Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An initial event in gram-negative bacteremia is activation of the complement cascade with production of C5a. C5a, in turn, acts as a chemotactic stimulus for leukocytic aggregation and, in conjunction with bacterial products, stimulates the release of oxygen free radicals from leukocytes. We have hypothesized that these oxygen free radicals (.O2-, superoxide anion; .OH, hydroxyl radical; H2O2, hydrogen peroxide) contribute to the characteristic myocardial dysfunction of endotoxin shock, Isolated canine cardiac sarcoplasmic reticulum (SR) was used as a subcellular determinant of mechanical function. SR was incubated for 20 min at 37 degrees C in the presence of phorbol myristate acetate activated leukocytes (A-L) and calcium uptake and Ca2+-adenosine triphosphatase (ATPase) activities were measured. Activated leukocytes significantly depressed SR Ca2+ uptake rates (C = 1.12 +/- 0.05 mumol CA2+/mg-min; A-L = 0.73 +/- 0.05). The addition of catalase (CAT; 10 micrograms/ml) or superoxide dismutase (SOD: 10 micrograms/ml) plus CAT reversed the inhibition of SR Ca2+ uptake. SOD further depressed SR Ca2+ uptake (+SOD = 0.55 +/0 0.04 mumol Ca2+/mg-min). Mannitol had no effect. SR ATPase activity was inhibited with A-L (C = 1.41 +/- 0.04 mumol Pi/mg-min; A-L = 0.84 +/- 0.09). Neither mannitol, nor SOD nor CAT alone had any effect on the depression of SR ATPase activity. SOD plus CAT reversed the ATPase depression induced by A-L. It is concluded that phorbol myristate acetate activated leukocytes via free radical-mediated mechanisms can directly affect function and activity of the excitation-contraction coupling system of cardiac muscle. Free radical scavengers identified hydrogen peroxide as a major mediator of depressed Ca2+ uptake rates. In conjunction with the superoxide anion, hydrogen peroxide contributes to the depressed ATPase activity.
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PMID:Interaction of oxygen free radicals and cardiac sarcoplasmic reticulum: proposed role in the pathogenesis of endotoxin shock. 685 Oct 3

Myelomonocytic myeloproliferative disease in a horse was diagnosed on the basis of hematologic, enzymatic, and histopathologic findings. It was characterized clinically by depression, weight loss splenomegaly, lymphadenopathy, coagulopathy, and bacteremia. Hematologic findings included severe refractory anemia, thrombocytopenia, monocytosis, and pleomorphic leukocytes, with a left shift of the myeloid series. The serum lysozyme concentration was 14.5 microgram/ml (normal, less than 5 microgram/ml). The bone marrow contained many immature cells of the myeloid series and had a myeloid-to-erythroid ratio of 30.5 to 1. The horse died after brief hospitalization. Necropsy revealed generalized lymphadenopathy and hemorrhages throughout the body. Histopathologically, primitive cells were seen in several tissues. Cells that proliferated in the bone marrow were primarily myeloblastic, with some additional erythropoietic cells. Myeloblastic cells with evidence of normal erythropoiesis were seen in numerous lymph nodes and in the spleen, whereas primarily normal erythropoietic cells proliferated in the adrenal glands. Myeloid blast-type cells predominated in the lungs, myocardium, liver, and kidneys.
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PMID:Myelomonocytic myeloproliferative diseases in a horse. 705 85

Bovine viral diarrhea virus infection of cattle interfered with normal blood clearance mechanisms, as evidenced by the detection of an endogenous bacteremia in up to 85% of infected calves during the first 5 days after infection. The occurrence of detectable bacteremia correlated with the period of leukopenia and depression of lymphocyte responses to mitogens. Noninoculated control animals, reinoculated immune calves, or calves inoculated with infectious bovine rhinotracheitis virus yielded consistently negative cultures. Bacillus spp were isolated in almost all calves. Similar organisms were isolated from the blood of normal calves when medium containing sodium poly-anetholesulfonate was used for culture. It was concluded that bovine viral diarrhea virus infection depressed the normal defense mechanisms, presumably humoral factors or phagocytic function, resulting in uninhibited blood circulation of bacteria during infection.
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PMID:Detection of bacteremia in cattle inoculated with bovine viral diarrhea virus. 725 71

There is an ongoing discussion whether the heart is the primary target organ responsible for the development of cardiovascular failure during septic shock as well as its onset. We tried to study the reaction of the heart to sepsis in the early phase of 8 h, using a sublethal model of sepsis in six awake cross-bred Austrian mountain sheep. Sepsis was induced by infusion of a live Escherichia coli suspension at a dose of 5 x 10(7) colony-forming units per kg body weight over 8 h. Standard hemodynamic, hematologic and serum tumor necrosis factor (TNF) measurements were obtained. For evaluation of left ventricular performance we used the following methods, tested in five pilot experiments: 1) The shift of the end-systolic pressure-diameter relation. This was characterized by the calculated shift of the transverse external end-systolic diameter of the left ventricle at a "midrange" end-systolic pressure of 100 mmHg (end-systolic ventricular diameter deviation, ESVDD100). Calculations were performed using a second order regression function of the end-systolic pressure diameter points obtained by variation of afterload by a cuff occluder on the aorta; 2) The shift of the (dP/dt)max over end-diastolic diameter ratio compared to control values estimated by a graphical approach. Mean pulmonary pressure increased from 21 +/- 1 to 36 +/- 2 mmHg in the first hour after starting the E. coli infusion and remained elevated during the entire 8 h observation period. Serum TNF was found to peak 1 hour after start of E. coli infusion and was hardly detectable after 3 hours of bacteremia. Mean aortic pressure showed minor changes (maximum 105 +/- 3 mmHg, minimum 91 +/- 2 mmHg) and there were no statistically significant alterations of the cardiac index. ESVDD100 showed an "oscillatory" reaction in the first phase and a statistically significant decrease of contractility in the second phase (at 4 h). This was confirmed by the graphical method of the (dP/dt)max over end-diastolic diameter ratio. We may therefore conclude that there is no early depression of myocardial function or if so, it may be masked by adrenergic stimulation. In the later phase of the 8 h experiment there is a significantly decreased contractility of the heart. This may be compensated (e.g., "Starling" mechanism or heart rate increase) in this sublethal model.
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PMID:Myocardial function in septic sheep. 774 34

To evaluate the clinical relevance of the experimental findings of a more severe cardiac depression in Pseudomonas (P.) than in non-P. sepsis, we retrospectively compared the hemodynamic data in 26 patients with P. sepsis (20 cases, single pathogen; six cases, more positive cultures with P. than with non-P. species), and 102 with non-P. sepsis. As in other studies, the left ventricular stroke work index (LVSWI) was used to assess cardiac performance. The two groups (all numbers are means) had a similar disease and sepsis severity profile (P. vs. non-P: septic shock, 81% vs. 87%; APACHE II scores, 29.1 vs. 29.2; Elebute sepsis scores, 18.1 vs. 18.1; mortality, 58% vs. 62%). Preload (pulmonary capillary wedge pressure 15.0 vs. 16.3 mm Hg) and systemic vascular resistance (588 vs 572 dyn.cm-5.sec) were comparable. Cardiac performance displayed no significant difference (LVSWI, 42.8 vs. 38.3 g.m/m2), a result reproduced in the subgroups with culture-proven bacteremia, with or without preexisting cardiovascular disease or septic shock. Thus, our data suggest that there is no difference in the degree of cardiovascular dysfunction in patients with Pseudomonas compared to non-Pseudomonas sepsis of otherwise equivalent disease severity.
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PMID:Pseudomonas sepsis does not cause more severe cardiovascular dysfunction in patients than non-Pseudomonas sepsis. 805 63

The signs of pneumonic plague in sacred baboons infected by aerosol are: fever, hurried breathing, depression and constantly increasing bacteremia. Some infected animals isolate the plague microbes while coughing and thus could be a source of the infection. By the clinical and pathomorphological signs, pneumonic plague in sacred baboons is similar to that in humans which makes it possible to use the animals in the development of schemes for special prophylaxis and treatment of the disease. In efficacy estimation of antibacterial drugs sacred baboons should be infected by aerosol by highly virulent strains of Y. pestis in doses of 1.10(4)-1.10(5) live microbes. The treatment of the animals should be started from the moment of the rectal temperature increase to 39.5 degrees C or higher after collecting the blood specimens for the bacteriological tests. It was shown that a two-day course of the treatment with antibacterial drugs was not efficient in the animals with pneumonic plague. The use of streptomycin, gentamicin, netilmicin or ciprofloxacin for 7 days cured all the infected animals. The use of streptomycin in the therapeutic doses was not efficient in the animals whose blood specimens of 1 cm3 contained 4.10(4) or more plague microbes by the moment when the treatment was started.
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PMID:[Standardization of conditions for the evaluation of effectiveness of antibacterial drugs in pneumonic plague in sacred baboons]. 859 90

Cardiovascular responses to systemic bacteremia were evaluated in a pre-instrumented, conscious pigs. Basal observations were obtained 5-7 days after instrumentation. On the next day, Escherichia coli 0111.B4 (1.1 to 33 x 10(9) CFU/kg)-laden fibrin clots were implanted intraperitoneally. Nonsurvivors (9/18) demonstrated rapid cardiovascular decompensation. Survivors (9/18) demonstrated significant cardiovascular injury, which was reversed by 5-7 days postimplant. Cardiac inotropicity was significantly reduced in this period, but recovered by day 7. Circulating myocardial depressant substance activity (assayed by serum-induced depression of beating neonatal rat myocytes) was present on days 1-4 of bacteremia and recovered to basal values on day 6. No clinical or cardiovascular changes were seen in pigs implanted with sterile clots (n = 4). These data demonstrate that implantation of bacteria-laden fibrin clots in pigs induces cardiovascular alterations that mimic responses seen in human sepsis.
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PMID:A porcine model of peritonitis and bacteremia simulates human septic shock. 896 95

The objectives of this study were to estimate the prevalence of bacteremia in critically ill, neonatal calves with severe diarrhea or depression, and to describe the variety of bacteria involved. Two studies were conducted in the summers of 1991 and 1993 involving 190 neonatal calves, 1-day to 19-days-old. Bacteremia was detected by blood culture in 31% (28/90) of calves in study 1, and in 24% (19/79) of ill calves and 0% (0/21) of control calves in study 2. Bacteria cultured from blood included Escherichia coli (51% of all isolates), other gram-negative enterics (25.5%), gram-negative anaerobes (5.9%), gram-positive cocci (11.8%), and gram-positive rods (5.9%). Among clinically ill calves, the average age was significantly lower in the blood culture-negative group (5.5 d) than in the blood culture-positive group (7.5 d) (P = 0.004). Mean serum IgG concentration was significantly (P = 0.0001) lower in blood culture-positive calves (1.146 g/L) than in blood culture-negative calves (3.077 g/L). The mortality rate was significantly (P < 0.0001) higher in the blood culture-positive group (57.4%) than in the blood culture-negative group (15.1%). Bacteremia appeared to be a frequent entity in this particular rearing situation. Early recognition of the problem, as well as appropriate treatment, may be beneficial in increasing survival rates. Results also support the need to address the failure of passive transfer of maternal antibodies to prevent bacteremia in calves.
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PMID:Bacteriological culture of blood from critically ill neonatal calves. 902 92

Cardiovascular diseases, including atherosclerosis and myocardial ischemia, occur as a result of a complex set of genetic and environmental factors. During periodontitis, dental plaque microorganisms may disseminate through the blood to infect the vascular endothelium and contribute to the occurrence of atherosclerosis and risk of myocardial ischemia and infarction. Myocardial ischemia and infarction are often preceded by acute thromboembolic events. In an in vitro model of thrombosis, certain dental plaque bacteria induce platelets to aggregate. Aggregation of platelets is induced by the platelet aggregation-associated protein [PAAPJ expressed on plaque bacteria, including Streptococcus sanguis and Porphyromonas gingivalis. Intravenous infusion of S. sanguis into rabbits has been shown previously to cause changes in the electrocardiogram (ECG), heart rate, blood pressure, and cardiac contractility. These changes are consistent with the occurrence of myocardial infarction. The ECG changes are now shown to begin within 30 seconds after infusion of PAAP+ S. sanguis, followed by alterations in blood pressure and respiratory rate. These changes occurred intermittently over a 30-minute period and changed within one heartbeat to a normal pattern and suddenly back to abnormal. Intermittent ECG abnormalities were seen in 13 of 15 rabbits, including left axis deviation, ST-segment depression, preventricular contractions, alternans, and bigemnia. Dose-dependent thrombocytopenia, accumulation of 111Indium-labeled platelets in the lungs, and tachypnea also occurred. No changes occurred with the PAAp- strain. The data indicated that PAPP+ S. sanguis interacts with circulating platelets, inducing thromboemboli to cause the pulmonary and cardiac abnormalities. During periodontitis, therefore, PAAP+ S. sanguis and P. gingivalis bacteremia may contribute to the chance of acute thromboembolic events.
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PMID:Dental plaque, platelets, and cardiovascular diseases. 972 99

The systemic infections caused by E. rhusiopathiae and reported in literature are very rare, majority evolving with endocarditis. The authors present a child with acute leukemia, to whom the blood culture during a high temperature episode allows to isolate this bacterium, without valvular lesions. The case is interesting because of the arisen bacteriological diagnosis problems and because of the pathogenic aspects of the infection. An animal source contact being absent, we took in account the intestinal carriage which, under the profound depression of the defence (the underlaying disease and the cytostatic therapy) could result in a persistent bacteremia. The treatment with cefazolin allows the infection to be cured.
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PMID:[Erysipelothrix rhusiopathiae bacteremia in a child with acute leukemia]. 1075 59


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