A new method of measuring intracellular Na and K using Li substitution was applied to a study of vascular smooth muscle and red cell Na changes in haemorrhagic shock. A rat haemorrhagic shock model was used. Controlled haemorrhage was allowed with a syringe reservoir and the arterial blood pressure was maintained at 30 mm Hg. In a pilot study, using 20 rats, the plasma Na and plasma K were monitored. A fall in plasma Na and a rise in plasma K were observed. Both returned towards normal following retransfusion and recovery for one hour. In vascular smooth muscle, significant changes in both cell Na and K occurred following a 2 hour period of haemorrhagic shock. The vascular smooth muscle cell Na in control animals was 27.0±1.5 mEq/kg dry weight and 42.7±1.4 mEq/kg dry weight in the shocked animals (P<0.001). The cell K was 127.8±6.0 in the control animals and 74.7±4.2 in the shocked animals. In red cell studies, significant increases in red cell Na were found. The red cell Na in controls was 7.09±0.29 mEq/litre cells, whilst in the shocked animals the red cell Na was 8.26±0.33 mEq/litre cells (P<0.025). This was associated with a small but not statistically significant fall in red cell K. In both sets of experiments, the plasma Na and K were monitored and similar changes to those of the pilot study were found. Following retransfusion and recovery for 1 hour in the vascular tissue study and 2 hours in the red cell study, no significant recovery of cellular Na or K occurred. The results of these studies are consistent with a significant impairment of cell membrane function in haemorrhagic shock. The importance of both normal vascular responses and red cell function following severe haemorrhage is obvious. The fact that both may be impaired may have important implications in relation to the treatment and prognosis of haemorrhagic shock. / Medicine, Faculty of / Cellular and Physiological Sciences, Department of / Graduate

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Thesis (M.S.)--Wisconsin. / Includes bibliographical references (leaves 79-82).

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A thesis submitted to the Faculty of Health Sciences University of the Witwatersrand. Johannesburg for the degree of Doctor of Philosophy Johannesburg 1997 / a) to develop sensitive tests for the early diagnosis of Crimean-Congo haemorrhagic fever {( '( "II;) infection or humans. based on the detection of viral nucleic add and antibody in serum: [Abbreviated Abstract. Open document to view full version] / MT2017

T V Gale

Acute Respiratory Distress Syndrome is a late cause of morbidity and mortality following hemorrhagic shock and resuscitation. Previous work in our laboratory showed that alveolar macrophages were primed for increased responsiveness to lipopolysaccharides, as evidenced by augmented inflammatory cytokine production. Recent studies have shown that macrophages can be polarized into two phenotypes, namely pro-inflammatory M1 and anti-inflammatory M2 macrophages, in response to various environmental cues. The major hypothesis to be tested in this thesis is that HS/R shifts the M1/M2 polarization of alveolar macrophages to favour a pro-inflammatory milieu in the lung. A biphasic shift in the phenotype of alveolar macrophages in response to HS/R characterized by an early reduction of M2 cells followed by a late up-regulation of M1 macrophages was observed. The administration of M2- polarizing PPAR&gamma; agonists prior to HS/R restored the M1/M2 balance of alveolar macrophages and reduced lung injury.

Acute Respiratory Distress Syndrome is a late cause of morbidity and mortality following hemorrhagic shock and resuscitation. Previous work in our laboratory showed that alveolar macrophages were primed for increased responsiveness to lipopolysaccharides, as evidenced by augmented inflammatory cytokine production. Recent studies have shown that macrophages can be polarized into two phenotypes, namely pro-inflammatory M1 and anti-inflammatory M2 macrophages, in response to various environmental cues. The major hypothesis to be tested in this thesis is that HS/R shifts the M1/M2 polarization of alveolar macrophages to favour a pro-inflammatory milieu in the lung. A biphasic shift in the phenotype of alveolar macrophages in response to HS/R characterized by an early reduction of M2 cells followed by a late up-regulation of M1 macrophages was observed. The administration of M2- polarizing PPAR&gamma; agonists prior to HS/R restored the M1/M2 balance of alveolar macrophages and reduced lung injury.

Thesis (M.S.)--University of Wyoming, 2007. / Title from PDF title page (viewed on Nov. 4, 2008). Includes bibliographical references (p. 63-68).

Dengue virus infection affects the heart structurally and functionally. Clinical manifestations of cardiac complications secondary to dengue virus infection vary from self-limiting arrhythmias to severe myocardial infarction, leading to hypotension, pulmonary edema, and cardiogenic shock. However, we report a case of dengue hemorrhagic fever (DHF) complicated by a complete heart block. A female with DHF due to dengue virus serotype 2, presented to the emergency department with fever, headache, rash, and fatigue followed by an episode of syncope. She was found to have a third-degree atrioventricular block, with pulseless polymorphic ventricular tachycardia. Patient was resuscitated and a temporary trans-venous pacemaker was placed. She reverted back to normal sinus rhythm after 4 days of syncope and was subsequently discharged from the hospital after complete resolution of symptoms, without the need for a permanent pacemaker. Physicians are warranted to have high index of suspicion for dengue virus infection as an etiology in patients with acute cardiovascular compromise, especially in tropical areas.