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At least 811 records · Page 45Linked to original sources
PubMed2003

Superoxide is involved in the central nervous system activation and sympathoexcitation of myocardial infarction-induced heart failure.

Increased angiotensin II signaling in the brain has been shown to play a critical role in the excessive sympathoexcitation and development of heart failure (HF) after myocardial infarction (MI). We have recently demonstrated that reactive oxygen species mediate the actions of angiotensin II in the brain. In this study, we tested the hypothesis that increased redox signaling in central cardiovascular control regions is a key mechanism in the neurocardiovascular dysregulation that follows MI. Ligation of the left coronary artery induced a large MI and subsequent HF in adult C57BL/6 mice, as demonstrated by cardiac hypertrophy, hydrothorax, and ascites. Immunohistochemical analysis of Fos, a marker of neuronal activation, revealed a significant increase in the number of Fos-positive neurons in the paraventricular nucleus and supraoptic nucleus at 2 and 4 weeks after MI compared with sham mice. Intracerebroventricular injection of an adenoviral vector encoding superoxide dismutase (Ad-Cu/ZnSOD) caused a significant decrease in the number of Fos-positive neurons in the paraventricular nucleus and supraoptic nucleus at 2 weeks after MI compared with mice receiving either saline or a control vector (Ad-LacZ). There was also a diminished role of sympathetic drive in post-MI mice treated centrally with Ad-Cu/ZnSOD, as demonstrated by significantly attenuated falls in heart rate and mean arterial pressure to the ganglionic blocker hexamethonium and decreased urinary norepinephrine levels in these mice compared with Ad-LacZ-treated MI mice. These results suggest that superoxide plays a key role in the central activation and sympathetic hyperactivity after MI in mice and that oxygen radicals in the brain may be important new targets for therapeutic treatment of heart failure.

Adenoviridae↗
PubMed1995

Clinical, echocardiographic, and hemodynamic evidence of cardiac tamponade caused by large pleural effusions.

Large pleural effusions are typically associated with dyspnea and potential respiratory compromise. Experimental evidence suggests that with large effusions, increased intrapleural pressure may be transmitted to the pericardial space, resulting in impaired cardiac filling and reduced stroke volume. We report two cases in which large pleural collections were complicated by hypotension. The effusions were due to an infected right hepatic hydrothorax (Case 1) and a left malignant effusion (Case 2). Echocardiography demonstrated right and left ventricular diastolic collapse, respectively, confirming a diagnosis of cardiac tamponade. Large volume thoracentesis resulted in immediate hemodynamic improvement as demonstrated by a reduction in right ventricular and atrial pressures (Case 1) and echocardiographic resolution of left ventricular diastolic collapse (Case 2). These cases establish that large pleural effusions can cause hemodynamically significant cardiac tamponade. In addition, they illustrate how the demonstration of cardiac compressive physiology can significantly alter the therapeutic approach to large pleural effusions.

Adult↗
PubMed1989

Percutaneous subclavian vein catheterization for hemodialysis: a report of 57 insertions.

The authors report an analysis of 57 subclavian vein catheterizations for hemodialysis. A total of 51 patients (34 men, 17 women) kept the Cobe single- and double-lumen catheters for 1,726 days. The youngest patient was eighteen and the oldest seventy-two years of age. There were no catheter-related deaths. Complications were encountered in 9 patients. The only life-threatening complication was cardiac arrest, which occurred during flushing of the catheter. The patient was successfully revived. The other complications were pneumothorax and hydrothorax in 1 patient, catheter site infection in 5 patients, and arrhythmias in 2 patients, which stopped after readjustment of the catheter tips. Their experience indicates that percutaneous subclavian vein catheterization is safe and provides quick access for hemodialysis with no morbidity and mortality if done correctly, patiently, and meticulously. The authors believe that this should be the first choice in patients with reversible renal failure and in patients with chronic renal failure, who are usually elderly and medically compromised, till a permanent vascular access is ready for use.

Adult↗
PubMed1990

Central venous pressure monitoring for the critically ill in Zambia.

The safety and value of central venous pressure (CVP) monitoring in 100 critically ill patients in Zambia was studied prospectively. There were six complications related to insertion, the only serious one being a hydrothorax which was recognized and treated. One patient developed catheter-related septicaemia. CVP measurement altered proposed fluid management in 19 cases, determined management in 31 in whom fluid status was uncertain and confirmed fluid therapy in 50. Additional benefits of central venous catheterization were drug infusion in 33 patients and venous access in 53. Technical problems during monitoring occurred in 54 cases and were due to kinking of the catheter, blockage or inadvertent removal. In our circumstances the risks of cannulation of central veins seem justified in selected patients but good nursing supervision of patients is necessary.

Adolescent↗
PubMedDate not supplied

Mechanical complications from insertion of subclavian venous feeding catheters: comparison of de novo percutaneous venipuncture to change of catheter over guidewire.

Since a percutaneous catheter insertion into the subclavian vein can be tedious, time consuming, and risky, we have compared the morbidity of 137 de novo subclavian catheter insertions to that of 93 reinsertions over guidewire. Mechanical complications were significantly higher (p less than 0.03) in those with catheter insertions (8.8%) than in those with the guidewire insertions (2.2%). These included pneumothorax (4), arterial puncture (4), catheter-size bleed (3), and hemothorax (1) in the catheter insertion group and local bleeding (1) and hydrothorax (1) in the guidewire insertion group. The difference in complications between methods is probably inherent in the techniques. Operator experience was not a factor: 55% of the physicians in each group had previously done less than 26 subclavian venous catheterizations. Preliminary analysis indicates that the infection rate, as determined by semiquantitative, cultures, is the same in each group. When considering the equal potential for infection, we conclude that change over a guidewire is an acceptable alternative to contralateral de novo percutaneous subclavian venipuncture for feeding catheter insertion. In view of fewer mechanical complications and greater ease of insertion, change of subclavian feeding catheters by guidewire is probably the method of choice.

Arteries↗
PubMed1987

Tissue polypeptide antigen (TPA) in pleural effusions.

The usefulness of tumor marker assay in pleural effusions for differential diagnosis is still debated. From the observation of common antigens on tissue polypeptide antigen (TPA) and keratins 8, 18 and 19 and vimentin, all substances contained in normal and neoplastic mesothelium, we felt it opportune to evaluate the use of TPA assay in 105 pleural effusions (46 benign and 59 malignant). The values were much higher than those found in blood. In hydrothorax the median value was 454 U/l (range, 59-1923), in exudative effusions 846 U/l (range, 258-4485), in metastatic pleural effusions 1277 U/l (range, 58-32352) and in mesotheliomas 7705 (range, 759-16000). The maximum value found in nonmalignant effusions was 4485 U/l; this value was taken as a cutoff level, so only 29.9% of the tumors were positive to the test. Our results showed this assay to be not very important for a differential diagnosis of malignant and nonmalignant pleural effusions. Nevertheless, the different TPA patterns in mesotheliomas (66.6% positive) and metastatic pleural effusions (15.9%) suggest that further studies are warranted.

Adult↗
PubMed1979

Mycotoxicosis produced in swine by cultural products of an isolate of Aspergillus ochraceus. I. Clinical observations and pathology.

Pigs fed a ration, 25% of which was rice culture, of Aspergillus ochraceus lost weight or failed to gain and became depressed. Some pigs died and most developed subcutaneous edema, hydrothorax, hydroperitoneum, pulmonary atelectasis, edema of the mesentery and perirenal edema. Microscopic lesions in addition to edema were primarily renal and consisted of tubular degeneration and necrosis, hyaline tubular casts, interstitial fibrosis and tubular cell regeneration. The first change found after 3 days was cytoplasmic vacuolation of the convoluted and straight segments of the proximal tubules. Necrotic proximal tubules were found after 4 days and after 9 days degeneration and necrosis involved predominantly proximal tubular segments. Pigs fed a ration, 12.5% of which was rice culture, for 8 weeks did not develop perirenal edema but had firm kidneys. Extensive interstitial fibrosis of the cortical labyrinth was the principal change. Within the fibrous connective tissue, some tubules were necrotic and others were atrophied.

Animals↗
PubMed1984

Monocytic leukemia in a horse.

On clinical examination, a six-year-old Hassian gray gelding with a history of impaired performance, slight cough, colic, and edema of the ventral abdomen, prepuce and the legs had reduced skin turgor, pale mucous membranes, forced costoabdominal breathing, reduced venous return, enlarged lymph nodes, and splenomegaly. Hematologic findings revealed anemia, leukocytosis and a high percentage of monocytoid leukemic cells. Generalized lymphadenopathy, splenomegaly, ascites, hydrothorax, and a diffusely thickened gut wall were found at necropsy. Massive infiltration with monocytoid leukemic cells was detected in lymph nodes, spleen, bone marrow, liver, gut wall, kidneys, and choroid plexus. Incubation of living cells obtained from a leukocyte concentrate with latex particles revealed phagocytosis in the leukemic cells on light and electron microscopy. The leukemic cells also had a marked alpha-naphthyl-acetate and naphthol-AS-acetate esterase activity, but were only weakly positive to naphthol-AS-D-chloroacetate esterase. A very weak alkaline phosphatase activity only was demonstrated in a few leukemic cells. On scanning electron microscopy, the leukemic cells had prominent ruffles and ridge-like profiles. These features of the leukemic cells excluded lymphocytic and granulocytic leukemia, and monocytic leukemia was diagnosed.

Alkaline Phosphatase↗
PubMed1996

Spontaneous cardiomyopathy and exophthalmos in cotton rats (Sigmodon hispidus).

Exophthalmos and clinical signs of heart failure occurred sporadically in 3- to 12-month-old cotton rats (Sigmodon hispidus) in a colony originally derived from three male and four female littermates. Macroscopic lesions in severely affected animals included subcutaneous edema, hydrothorax, right ventricular dilatation, unilateral or bilateral atrial thrombosis, and exophthalmos. Hearts from 17 cotton rats that were found dead or were euthanatized because of exophthalmos or dyspnea and 33 control cotton rats were examined microscopically. Myocardial lesions were present in 46 of 46 cotton rats > or = 1 month of age and consisted of multifocal cardiac myocyte necrosis, mineralization, and mononuclear inflammatory cell infiltration. Cotton rats > 5 months of age also had foci of interstitial fibrosis and myocyte atrophy. Twelve of 24 (50%) necropsied cotton rats had chronic pulmonary congestion, and livers from eight of 24 (33%) had chronic periacinar congestion and atrophy. Thrombi were present in one or both cardiac atria in nine of 50 (18%) hearts, and in at least one orbital venous sinus in 14 of 24 (58%) necropsied cotton rats and in 12 of 14 (86%) with exophthalmos. Exophthalmos in this colony of cotton rats appears to have resulted predominantly from orbital venous sinus thrombosis caused by stasis of venous blood secondary to right heart failure associated with a heritable cardiomyopathy.

Animals↗
PubMed1997

The lesions of experimental equine morbillivirus disease in cats and guinea pigs.

Nine cats and four guinea pigs became affected with severe disease during experiments on the infectivity of equine morbillivirus, a newly recognized cause of respiratory disease in horses and humans. Four of the cats were challenged by subcutaneous inoculation, two by intranasal installation, two by oral dosage, and one by direct contact with a cat previously infected by subcutaneous inoculation. All four guinea pigs were inoculated subcutaneously. Gross pathology seen in all affected cats was characterized by hydrothorax and dark, heavy, wet, congested and/or hemorrhagic lungs with froth sometimes found in the respiratory passages. Pulmonary lymph nodes were enlarged and edematous. Six cats also had congested ceca with accompanying edema of mesenteric lymph nodes. Histologically, the lesions in the lungs of the cats were those of severe interstitial pneumonia characterized by serofibrinous alveolar edema, alveolar macrophages, intra-alveolar hemorrhage, thrombosis of small veins, alveolar wall necrosis, and syncytial cells. Clearly defined vascular lesions included intramural hemorrhage, edema, and necrosis and syncytial cells in the endothelium of pulmonary arteries and veins, 20-80 microm in diameter. Vascular lesions accompanied by parenchymal degeneration were also seen in the gastrointestinal and lymphoid organs. Syncytial cells were also visible in the lymphoid tissues of lymph nodes, spleen, and Peyer's patches. At necropsy, all guinea pigs were cyanosed and had congestion and edema in the gastrointestinal tract. Histologically, there was widespread vascular disease in arteries and veins, 20-80 microm in diameter, in many organs such as the lungs, kidneys, spleens, lymph nodes, gastrointestinal tracts, and skeletal and intercostal muscles, but there was no severe pulmonary edema as seen in horses and cats. Sections of tissues of the cats and guinea pigs, examined by indirect immunocytochemical stains, confirmed that the vascular damage was associated with the presence of equine morbillivirus antigen. The syncytia in small blood vessels in the lungs and other organs of both cats and guinea pigs were similar to those seen in horses, and their presence was interpreted as an important characteristic of the disease consistent with a reaction to a morbillivirus.

Animals↗
PubMed2000

Cardiomyopathy in captive African hedgehogs (Atelerix albiventris).

From 1994 to 1999, 16 captive African hedgehogs (Atelerix albiventris), from among 42 necropsy cases, were diagnosed with cardiomyopathy. The incidence of cardiomyopathy in this study population was 38%. Fourteen of 16 hedgehogs with cardiomyopathy were males and all hedgehogs were adult (>1 year old). Nine hedgehogs exhibited 1 or more of the following clinical signs before death: heart murmur, lethargy, icterus, moist rales, anorexia, dyspnea, dehydration, and weight loss. The remaining 7 hedgehogs died without premonitory clinical signs. Gross findings were cardiomegaly (6 cases), hepatomegaly (5 cases), pulmonary edema (5 cases), pulmonary congestion (4 cases), hydrothorax (3 cases), pulmonary infarct (1 case), renal infarcts (1 case), ascites (1 case), and 5 cases showed no changes. Histologic lesions were found mainly within the left ventricular myocardium and consisted primarily of myodegeneration, myonecrosis, atrophy, hypertrophy, and disarray of myofibers. All hedgehogs with cardiomyopathy had myocardial fibrosis, myocardial edema, or both. Other common histopathologic findings were acute and chronic passive congestion of the lungs, acute passive congestion of the liver, renal tubular necrosis, vascular thrombosis, splenic extramedullary hematopoiesis, and hepatic lipidosis. This is the first report of cardiomyopathy in African hedgehogs.

Animals↗
PubMed2006

Monensin toxicosis in water buffaloes (Bubalus bubalis).

The consumption of monensin-containing feed resulted in deaths of water buffaloes from a feedlot in which cattle and buffaloes were kept together. The monensin formulation was recommended only for use in cattle. Anorexia, muscular weakness, dyspnea, and recumbency were the major clinical findings. The most significant gross lesions were focal pale areas in semitendinosus and semimembranosus muscles, in which segmental necrosis of myofibers was seen microscopically. To compare susceptibilities of species to monensin, 3 bovine calves and 3 buffalo calves were orally dosed. At 5, 7.5, and 10 mg/kg of monensin, only the buffaloes became ill and died. Clinical signs initiated 18-20 h postdosing and were comparable to those from field cases. Gross changes consisted of ascites, hydrothorax, hydropericardium, hepatomegaly, and focal pale areas in the myocardium and to a lesser degree in semitendinosus and semimembranosus muscles. Histopathological changes also resembled those from the field cases, but were especially pronounced in the myocardial cells. The hypothesis that buffaloes could have a lower tolerance to monensin than cattle has been supported by experimental cases.

Animals↗
PubMed1992

Characterization of an epizootic of pulmonary edema in swine associated with fumonisin in corn screenings.

In 1989, corn screenings were associated with acute interstitial pulmonary edema, hydrothorax, and death in swine. Attack rate was 5-50%, case fatality rate was 50-90%, and clinical course was 1-2 days. Screenings from farms with pigs affected with pulmonary edema contained 20-330 micrograms fumonisin B1 per gram. Screenings containing 92 micrograms fumonisin B1 per gram fed to weanling pigs caused pulmonary edema and death. Sterilized corn inoculated with Fusarium moniliforme and diluted 1:1 with clean corn contained fumonisin B1 (17 micrograms/g) and caused acute pulmonary edema when fed for 5 days. Survivors developed subacute hepatotoxicosis with individual hepatocellular necrosis, hepatomegalocytosis, and increased numbers of mitotic figures. Similar liver lesions occurred in pigs given fumonisin B1 intravenously at 0.8 mg/kg body weight for 14 days.

Animal Feed↗
PubMed1993

Fumonisin toxicosis in swine: clinical and pathologic findings.

From a series of experimental studies with pigs (12-16 kg), either pulmonary edema or liver failure emerged as a distinct pathogenetic expression of fumonisin B1 (FB1) toxicosis. The primary determinant as to which pathogenetic consequence developed was the quantity (dose) of the mycotoxin fed or intubated per kilogram of body weight per day. Pigs intubated with a minimum of 16 mg FB1/kg/day developed severe interlobular edema with or without hydrothorax and variably severe pulmonary edema. Pigs intubated with < 16 mg FB1/kg/day or pigs fed diets containing 200 mg FB1/kg of feed developed marked icterus and hepatocellular necrosis. The spectrum of degrees of severity of pulmonary edema observed in the experimental pigs allowed rational speculation regarding evolution of the pathologic changes.

Animals↗
PubMed2004

A model of chronic heart failure in spontaneous hypertensive rats (SHR).

Common models of chronic heart failure (CHF) do not always result in parameters and symptoms that can be extrapolated to the clinical situation of patients with end-stage heart failure. The aim of this study was to establish and validate a new model of CHF in the rat. CHF was induced in Wistar Kyoto (WKY/NHsd) and spontaneously hypertensive (SHR/NHsd) rats by creating a permanent (8-week) occlusion of the left coronary artery 2 mm distal to the origin from the aorta by a modified technique. This resulted in a large infarction of the free left ventricular wall. The focus of attention was the validation of the geometric properties of the left ventricle and its contractility. The validation of the geometric properties of the left ventricle was done by a non-invasive magnetic resonance imaging (MRI) technique and by planimetry (stereology). Cardiodynamics (e.g. contractility) were evaluated in the isolated 'working heart' model. We were able to establish a new and predictive model of heart failure in the spontaneously hypertensive rat 8 weeks after coronary artery ligation. At this time point, the WKY rat did not show any symptoms of CHF. The model represents characteristic parameters and symptoms that can be extrapolated to the clinical situation of patients with end-stage heart failure (NYHA III-IV). Upon inspection, severe clinical symptoms of congestive heart failure were prominent, such as dyspnoea, subcutaneous oedema, pale-bluish limbs and impaired motion. Non-invasive sequential measurements by NMR techniques showed lung oedema, hydrothorax, large dilated left and right ventricular chambers and hypertrophy of the septum. The infarcted animals showed a reduced heart power, diminished contractility and enhanced heart work, much more so in the SHR/NHsd rat than in the WKY/NHsd rat. Furthermore the infarcted animals showed enhanced levels of hydroxyproline/proline ratios, again much more so in the SHR/NHsd rat than in the WKY/NHsd rat.

Animals↗
PubMed2005

The isolated working heart model in infarcted rat hearts.

Congestive heart failure (CHF) is one of the most common causes of death in western countries. The aim of this study was to establish and validate the working heart model in rat hearts with CHF. In the rat model the animals show parameters and symptoms that can be extrapolated to the clinical situation of patients with end-stage heart failure. The focus of attention was the evaluation of cardiodynamics (e.g.contractility) in the isolated 'working heart' model. The geometric properties of the left ventricle were measured by planimetry (stereology). Formulae available in the past for determining certain parameters in the working heart model (e.g.external heart work) have to be fitted to the circumstances of the infarcted rat hearts with its different organ properties.CHF was induced in Wistar Kyoto (WKY/NHsd) and spontaneously hypertensive rats (SHR/NHsd) by creating a permanent (8 week) occlusion of the left coronary artery, 2 mm distal to the origin from the aorta, by a modified technique (Itter et al. 2004). This resulted in a large infarction of the free left ventricular wall. We were able to establish and adapt a new and predictive working heart model in spontaneously hypertensive rat hearts with myocardial infarction (MI) 8-12 weeks after coronary artery ligation. At this stage the WKY rat did not show any symptoms of CHF. The SHR rat represented characteristic parameters and symptoms that could be extrapolated to the clinical situation of patients with end-stage heart failure (NYHA III-IV). Upon inspection, severe clinical symptoms of CHF such as dyspnoea, subcutaneous oedema, palebluish limbs and impaired motion were prominent. On necropsy the SHR showed lung oedema, hydrothorax, large dilated left and right ventricular chambers and hypertrophy of the septum. In the working heart model the infarcted animals showed reduced heart power, diminished contractility and enhanced heart work, much more so in the SHR/NHsd than in the Wistar Kyoto rat (WKY/NHsd). The aim for the future is to find a causal therapy of heart failure treatment. At present, only palliative therapy is possible for patients with heart failure. For this reason the working heart model in CHF rat hearts should provide a valuable method for early testing of new therapeutic approaches for patients with CHF.

Animals↗