Hemorrhagic shock is a clinical syndrome involving widespread cellular dysfunction and resulting in injury to many organs. Resuscitation from hemorrhagic shock is similar to reperfusion after ischemia, but differs in that some blood flow persists during shock. Ischemia-reperfusion produces oxygen radicals in many organs, including the liver of the rat and the human. The hypothesis of this project was that oxygen radicals are produced and cause hepatic injury during resuscitation from hemorrhagic shock. The production of oxygen radicals within the liver should cause lipid peroxidation and tissue injury. Manipulation of defenses against oxygen radicals should decrease the hepatic injury caused by hemorrhagic shock and resuscitation. The blood pressure of Sprague-Dawley rats was reduced to 35-40 mm Hg by blood withdrawal for two hours, followed by reinfusion of withdrawn blood. Plasma alanine aminotransferase (ALT) levels rose and injury to hepatocytes and non-parenchymal cells was found on transmission electron microscopy. The presence of lipid peroxidation was determined by quantitation of ethane exhalation and hepatic content of thiobarbituric acid reactive substances (TBARS). Ethane exhalation was elevated during the hypotensive phase and after resuscitation. Hepatic TBARS levels were elevated after resuscitation only. The same hemorrhagic shock protocol was used to determine the effect of antioxidant manipulation on hepatic injury. The antioxidants superoxide dismutase, catalase, or deferoxamine produced no reduction in hepatic injury. The administration of phorone reduced hepatic non-protein sulfhydryl content and increased plasma ALT levels nine fold at 24 hours after resuscitation. The development of lipid peroxidation and the exacerbation of liver injury by the administration of phorone suggest that oxygen radicals are produced in the liver during hemorrhagic shock and resuscitation. However, the administration of antioxidants provided no protection. Therefore, it seems unlikely the oxygen radicals are involved in the pathogenesis of liver injury in this model. It is possible that the lipid peroxidation occurs after the cell is irreversible injured.

Class of 2010 Abstract / OBJECTIVES: The purpose of this study was to demonstrate that an increase in INR is associated with a hemorrhagic event in patients taking the oral anticoagulant warfarin. METHODS: A retrospective review of data from 18 patients previously stable on warfarin therapy with an elevation in INR at the time of a hemorrhagic event. Patients were receiving warfarin treatment in the anticoagulation clinic at the Southern Arizona VA Healthcare system from April 2008 to December 2009. Primary outcome measures included a comparison of INR, warfarin dose, and hematocrit at baseline, within 7 days of the event, and during follow-­‐up. RESULTS: A significant increase in INR was observed from baseline to the event (2.5 +/-­‐ 0.36 vs 6.2 +/-­‐ 3.2; p = 0.0002) but differences in INR during all periods of follow-­‐up did not differ from baseline (p = 0.35 – 0.99). When compared with baseline, differences in warfarin dose reached statistical significance when all 12 weeks of follow-­‐up were included (34.4 +/-­‐ 13.8 mg vs 32.4+/-­‐ 15.5 mg; p = 0.01) but were not significant when only the last 8 weeks (p = 0.06) or 4 weeks (p = 0.16) were included. Hematocrit values decreased significantly following hemorrhage (39.8 +/-­‐ 3.63 vs 33.5 +/-­‐ 5.72; p = 0.0002) before trending toward baseline (39.85 +/-­‐ 3.63 vs 37.13 +/-­‐ 4.72; p = 0.007). CONCLUSIONS: Hemorrhagic events were associated with an increased INR in previously stable warfarin patients. The mean weekly warfarin dose required to maintain a therapeutic INR returned to baseline within 8 weeks of the hemorrhagic event.

A dissertation submitted to the Faculty of Health Sciences University of the Witwatersrand, Johannesburg for the degree of Master of Science. / The Special Pathogens Unit (SPU) of the National Institute for Virology has diagnosed a total of 158 cases of Crimean-Congo haemorrhagic fever (CCHF) from the time that the disease was first recognized in South Africa in 1981 up until the end of 2000. The virus has a propensity to cause nosocomial infections, and consequently rapid diagnosis is important for the isolation of the patient and the institution of barrier-nursing to protect medical staff and the community at large. Thus it is essential that the SPU should have the latest diagnostic and research tools available. Diagnosis of CCHF is generally confirmed by isolation of the virus, detection of viral RNA amplified by reverse transcriptase polymerase chain reaction (RT-PCR), demonstration of seroconversion or a >4-fold increase in IgG antibody titre, or detection of specific IgM antibody activity. Virus can be isolated in 1-6 days in cell culture, but the method is less sensitive for the isolation of low concentrations of virus than the use of suckling mice which, however, takes 7-9 days.

archives@tulane.edu / 1 / Angela Crist

The Ebola viruses cause sporadic outbreaks of Ebola hemorrhagic fever (EHF) where origins have been traced to the continent of Africa and the Philippines. Since the initial discovery of Zaire and Sudan ebolavirus in 1976, the Ebola viruses have been responsible for severe hemorrhagic fever outbreaks in Africa with case fatality rates between 40-90%. The natural reservoir(s) of the Ebola viruses is currently unknown, but there is mounting evidence that fruit bats may play a key role. The goal of the current study is to screen a large variety of bat species from Africa and Asia where Ebola is known to be endemic for the presence of IgG specific antibody to Ebola virus in order to see which bat species may show evidence of past Ebola virus infection. Ebola virus would not be expected to cause lethal disease in its natural reservoir; therefore the presence of IgG antibody would be present. Identifying the species of bats that have been infected will allow researchers to hopefully isolate Ebola virus from bats adding to the evidence that bats are a reservoir species. The knowledge gained may also provide clues to new species of bats yet to be identified as possible natural reservoir(s) as well as expand the known geographical range of known Ebola virus outbreaks. Knowing which species of bats as well as their geographic range may help prevent future Ebola outbreaks by minimizing human-reservoir contact.

No description available.

Thesis (M.S.)--University of Wisconsin--Madison, 1982. / Typescript. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Made available in DSpace on 2014-06-11T19:30:29Z (GMT). No. of bitstreams: 0 Previous issue date: 2008-12-19Bitstream added on 2014-06-13T20:00:44Z : No. of bitstreams: 1 silva_ae_dr_botfm.pdf: 677283 bytes, checksum: 81300198b62fe55885f8b966cdd716bf (MD5) / Os anestésicos inalatórios halogenados podem apresentar papel importante na patogênese das alterações cardiocirculatórias e renais durante o choque hemorrágico por alterarem, de maneira dose dependente, os mecanismos de defesa compensatórios. O presente estudo teve como objetivo comparar os efeitos de uma concentração alveolar mínima (CAM) de halotano, sevoflurano e isoflurano sobre o sistema cardiovascular e renal em cães submetidos a choque hemorrágico e reposição volêmica com o sangue retirado do animal. O estudo aleatório foi realizado em trinta cães, sem raça definida, distribuídos em três grupos de acordo com o anestésico inalatório halogenado utilizado durante a anestesia, em concentrações eqüipotentes de uma CAM: GH (n=10) - halotano a 0,89%; GS (n=10) - sevoflurano a 2,4%; e GI (n=10) - isoflurano a 1,4%. Todos os cães foram ventilados mecânicamente, esplenectomizados e submetidos a sangramento, com retirada em torno de 40% do volume sangüíneo, visando manter a pressão arterial média de 40 a 50 mm Hg durante 45 minutos. A seguir, os cães foram submetidos à expansão volêmica com o sangue removido. Os atributos hemodinâmicos foram determinados no momento controle, após 45 minutos de hemorragia, e 15 e 60 minutos após a reposição sangüínea. Os atributos renais foram medidos nos mesmos momentos, exceto no período hemorrágico, pela ausência de diurese. No momento controle, a maioria das variáveis hemodinâmicas e renais foram semelhantes entre os grupos, com exceção da fração de filtração, cujos valores foram menores no grupo GI, em relação aos grupos GH e GS (p < 0,05), e da osmolalidade urinária, cujos valores foram maiores no grupo GS, em comparação com o grupo GH (p < 0,05). Após a hemorragia... / Halogenated anesthetics may play an important role in the pathogenesis of cardiovascular and renal changes during hemorrhagic shock because they modify, in a dose-dependent manner, compensatory defense mechanisms. The aim of the present study was to compare the effects of a minimum alveolar concentration (MAC) of halothane, sevoflurane and isoflurane on the cardiovascular and renal systems of dogs subjected to hemorrhagic shock followed by restoration of blood volume with shed blood. Thirty mongrel dogs were randomly distributed into three groups according to the halogenated anesthetic used for anesthesia. They were anesthetized with halothane (H group; n=10), sevoflurane (S group; n=10) or isoflurane (I group; n=10) and anesthesia was maintained at 1.0 MAC: 0.89%, 2.4%, and 1.4%, respectively. All the dogs were mechanically ventilated, splenectomized and subjected to bleeding with 40% blood reduction to keep mean arterial pressure between 40 and 50 mm Hg for 45 min. Thereafter, the dogs were resuscitated with shed blood. The hemodynamic attributes were determined at the control moment, after 45 min of hemorrhage, 15 and 60 min after restoration of blood volume. The renal attributes were determined at the described moments, except during the hemorrhage period, for lack of diuresis. At the control moment, most of the hemodynamic and renal variables were similar among the groups, except for the filtered fraction, Introdução e Literatura 11 which was lower in GI than in groups GH and GS (p < 0.05), and for urinary osmolarity, which was higher in GS compared to GH (p < 0.05). After hemorrhage, the hemodynamic attributes decreased, without significant differences among the groups (p > 0.05). Fifteen minutes after resuscitation, most of the hemodynamic and renal attributes were... (Complete abstract click electronic access below)

Bone circulation in Hemorrhagic Shock was studied in 35 male mongrel dogs. The term hemorrhagic shock is defined in this thesis as persistent profound hypotensive syndrome, due to acute hemorrhage of more than one third of blood volume. The method of induction of shock consisted of removal of one third of estimated blood volume (8% of body weight) at a rate of 25 - 50 ml/min, and subsequently dropping the systemic blood pressure in a stepwise manner until the maintaining level of 30 - 35 mmHg is reached. The central venous pressure, pulse and respiratory rates were also recorded. Bone circulation was studied by (1) recording the blood flow through a cannula inserted into the tibial nutrient vein or artery and (2) recording the intramedullary pressure of tibia. When one third of estimated blood volume was removed, the bone blood flow through the nutrient vessel decreased to 22.5 ± 3.4% of control level. The decreased bone blood flow persisted as long as the hemorrhagic shock was maintained for 4-18 hours. The decreased bone blood flow was also evidenced by a profound and persistent fall of the intramedullary pressure of bone. Reinfusion into the animal of lost blood within fifteen minutes to six hours after hemorrhage resulted in a complete or partial recovery of the control systemic blood pressure as well as the control rate of bone blood flow and the control level of intramedullary pressure of bone. The curve showing relationship between the changes in bone blood flow and the systemic blood pressure is an exponential one with concavity towards the flow axis. This indicates that bone has a vasomotor control mechanism of increasing peripheral resistance during hemorrhagic shock. This was substantiated by the following observations: (1) The severity of decrease in bone blood flow on the side of lumbar sympathectomy was much milder (16% less) compared to the side of the intact sympathetic nerve; (2) Dibenzyline (phenoxybenzamine) a sympatholytic drug or alpha-receptor blocking agent alters the pressure-flow curve of bone circulation in chock to a linear pattern which indicates that the drug blocks the bone vasoconstricting mechanism(s). It is concluded that bone blood flow decreases in hemorrhagic shock and is not merely due to a decrease in circulatory blood volume, but also due to sympathetic and catecholamine hormonal vasoconstrictor mechanisms. / Surgery, Department of / Medicine, Faculty of / Graduate

By specifically analysing for the various active principles of plasma, platelets, tissues and their fractions, much new information has been obtained concerning the role of lipoids and platelets in blood coagulation and in the hemostatic mechanisms in health and disease. Analysed components are studied in artificial clotting systems, especially a two-stage thrombin- forming system. Some 86 cases of bleeding disorders, 32 new born normal infants and their mothers, and many normal adult bloods have been analysed with respect to components of the clotting and hemostatic functions. The detailed considerations embodied in the thesis are encompassed under the following heads: 1) the importance of certain lipoids, especially cephalin 2) the normal need, in plasma clotting, for platelets, 3) the particular significance of a platelet component, which has many analogies to cephalin, in the thromboplastic system, 4) potentiation of the thromboplastic actions of cephalin, of platelets, and of tissue thromboplastin (to some extent) by a variety of experimental additives. Part of this may be explained as a 'thromboplastin generation' through co-participation of certain plasmatic components (antihemophilic globulin, PTC" etc. ) . Part, however, may be the result of certain proteolytic enzymes, particularly trypsin, 'disaggregating' lipoproteins and thus rendering their phospholipid (and sometimes calcium) available for participation in the clotting reactions, 5) possible Ca-containing and lipid-containing 'intermediates’ in the thrombin-forming reactions, 6) myelin figure formation as an explanation of ‘alterations' of platelets and certain other formed elements such as thrombocytes, megakaryocytes, and stromatolytic erythrocytes 7) the multiplicity of factors which platelets may contribute to the blood clotting and hemostatic mechanisms 8) the occurrence of many clinical disorders due to deficiency of platelet functions. Thrombocytopenias denote deficient numbers ('counts' and total bulk in body). Thrombocytopathies are deficiencies of specific platelet components, e . g. thromboplastic factor, accelerator, vasoconstrictor (5-hydroxy tryptamine), or retractor factor. Such deficiencies can be clinically significant even when the platelet count is normal. Bleeding in leukaemias, uremias, etc. may often be accounted for in these terms, 9) the nature and modes of action of heparin and other 'antithromboplastic’ inhibitors, and of some antiproteases, in relation to the mechanisms discussed 10) the ‘cephalin availability theory' of the author, as a useful working hypothesis to explain the importance of the natural thromboplastic phospholipid. Lipid release from platelet, tissue, or possibly plasma sources may very well be the long-obscure 'trigger mechanism' which initiates blood coagulation.