Pericardial Effusion in a Dog with Pericardial Hemangiosarcoma.

An adult Jack Russel terrier dog presented for evaluation of large-volume peritoneal and pleural effusion. Echocardiography revealed scant pericardial effusion and abnormally thickened pericardium. Electrocardiography revealed complete atrioventricular block with junctional and ventricular escape beats and occasional ventricular premature complexes. Computed tomography of the thorax confirmed diffuse abnormal thickening of the pericardium, and a tentative diagnosis of constrictive-effusive pericarditis was made. The dog underwent subtotal pericardiectomy to remove the parietal pericardium and permanent epicardial pacemaker implantation to manage bradycardia. Based on pericardial histopathology and immunohistochemistry, a diagnosis of pericardial hemangiosarcoma was made. Systemic chemotherapy was initiated with doxorubicin 1 month after surgery. Despite initial improvement with chemotherapy, the dog was euthanized 4 months after surgery because of development of recurrent pleural effusion. To the author's knowledge, this is the first case report in dogs to describe isolated pericardial location of hemangiosarcoma resulting in constrictive-effusive pericarditis.

Effects of alpha-lipoic acid on biomarkers of oxidative stress in streptozotocin-induced diabetic rats.

Increased oxidative stress and impaired antioxidant defense mechanisms are important factors in the pathogenesis and progression of diabetes mellitus and other oxidant-related diseases. This study was designed to determine whether alpha-lipoic acid, which has been shown to have substantial antioxidant properties, when administered (10 mg/kg ip) once daily for 14 days to normal and diabetic female Sprague-Dawley rats would prevent diabetes-induced changes in biomarkers of oxidative stress in liver, kidney and heart. Serum glucose concentrations, aspartate aminotransferase activity, and glycated hemoglobin levels, which were increased in diabetes, were not significantly altered by alpha-lipoic acid treatment. Normal rats treated with a high dose of alpha-lipoic acid (50 mg/kg) survived but diabetic rats on similar treatment died during the course of the experiment. The activity of glutathione peroxidase was increased in livers of normal rats treated with alpha-lipoic acid, but decreased in diabetic rats after alpha-lipoic acid treatment. Hepatic catalase activity was decreased in both normal and diabetic rats after alpha-lipoic acid treatment. Concentrations of reduced glutathione and glutathione disulfide in liver were increased after alpha-lipoic acid treatment of normal rats, but were not altered in diabetics. In kidney, glutathione peroxidase activity was elevated in diabetic rats, and in both normal and diabetic animals after alpha-lipoic acid treatment. Superoxide dismutase activity in heart was decreased in diabetic rats but normalized after treatment with alpha-lipoic acid; other cardiac enzyme activities were not influenced by either diabetes or antioxidant treatment. These results suggest that after 14 days of treatment with an appropriate pharmacological dose, alpha-lipoic acid may reduce oxidative stress in STZ-induced diabetic rats, perhaps by modulating the thiol status of the cells.

Effects of pycnogenol treatment on oxidative stress in streptozotocin-induced diabetic rats.

Free radicals and oxidative stress have been implicated in the etiology of diabetes and its complications. This in vivo study has examined whether subacute administration of pycnogenol, a French pine bark extract containing procyanidins that have strong antioxidant potential, alters biomarkers of oxidative stress in normal and diabetic rats. Diabetes was induced in female Sprague-Dawley rats by a single injection of streptozotocin (90 mg/kg body weight, ip), resulting (after 30 days) in subnormal body weight, increased serum glucose concentrations, and an increase in liver weight, liver/body weight ratios, total and glycated hemoglobin, and serum aspartate aminotransferase activity. Normal and diabetic rats were treated with pycnogenol (10 mg/kg body weight/day, ip) for 14 days. Pycnogenol treatment significantly reduced blood glucose concentrations in diabetic rats. Biochemical markers for oxidative stress were assessed in the liver, kidney, and heart. Elevated hepatic catalase activity in diabetic rats was restored to normal levels after pycnogenol treatment. Additionally, diabetic rats treated with pycnogenol had significantly elevated levels of reduced glutathione and glutathione redox enzyme activities. The results demonstrate that pycnogenol alters intracellular antioxidant defense mechanisms in streptozotocin-induced diabetic rats.

Effects of quercetin on antioxidant defense in streptozotocin-induced diabetic rats.

In light of evidence that some complications of diabetes mellitus may be caused or exacerbated by oxidative damage, we investigated the effects of subacute treatment with the antioxidant quercetin on tissue antioxidant defense systems in streptozotocin-induced diabetic Sprague-Dawley rats (30 days after streptozotocin induction). Quercetin, 2-(3,4-dihydroxyphenyl)-3,5,7-trihydroxy-4H-1-benzopyran-4-one, was administered at a dose of 10mg/kg/day, ip for 14 days, after which liver, kidney, brain, and heart were assayed for degree of lipid peroxidation, reduced and oxidized glutathione content, and activities of the free-radical detoxifying enzymes catalase, superoxide dismutase, glutathione peroxidase, and glutathione reductase. Treatment of normal rats with quercetin increased serum AST and increased hepatic concentration of oxidized glutathione. All tissues from diabetic animals exhibited disturbances in antioxidant defense when compared with normal controls. Quercetin treatment of diabetic rats reversed only the diabetic effects on brain oxidized glutathione concentration and on hepatic glutathione peroxidase activity. By contrast, a 20% increase in hepatic lipid peroxidation, a 40% decline in hepatic glutathione concentration, an increase in renal (23%) and cardiac (40%) glutathione peroxidase activities, and a 65% increase in cardiac catalase activity reflect intensified diabetic effects after treatment with quercetin. These results call into question the ability of therapy with the antioxidant quercetin to reverse diabetic oxidative stress in an overall sense.

Effects of isoeugenol on oxidative stress pathways in normal and streptozotocin-induced diabetic rats.

Because some complications of diabetes mellitus may result from oxidative damage, we investigated the effects of subacute treatment (10mg/kg/day, intraperitoneal [ip], for 14 days) with the antioxidant isoeugenol on the oxidant defense system in normal and 30-day streptozotocin-induced diabetic Sprague-Dawley rats. Liver, kidney, brain, and heart were assayed for degree of lipid peroxidation, reduced and oxidized glutathione content, and activities of the free radical-detoxifying enzymes catalase, superoxide dismutase, glutathione peroxidase, and glutathione reductase. All tissues from diabetic animals exhibited disturbances in antioxidant defense when compared with normal controls. Treatment with isoeugenol reversed diabetic effects on hepatic glutathione peroxidase activity and on oxidized glutathione concentration in brain. Treatment with the lipophilic compound isoeugenol also decreased lipid peroxidation in both liver and heart of normal animals and decreased hepatic oxidized glutathione content in both normal and diabetic rats. Some effects of isoeugenol treatment, such as decreased activity of hepatic superoxide dismutase and glutathione reductase in diabetic rats, were unrelated to the oxidative effects of diabetes. In heart of diabetic animals, isoeugenol treatment resulted in an exacerbation of already elevated activities of catalase. These results indicate that isoeugenol therapy may not reverse diabetic oxidative stress in an overall sense.

Effects of coenzyme Q10 treatment on antioxidant pathways in normal and streptozotocin-induced diabetic rats.

Coenzyme Q10 is an endogenous lipid soluble antioxidant. Because oxidant stress may exacerbate some complications of diabetes mellitus, this study investigated the effects of subacute treatment with exogenous coenzyme Q10 (10 mg/kg/day, i.p. for 14 days) on tissue antioxidant defenses in 30-day streptozotocin-induced diabetic Sprague-Dawley rats. Liver, kidney, brain, and heart were assayed for degree of lipid peroxidation, reduced and oxidized glutathione contents, and activities of catalase, superoxide dismutase, glutathione peroxidase, and glutathione reductase. All tissues from diabetic animals exhibited increased oxidative stress and disturbances in antioxidant defense when compared with normal controls. Treatment with the lipophilic compound coenzyme Q10 reversed diabetic effects on hepatic glutathione peroxidase activity, on renal superoxide dismutase activity, on cardiac lipid peroxidation, and on oxidized glutathione concentration in brain. However, treatment with coenzyme Q10 also exacerbated the increase in cardiac catalase activity, which was already elevated by diabetes, further decreased hepatic glutathione reductase activity, augmented the increase in hepatic lipid peroxidation, and further increased glutathione peroxidase activity in the heart and brain of diabetic animals. Subacute dosing with coenzyme Q10 ameliorated some of the diabetes-induced changes in oxidative stress. However, exacerbation of several diabetes-related effects was also observed.

Effects of piperine on antioxidant pathways in tissues from normal and streptozotocin-induced diabetic rats.

Using diabetes mellitus as a model of oxidative damage, this study investigated whether subacute treatment (10 mg/kg/day, intraperitoneally for 14 days) with the compound piperine would protect against diabetes-induced oxidative stress in 30-day streptozotocin-induced diabetic Sprague-Dawley rats. Liver, kidney, brain, and heart were assayed for degree of lipid peroxidation, reduced and oxidized glutathione (GSH and GSSG, respectively) content, and activities of the free-radical detoxifying enzymes catalase, superoxide dismutase, glutathione peroxidase, and glutathione reductase. Piperine treatment of normal rats enhanced hepatic GSSG concentration by 100% and decreased renal GSH concentration by 35% and renal glutathione reductase activity by 25% when compared to normal controls. All tissues from diabetic animals exhibited disturbances in antioxidant defense when compared with normal controls. Treatment with piperine reversed the diabetic effects on GSSG concentration in brain, on renal glutathione peroxidase and superoxide dismutase activities, and on cardiac glutathione reductase activity and lipid peroxidation. Piperine treatment did not reverse the effects of diabetes on hepatic GSH concentrations, lipid peroxidation, or glutathione peroxidase or catalase activities; on renal superoxide dismutase activity; or on cardiac glutathione peroxidase or catalase activities. These data indicate that subacute treatment with piperine for 14 days is only partially effective as an antioxidant therapy in diabetes.

Atrophic ununited diaphyseal fractures of the humerus with a bony defect: treatment by wave-plate osteosynthesis.

We treated 15 patients with atrophic nonunion of a diaphyseal fracture of the humerus with an associated bony defect using an autogenous cancellous bone graft and a plate to bridge the defect. There were nine men and six women with a mean age of 48 years. The mean length of the bony defect was 3 cm. At a mean follow-up of 30 months only one fracture failed to unite. This suggests that, in the presence of a well-vascularised envelope of muscle, the application of an autogenous cancellous bone graft in conjunction with a bridging plate represents a good alternative to more demanding surgical techniques.

Streptozotocin-induced diabetes increases gamma-glutamyltranspeptidase activity but not expression in rat liver.

Earlier work describing increased biliary excretion of the acetaminophen-cysteine conjugate advanced the hypothesis that streptozotocin-induced diabetes increases gamma-glutamyltranspeptidase (GGT) expression in Sprague-Dawley rats. To test this hypothesis, rats were divided into control, diabetic, and insulin-treated diabetic groups. Diabetes was induced by intravenous injection of 45 mg streptozotocin/kg body weight and was effectively controlled by insulin treatment in the appropriate group. Densitometric quantification demonstrated that hepatic GGT activity in diabetic rats was significantly increased when compared to normal and insulin-treated diabetic controls. Histochemical staining of liver was greater in female than in male rats, and staining increased in female rat liver as the duration of diabetes lengthened from 30 to 90 days. GGT activity was increased by diabetes in liver canalicular-enriched and basolateral-enriched membrane preparations, and it was unchanged in renal brush border-enriched membranes. Total mRNA isolated from diabetic and insulin-treated diabetic rat livers did not conclusively demonstrate an elevation of GGT mRNA relative to normal. Western blot analysis showed no differences in the amount of GGT in diabetic versus normal rat livers. These data indicate that streptozotocin-induced diabetes does not alter the expression of, but does increase the activity of, GGT in liver.

Hepatobiliary excretion of bile acids and rose bengal in streptozotocin-induced and genetic diabetic rats.

Divergent opinions regarding the effect of streptozotocin- (STZ) induced diabetes on bile flow rate may be due to the differing lengths of time after STZ administration at which bile flow was measured. Also, the biliary excretion of bile acids can influence the canalicular transport of several organic anions. Therefore, the hepatic clearance of the bile acid-dependent organic anion rose bengal was studied over a 30-day period in STZ-induced insulin-dependent Sprague-Dawley diabetic rats with elevated bile acid pools and in fatty noninsulin-dependent diabetic and lean Wistar rats. Excretion of total bile acids and rose bengal was higher in diabetic rats than in Sprague-Dawley control or lean or fatty Wistar rats. Depletion of bile acids for 10 hr in the 30-day STZ rat prevented the increased excretion of rose bengal. Bile flow rates in fatty and lean Wistar rats were similar to that in Sprague-Dawley controls. Increased bile acid excretion 7 and 14 days after STZ was not accompanied by the expected significant increase in bile flow, reflecting decreased bile acid-independent bile flow, regardless of method of calculation of bile flow (per g liver or per kg body weight). By 30 days, there were significant increases in bile acid excretion and bile flow. The increased clearance of rose bengal 7 days after STZ indicates that pathophysiological changes in the hepatocyte begin soon after the initiation of diabetes. Studies of taurocholate uptake into liver plasma membrane vesicles indicated that the maximal velocity of transport across the basolateral membrane was increased with no change in Km. This change was not observed in vesicles from insulin-treated diabetic rats. Therefore, studies employing STZ need to allow time for STZ toxicity to be overcome and for the pathology of diabetes to become established, to accurately reflect the diabetic condition.

Complex nonunion of fractures of the femoral shaft treated by wave-plate osteosynthesis.

We have treated 42 consecutive complex ununited fractures of the femoral shaft by wave-plate osteosynthesis at five different medical centres. There were 13 with previous infection, 12 with segmental cortical defects, and 3 were pathological fractures. In 39 cases there had been previous internal fixation and 21 patients had had more than one earlier operation. Union was achieved in 41 patients at an average of six months, although three had required a second bone graft. Two patients had recurrence of infection and in one this resulted in the persistence of nonunion. There were no failures of the implant. All 41 patients with union are now fully weight-bearing, but four have a leg-length discrepancy, one has axial malalignment, and nine have residual stiffness of the knee. These results are surprisingly good, despite the complexity of the initial problem, and appear to confirm the biological and mechanical advantages of the wave plate over the conventional plate for such cases.

Hepatobiliary excretion of cysteinyl leukotrienes in three experimental models of acute hepatic injury.

The acute phase response to chemically-induced organ damage involves inflammation and the production of leukotrienes. The liver ordinarily takes up, metabolizes and excretes into bile cysteinyl leukotrienes, but the effect of hepatic injury on these processes is unknown. The hepatic uptake and biliary excretion of LTC4 was studied in male Sprague-Dawley rats after exposure to either streptozotocin (45 mg/kg iv 30 days before experimentation), estradiol-17 beta-valerate (1 mg/kg sc once a week for 3 weeks) or lipopolysaccharide/D-galactosamine (33 micrograms/ kg ip; 300 mg/kg ip at 6 h and 3 h, respectively, before experimentation). Acute liver injury is produced by these treatment paradigms. Glucose concentrations and activities of several marker enzymes in plasma were measured to demonstrate hepatic injury. Biliary excretion of 3H-LTC4 was similar to normal control rats in the three types of acute liver injury. Bile flow rates after 3H-LTC4 injection were reduced in lipopolysaccharide-pretreated rats and increased in estradiol-treated animals. Total biliary excretion of leukotrienes was not altered in any disease group. Thus, these models of acute hepatic injury do not appear to influence the hepatobiliary clearance of leukotrienes.

Dental surgery standards for perioperative nurses. Medical Center of Central Georgia.

Practice standards for dental surgery are necessary to maintain quality care for dental patients. Specific standards or recommended practices for dental surgery have not been addressed by AORN, and none are available from the American Dental Association or the Georgia Dental Association. We incorporated the Centers for Disease Control and Prevention guidelines, and Occupational Safety and Health Administration regulations had to be incorporated into existing perioperative standards to institute dental surgery standards for our facility. The standards for dental surgery at the Medical Center of Central Georgia, Macon, evolved with the leadership of perioperative nurses.

Chronic voluntary exercise may alter hepatobiliary clearance of endogenous and exogenous chemicals in rats.

A chronic voluntary exercise paradigm, which mimics the exercise pattern of many humans, influences the hepatic clearance of several organic anions and a bile acid, whereas a neutral organic compound is seemingly unaffected. To extend these observations, the present work has evaluated in female Sprague-Dawley rats the effect of 6 weeks of voluntary running on the hepatobiliary elimination of endogenous bile acids and glutathione and exogenously injected rose bengal, digoxin, and acetaminophen. Inactive rats had mobility limited to their cages, whereas exercised rats had free access to a 44-in running wheel. In comparison to weight-matched sedentary rats, the exercised rats ran 4.3 +/- 0.3 miles/day, consumed 45% more food daily, had slightly greater liver/body weight ratios, and slightly elevated basal bile flow rates. Biliary excretion of endogenous bile acids was increased significantly, and excretion of reduced and oxidized glutathione was increased in exercised rats by 190% and 173% of sedentary levels, respectively. Total clearance, biliary clearance, and maximal biliary excretion of the injected organic anion rose bengal (60 mumol/kg) were elevated in exercised rats by 86%, 440%, and 85%, respectively. In contrast, there were no observed differences in pharmacokinetic parameters, serum elimination, or biliary excretion for the clinically important cardiac glycoside digoxin (dose of 100 nmol/kg). Finally, study of the analgesic acetaminophen (330 mumol/kg) revealed that total and biliary clearances were increased by 37% and 42%, respectively, in exercised rats, whereas steady-state volume of distribution and elimination half-life were not significantly different.(ABSTRACT TRUNCATED AT 250 WORDS)

Chronic physical activity: hepatic hypertrophy and increased total biotransformation enzyme activity.

Does chronic voluntary physical activity alter hepatic or intestinal capacities for xenobiotic biotransformation? This question was investigated by comparing biotransformation enzyme activities in liver and small intestine of active and sedentary rats. Male rats allowed unlimited access to a running wheel and fed ad lib. for 6 weeks were weight-matched to sedentary controls; the active rats ate 22% more food than the sedentary rats (P less than 0.05). Active rats ran 2.8 +/- 0.6 miles/day. Liver weights were higher in the active rats (11.2 +/- 0.2 vs 9.8 +/- 0.2 g; P less than 0.05), as were total liver protein, and liver microsomal and cytosolic protein (P less than 0.05). As a result of liver hypertrophy, the active rats showed higher total liver activity of several biotransformation enzymes, including 2-naphthol sulfotransferase, styrene oxide hydrolase, benzphetamine N-demethylase, ethacrynic acid glutathione S-transferase and morphine UDP-glucuronosyltransferase (P less than 0.05). In contrast, there was no detectable difference in total liver N-acetyltransferase activity toward p-aminobenzoic acid, 2-naphthylamine, and 2-amino-fluorene as well as, relative hepatic enzyme activity (expressed per g liver or per mg protein) and total and relative intestinal enzyme activity. We conclude that chronic voluntary physical activity, accompanied by an increased food intake, results in liver hypertrophy and potentially increases total hepatic capacity to biotransform certain xenobiotic chemicals.

The Sauvé-Kapandji procedure: a salvage operation for the distal radioulnar joint.

The Sauvé-Kapandji procedure, a distal radioulnar arthrodesis with surgical creation of a pseudoarthrosis in the distal ulna, was used to treat 11 patients. Although all patients had had at least one previous operation on the involved wrist, they were still having pain and functional limitations. Ten patients were available for follow-up, which averaged 33 months. Of the nine patients with posttraumatic arthritis, six had excellent results (a painless wrist that averaged 82 degrees of pronation and 83 degrees of supination). Three patients had good results (mild pain during activities with an identical range of forearm rotation). One patient who had rheumatoid arthritis had an excellent result for 3 years but recently had a radiocarpal wrist fusion because of radiocarpal arthritis. We have found the Sauvé-Kapandji procedure to be a reliable treatment option for intractable disorders of the distal radioulnar joint and recommend it as a salvage procedure when previous treatment has failed.

External fixation of distal radial fractures: results and complications.

External fixation of unstable fractures of the distal radius yields satisfactory results but has a high complication rate. We studied thirty-five fractures in thirty-four patients to determine whether the results obtained with external fixation warranted it use. At a mean follow-up period of 31 months, the results of treatment were assessed by interviews and clinical and radiographic examination of both wrists. Twelve fractures had an excellent result, twelve had a good result, ten had a fair result, and one had a poor result. Radiographic results were graded excellent in ten fractures, good in thirteen, fair in five, and poor in seven. No correlation was found between the anatomical results and the clinical results or the patients' subjective ratings. Complications that were related directly to the fixation pins occurred in fourteen of the fractures. There were forty-five additional complications. The frequency of complications and the limitations of external fixation demand caution on the part of the surgeon to prevent iatrogenic morbidity, which would limit the benefits of the technique.

Open reduction and internal fixation of delayed union and nonunion of the distal humerus.

Nonunion of a condylar fracture of the distal humerus rarely occurs, but when present it is difficult to manage. We recommend internal fixation of the nonunion in combination with decortication and autogenous iliac crest bone grafting along with careful selection and placement of the implant. Postoperatively, the goal is preservation of elbow motion until the nonunion heals. We reviewed the cases of five patients who had surgery for nonunion of this fracture, all of which healed within 2-3 months after surgery. At final follow-up their average arc of motion was 88 degrees.

The use of MRI in the diagnosis of an occult wrist ganglion cyst.

Magnetic resonance imaging (MRI) has proved to be particularly useful in the evaluation of soft-tissue lesions. A case is presented in which MRI was used to diagnose an occult ganglion cyst of the wrist.

The effect of long-term streptozotocin-induced diabetes on the hepatotoxicity of bromobenzene and carbon tetrachloride and hepatic biotransformation in rats.

To exclude the possibility that changes in hepatotoxicity and biotransformation were induced by diabetogen administration, the influence of long-lasting experimental insulin-dependent diabetes on the activities of benzphetamine demethylase, styrene oxide hydrolase, and UDP-glucuronosyl-transferases toward 1-naphthol, diethylstilbestrol, estrone and testosterone, and glutathione S-transferases toward 1-chloro-2,4-dinitrobenzene, ethacrynic acid, and sulfobromophthalein was studied. Adult male Sprague-Dawley rats injected with 45 mg streptozotocin/kg rapidly developed the classical symptoms of diabetes which persisted throughout the 90-day test period. Ketonemia was detectable at 6 but not at either 35 or 90 days after streptozotocin administration. After acute challenge with bromobenzene or carbon tetrachloride (CCl4), aspartate and alanine aminotransferase activities in rats diabetic for 35 and 90 days were markedly higher than those in normal rats, suggesting that diabetes potentiated the hepatotoxicity of these chemicals. Administration of 25 microliters CCl4/kg, ip, to diabetic rats decreased enzyme activities toward benzphetamine, sulfobromophthalein, 1-chloro-2,4-dinitrobenzene, and 1-naphthol. In normal rats, a dose of 400 microliters CCl4/kg, ip, was required to cause similar changes in enzyme activities. Bromobenzene (500 microliters/kg, ip) elicited opposing responses in diabetic and normal rats in N-demethylase activity, in UDP-glucuronosyltransferase activity toward 1-naphthol, estrone, and testosterone, and in glutathione S-transferase activity toward 1-chloro-2,4-dinitrobenzene. Total cytochrome P450 concentrations were reduced by both induction of diabetes and hepatotoxicant challenge. Thus, chronic uncontrolled diabetes alters the response of hepatic xenobiotic biotransformation enzymes in a non-uniform, substrate-dependent manner, independent of initial diabetogen effects. The role of cytochrome P450j in potentiating CCl4 toxicity is discussed.