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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Intensive care medicine 23 (1997), S. 379-385 
    ISSN: 1432-1238
    Keywords: Key words Platelet ; Sepsis ; Multiple organ dysfunction syndrome ; Glycoproteins ; Aggregation ; Adhesion ; Endothelium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objective: Altered platelet function plays a role in the pathophysiology of multiple organ failure in sepsis. The purpose of the present study was to evaluate various aspects of platelet adhesive function in septic patients and its putative relevance for prognosis. Design: Prospective clinical study. Setting: Intensive Care Unit of the University Hospital. Patients and methods: A total of 41 patients admitted to the medical Intensive Care Unit were studied. On the day of admission, patients were evaluated by intensive care scoring systems (Elebute, APACHE II) to assess the severity of sepsis and multiple organ dysfunction syndrome (MODS), and platelet function tests were performed. All patients were observed for 28 days to assess their clinical outcomes. Eleven patients revealed septicemia without MODS (Elebute ≥12, APACHE II 〈20) and 20 septic patients suffered from MODS (Elebute ≥12, APACHE II ≥20). Ten non-septic patients without MODS served as a control group (Elebute 〈12, APACHE II 〈20). Flow cytometric determination of the activated fibrinogen (fg) receptor GPIIb-IIIa and as well as thrombospondin (TSP) on platelets and platelet-neutrophil adhesion (CD41 immunofluorescence) ex vivo was performed using monoclonal antibodies. The effect of plasma obtained from patients on normal platelet aggregation in vitro, and adhesion to cultured endothelial cells was evaluated. Results: The surface expression of TSP on platelets was increased in septic patients with MODS compared to controls (p〈0.03). Platelet-neutrophil adhesion was not significantly altered in septicemia (p〈0.09) but decreased significantly in the presence of MODS (p〈0.05) when compared to controls. Logistic regression analysis showed that platelet-neutrophil adhesion was an independent predictor for poor clinical outcome (p〈0.01). Plasma from septic patients sensitized normal platelets to hyperaggregate and to adhere to cultured endothelium (p〈0.01). Conclusion: In septic patients platelets become activated and are hyperadhesive to other vascular cells including neutrophils and endothelium. This may induce sequestration of platelets and microcirculatory arrest, thus the development of MODS.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    European journal of clinical pharmacology 39 (1990), S. S9 
    ISSN: 1432-1041
    Keywords: Cardiac microcirculation ; left ventricular hypertrophy ; myocardial ischemia ; stunned myocardium ; leukocytes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary I. Myocardial hypertrophy, for instance in patients with hypertensive heart disease, is characterized by a reduction of coronary vascular reserve, even in the presence of normal coronary arteries. In hypertensive animals, on the microcirculatory level functional changes can be observed before the onset of any structural rarefications. In 10 rats with renal hypertension and pressure-induced left ventricular hypertrophy (LVH), the microcirulation of the left ventricular myocardium was studied using in vivo fluorescence microscopy and morphometric analysis. Renal hypertension was provoked by clipping of the left renal artery. After 8 weeks, systolic blood pressure in LVH rats averaged 172 ± 8 mm Hg, compared to 91 ± 2 mmHg in 10 normotensive (NT) rats. In LVH rats, distances of plasma-perfused capillaries were significantly increased (NT = 17.7; LVH = 20 μm;p 〈 0.001). Volume density, surface density, and length density of capillaries in LVH rats were reduced by 20% compared to NT rats. Capillary red cell content as measured by the ratio of capillaries filled with red cells to those containing plasma alone (Q) in LVH animals exceeded that in NT rats (LVH: Q = 0.83 ± 0.04; NT Q = 0.77 ± 0.04;p 〈 0.025). During hypoxia (H, 5% 02) capillary red cell recruitment in LVH rats (Q: control c = 0.83; H = 0.95) was diminished by 33% as compared to NT rats (Q: c = 0.77; H = 0.95). Thus, in addition to the decreased capillary density, the reduction of capillary red cell recruitment may be responsible for chest pain in patients with LVH and normal coronary arteries. 2. In 11 rats, the microcirculation of the repeatedly ischemic (stunned) left ventricular myocardium (SM) was studied using in vivo fluorescence microscopy. Stunning was provoked by 6 subsequent 10 minute ligations of the left anterior descending coronary artery, each of them followed by a 20 min reperfusion period. In the SM showing hypokinetic wall motion mean capillary blood flow velocity was markedly reduced (control c =1312; SM = 694 μm/sec;p 〈 0.001): myocardial blood flow (hydrogen clearance) in the SM dropped by 55%. In SM, leukocytes often appeared in slow-flow capillaries plugging capillary branches: the percentage of capillaries and postcapillary venules with adherent leukocytes was markedly increased (c = 3%; SM = 68%). In close link to leukocyte adherence, a rise of microvascular permeability was documented by extravascular clouds of fluorescent dextran. The ratio of capillaries filled with red cells to those containing plasma alone was diminished in SM (c = 0.77; SM = 0.65;p 〈 0.001). In the SM there are microcirculatory disturbances which occur before the onset of detectable structural alterations of both the microvasculature and the myocyte.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1435-1803
    Keywords: Angioplasty ; catecholamines ; epinephrine ; norepinephrine ; myocardial ischemia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract This study investigated arterial and coronary venous catecholamine concentrations in patients undergoing either elective coronary angioplasty (PTCA) or direct PTCA for acute myocardial infarction. We included 17 patients with stenoses of the left anterior descending coronary artery (LAD) and 10 patients with acute anterior myocardial infarction (AMI) undergoing PTCA. During the initial balloon dilatation arterial and coronary venous plasma concentrations of norepinephrine and epinephrine were determined. In elective PTCA, coronary occlusion (2 min) resulted in a transient increase of arterial concentrations of norepinephrine (2.04±0.30 vs. 1.26±0.13 nmol/L before dilatation) and epinephrine (0.52±0.08 vs. 0.34±0.04 nmol/L) in the first minute of reperfusion, whereas coronary venous concentrations of catecholamines were not changed after dilation. Among the 10 patients with AMI, immediate reperfusion of the LAD (TIMI grade 3) was achieved in 6 patients. In these patients, baseline arterial concentrations for norepinephrine (3.91±1.16 nmol/L) and epinephrine (4.68±2.07 nmol/L) were elevated and no transcardiac gradient for catecholamines was found. In the first minute after successful reopening of the LAD we detected a distinct rise of the transcardiac norepinephrine gradient from −0.10±0.53 to 85.02±24.64 nmol/L, which declined in the fifth minute of reperfusion to 4.36±2.30 nmol/L. Conversely, venous epinephrine and arterial concentrations for both catecholamines remained unchanged within the observation period. In the four patients with incomplete (TIMI 0–2) reopening of the LAD, we found no cardiac washout of norepine phrine. In summary, a transient rise of systemic catecholamines, but no cardiac release of norepinephrine was observed in patients after brief coronary occlusion. Conversely, a massive washout of norepinephrine from the infarcted myocardium occurred during AMI.
    Type of Medium: Electronic Resource
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