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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Authors record a preliminary study led so as to develope techniques of preparation of the cardiac homograft valves. Eight human hearts have been appropriated in the course of medico-legal autopsy. Under sterile hodd, the heart was dissected, aortic and pulmonary valves as well as a mitral valve fragment were collected for a total of 24 valvular levies. After sterlization in an antibiotic solution, valves were preserved at 4 degrees C for the mitral fragment specimen of fresh allograft and to - 196 degrees C in Nitrogen liquidates for the pulmonary and aortic valves. The control of graft quality had consisted in tests of competence during the dissection, to the evaluation of the histological study as well as tests of sterility. Cellular cultures had shown a fibroblast proliferation in 3 cases. It concerned an indeed reliable method but difficult and little sensitivity. Histological tests had shown two types of injurie: the myxoid degeneration (7 times on 8 valves) cryopreserved and a coagulative necrosis whose distribution was identical forthe two modes of conservation. Antibiotic's solution seemed to induce these injuries as do heart ischemia, and the traumatism lihleed to the great cold. The tests of sterility had shown a rate of contamination to 25 % essentially by Pseudomonas. In view of the installation of a behle of allograft bank of quality, we'll need to improve conditions of leavy, to use a freezer adaptation for progressive cryocongelation and the choice of simple method to evaluate valvular viabilty.
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PMID:[Feasability of a heart valve bank in Dakar. (Preliminary study of 8 human hearts)]. 1577 50

War wounds are the most complex type of non-targeted injuries due to uncontrolled tissue damage of varied and multifold localizations, exposing sterile body areas to contamination with a huge amount of bacteria. Wound contamination is caused by both the host microflora and exogenous agents from the environment (bullets, cloth fragments, dust, dirt, water) due to destruction of the host protective barriers. War wounds are the consequence of destructive effects of various types of projectiles, which result in massive tissue devitalization, hematomas, and compromised circulation with tissue ischemia or anoxia. This environment is highly favorable for proliferation of bacteria and their invasion in the surrounding tissue over a relatively short period of time. War wounds are associated with a high risk of local and systemic infection. The infection will develop unless a timely combined treatment is undertaken, including surgical intervention within 6 hours of wounding and antibiotic therapy administered immediately or at latest in 3 hours of wound infliction. Time is a crucial factor in this type of targeted combined treatment consisting of surgical debridement, appropriate empirical antimicrobial therapy, and specific antitetanic prophylaxis. Apart from exposure factors, there are a number of predisposing factors that favor the development of polymicrobial aerobic-anaerobic infection. These are shock, pain, blood loss, hypoxia, hematomas, type and amount of traumatized tissue, age, and comorbidity factors in the wounded. The determinants that define the spectrum of etiologic agents in contaminated war wounds are: wound type, body region involved, time interval between wounding and primary surgical treatment, climate factors, season, geographical area, hygienic conditions, and patient habits. The etiologic agents of infection include gram-positive aerobic cocci, i. e. Staphylococcus spp, Streptococcus spp and Enterococcus spp, which belong to the physiological flora of the human skin and mucosa; gram-negative facultative aerobic rods; members of the family Enterobacteriacea (Escherichia coil, Proteus mirabilis, Klebsiella pneumoniae, Enterobacter cloacae), which predominate in the physiological flora of the intestines, transitory flora of the skin and environment; gram-negative bacteria, i. e. Pseudomonas aeruginosa, Serratia marcescens, Acinetobacter calcoaceticus - A. baumanii complex; environmental bacteria associated with humid environment and dust; anaerobic gram-positive sporogeneous rods Clostridium spp, gram-negative asporogeneous rods Bacteroides spp and gram-positive anaerobic cocci; Peptostreptococcus spp and Peptococcus spp. The latter usually colonize the intestine, primarily the colon, and the skin, while clostridium spores are also found in the environment. Early empirical antibiotic therapy is used instead of standard antibiotic prophylaxis. Empirical antimicrobial therapy is administered to prevent the development of systemic infection, gas gangrene, necrotizing infection of soft tissue, intoxication and death. The choice of antibiotics is determined by the presumed infective agents and localization of the wound. It is used in all types of war wounds over 5-7-10 days. The characteristics of antibiotics used in war wounds are the following: broad spectrum of activity, ability to penetrate deep into the tissue, low toxicity, long half-life, easy storage and application, and cost effectiveness. The use of antibiotics is not a substitution for surgical treatment. The expected incidence of infection, according to literature data, is 35%-40%. If the time elapsed until surgical debridement exceeds 12 hours, or the administration of antibiotics exceeds 6 hours of wound infliction, primary infection of the war wound occurs (early infection) in more than 50% of cases. The keys for the prevention of infection are prompt and thorough surgical exploration of the wound, administration of antibiotics and antitetanic prophylaxis, awareness of the probable pathogens with respect to localization of the wound, and optimal choice of antibiotics and length of their administration.
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PMID:[Characteristics of war wound infection]. 1704 90

There is now substantial evidence that compounds released during host stress directly activate the virulence of certain opportunistic pathogens. Here, we considered that endogenous opioids might function as such compounds, given that they are among the first signals to be released at multiple tissue sites during host stress. We tested the ability of various opioid compounds to enhance the virulence of Pseudomonas aeruginosa using pyocyanin production as a biological readout, and demonstrated enhanced virulence when P. aeruginosa was exposed to synthetic (U-50,488) and endogenous (dynorphin) kappa-agonists. Using various mutants and reporter strains of P. aeruginosa, we identified involvement of key elements of the quorum sensing circuitry such as the global transcriptional regulator MvfR and the quorum sensing-related quinolone signaling molecules PQS, HHQ, and HQNO that respond to kappa-opioids. The in vivo significance of kappa-opioid signaling of P. aeruginosa was demonstrated in mice by showing that dynorphin is released from the intestinal mucosa following ischemia/reperfusion injury, activates quinolone signaling in P. aeruginosa, and enhances the virulence of P. aeruginosa against Lactobacillus spp. and Caenorhabditis elegans. Taken together, these data demonstrate that P. aeruginosa can intercept opioid compounds released during host stress and integrate them into core elements of quorum sensing circuitry leading to enhanced virulence.
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PMID:Dynorphin activates quorum sensing quinolone signaling in Pseudomonas aeruginosa. 1736 9

Kynurenine 3-monooxygenase (KMO) is a flavin-dependent hydroxylase that catalyzes the conversion of l-kynurenine (l-Kyn) to 3-hydroxykynurenine (3OHKyn) in the pathway for tryptophan catabolism. KMO inhibition has been widely suggested as an early treatment for stroke and other neurological disorders that involve ischemia. We have investigated the reductive and the oxidative half-reactions of a stable form of KMO from Pseudomonas fluorescens (KMO). The binding of l-Kyn by the enzyme is relatively slow and involves at least two reversible steps. The rate constant for reduction of the flavin cofactor by NADPH increases by a factor of approximately 2.5 x 10(3) when l-Kyn is bound. The rate of reduction of the KMO.l-Kyn complex is 160 s(-1), and the K(d) for the NADPH complex is 200 microM with charge-transfer absorption bands for the KMO(RED).l-Kyn.NADP(+) complex accumulating after reduction. The reduction potential of KMO is -188 mV and is unresponsive to the addition of l-Kyn or other inhibitory ligands. KMO inhibitors whose structures are reminiscent of l-Kyn such as m-nitrobenzoylalanine and benzoylalanine also stimulate reduction of flavin by NADPH and, in the presence of dioxygen, result in the stoichiometric liberation of hydrogen peroxide, diminishing the perceived therapeutic potential of inhibitors of this type. In the presence of the native substrate, the oxidative half-reaction exhibits triphasic absorbance data. A spectrum consistent with that of a peroxyflavin species accumulates and then decays to yield the oxidized enzyme. This species then undergoes minor spectral changes that, based on flavin difference spectra defined in the presence of 3OHKyn, can be correlated with product release. The oxidative half-reaction observed in the presence of saturating benzoylalanine or m-nitrobenzoylalanine also shows the accumulation of a peroxyflavin species that then decays to yield hydrogen peroxide without hydroxylation.
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PMID:Kynurenine 3-monooxygenase from Pseudomonas fluorescens: substrate-like inhibitors both stimulate flavin reduction and stabilize the flavin-peroxo intermediate yet result in the production of hydrogen peroxide. 1895 92

In eukaryotes, small amounts of nitrite confer cytoprotection against ischemia/reperfusion-related tissue damage in vivo, possibly via reduction to nitric oxide (NO) and inhibition of mitochondrial function. Several hemeproteins are involved in this protective mechanism, starting with deoxyhemoglobin, which is capable of reducing nitrite. In facultative aerobic bacteria, such as Pseudomonas aeruginosa, nitrite is reduced to NO by specialized heme-containing enzymes called cd(1) nitrite reductases. The details of their catalytic mechanism are summarized below, together with a hypothesis on the biological role of the unusual d(1)-heme, which, in the reduced state, shows unique properties (very high affinity for nitrite and exceptionally fast dissociation of NO). Our results support the idea that the nitrite-based reactions of contemporary eukaryotes are a vestige of earlier bacterial biochemical pathways. The evidence that nitrite reductase activities of enzymes with different cellular roles and biochemical features still exist today highlights the importance of nitrite in cellular homeostasis.
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PMID:Nitrite reduction: a ubiquitous function from a pre-aerobic past. 1955 8

Acute appendicitis is the most frequent emergency in gastrointestinal surgery. Obstruction of the appendiceal lumen appears to be one of the most common physiologic mechanisms for the development of acute appendicitis. Once obstructed, the dilatation of the lumen causes ischemia and necrosis of the wall. The most common organisms involved in appendicitis are Escherichia coli, Peptostreptococcus, Bacillus fragilis and Pseudomonas. Rarely, Actinomyces is involved in this process. In this case report, we report a case of actinomycosis of the appendix vermiformis occurring in a 19-year-old male with no predisposing factors. Along with a review of the literature, we will define the risk factors, clinical characteristics, diagnostic methods, and treatment of actinomycosis.
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PMID:Appendicitis: When there is more than meets the eye. 2176 32

Hydrogen sulfide (H2S), an endogenously produced small molecule, protects animals from various stresses. Recent studies demonstrate that animals exposed to H2S are long lived, resistant to hypoxia, and resistant to ischemia-reperfusion injury. We performed a forward genetic screen to gain insights into the molecular mechanisms Caenorhabditis elegans uses to appropriately respond to H2S. At least two distinct pathways appear to be important for this response, including the H2S-oxidation pathway and the hydrogen cyanide (HCN)-assimilation pathway. The H2S-oxidation pathway requires two distinct enzymes important for the oxidation of H2S: the sulfide:quinone reductase sqrd-1 and the dioxygenase ethe-1. The HCN-assimilation pathway requires the cysteine synthase homologs cysl-1 and cysl-2. A low dose of either H2S or HCN can activate hypoxia-inducible factor 1 (HIF-1), which is required for C. elegans to respond to either gas. sqrd-1 and cysl-2 represent the entry points in the H2S-oxidation and HCN-assimilation pathways, respectively, and expression of both of these enzymes is highly induced by HIF-1 in response to both H2S and HCN. In addition to their role in appropriately responding to H2S and HCN, we found that cysl-1 and cysl-2 are both essential mediators of innate immunity against fast paralytic killing by Pseudomonas. Furthermore, in agreement with these data, we showed that growing worms in the presence of H2S is sufficient to confer resistance to Pseudomonas fast paralytic killing. Our results suggest the hypoxia-independent hif-1 response in C. elegans evolved to respond to the naturally occurring small molecules H2S and HCN.
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PMID:The response of Caenorhabditis elegans to hydrogen sulfide and hydrogen cyanide. 2184 Aug 52

When mice are subjected to a Pseudomonas aeruginosa challenge 5 days after cecal ligation and puncture (CLP), clearance of the Pseudomonas is diminished when compared to sham mice. The object of this study was to determine which component(s) of CLP contributed to the impairment of the innate immune response. Mice subjected to either trauma alone or cecal ischemia/necrosis alone did not have impaired ability to clear a subsequent Pseudomonas challenge (determined by colony-forming units (cfu's) after culture of spleen tissue). However, mice subjected to abdominal contamination with heat-killed cecal contents had reduced ability to clear the subsequent Pseudomonas challenge. In contrast to normobiotic mice, neither CLP performed in germ-free mice nor abdominal contamination of mice with cecal contents from germ-free mice adversely affected clearance of a subsequent Pseudomonas challenge. These data suggest that suppressed immune function after CLP is due to exposure to microbial ligands within the cecal lumen rather than tissue trauma, ischemia, or necrosis. However, suppression of immune function did not appear to be due to exposure to LPS as TLR4-deficient mice subject to abdominal contamination with cecal contents had diminished clearance of a Pseudomonas challenge similar to that seen in wild-type mice.
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PMID:CLP-induced impairment of innate immune function is caused by exposure to the cecal lumenal contents and not the tissue trauma or tissue ischemia/necrosis components. 2190 19

Eyelid necrosis is a very rare disease, usually secondary to trauma or infections. Pseudomonas aeruginosa (PA) eyelid necrosis remains principally a clinical diagnosis and it is often missed early in its presentation because of the difficulty in differentiating it from more common soft tissue infections. However, when the diagnosis is made we must act quickly due to the fatal evolution if not handled properly. We present the case of a non-neutropenic 53-year-old male patient with a history of alcoholism, smoking habit and lung cancer under chemotherapy treatment who developed ocular necrotizing fasciitis due to PA with perforation of his left eye and severe bilateral sclera ischemia despite intensive antibiotic treatment and surgical debridement.
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PMID:Ocular necrotizing fasciitis due to Pseudomonas aeruginosa in a non-neutropenic patient. 2437 25

Infections have been commonly implicated in lupus relapses and in some cases as initiating the diagnostic work up of systemic lupus erythematosus (SLE). We describe here the case of a young patient who presented with Pseudomonas aeruginosa bacteremia and was found to have a new diagnosis of SLE. 53% of patients with active SLE and abdominal pain have intestinal vasculitis. These vasculitic changes can cause intestinal ischemia with consequent translocation of pathogens from the gastrointestinal tract to the bloodstream causing sepsis.
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PMID:Pseudomonas bacteremia as an initial presentation of SLE. 2683 77


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