was not changed by hyperthermia. Exogenous amino acids at 10 times the normal plasma concentration stimulated hepatic ureogenesis sevenfold at 37 degrees and over twofold at 42 degrees.

Altered hepatic functions and microsomal activity in perfused rat liver by hyperthermia combined with alkylating agents.

Livers of fasted rats were perfused for one hour in the presence of cyclophosphamide (CP), mechlorethamine (HN2), or melphalan (L-PAM) at 37 degrees and 42 degrees C. Hepatic biosynthetic function was assessed by determining gluconeogenesis from lactate, ureogenesis from NH4Cl, and O2 consumption. Antipyrine (AP) metabolism was employed to assess microsomal mixed function oxygenase enzyme activity at elevated temperatures.