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- Sandstedt, Bengt, 1951-, et al.
(författare)
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Genuine effects of ventricular fibrillation upon myocardial blood flow, metabolism and catecholamines in patients with aortic stenosis.
- 2004
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Ingår i: Scandinavian cardiovascular journal : SCJ. - 1401-7431. ; 38:2, s. 113-20
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Tidskriftsartikel (refereegranskat)abstract
- Objective-Ventricular fibrillation (VF) is life-threatening because of its haemodynamic and metabolic effects. The purpose was to examine if VF also has primary effects per se. We therefore investigated the early effects of VF on myocardial blood flow, metabolic characteristics and catecholamine concentrations in patients undergoing surgery for aortic stenosis. Design-The immediate effects of up to 5 min of VF were studied in 21 patients during cardiopulmonary bypass (CPB) before valve replacement. Results-During VF the global myocardial oxygen consumption, coronary blood flow and vascular resistance were unchanged, and the mean arterial pressure (on CPB) decreased from 70 to 51 mmHg (p<0.02). Fibrillation induced a high myocardial tone and a probable functional aortic insufficiency, which instantly equilibrated left ventricular and aortic pressures. Signs of myocardial ischaemia and acidosis developed after 4 min: a decrease in the pH of coronary sinus blood from 7.38 to 7.32 (p<0.001), an increased release of lactate from 32 to 137 mumol/min (p<0.001) and potassium from 29 to 73 μmol/min (p<0.05). The noradrenaline net release increased from 0.021 to 0.58 nmol/min (p<0.02) after 1.5 min of VF and then decreased. The adrenaline net uptake remained low and unchanged (17-28%). Conclusion-VF in patients with aortic stenosis was rapidly followed by myocardial ischaemia, acidosis and a transient increase in the myocardial noradrenaline net release despite sufficient coronary perfusion and unchanged global myocardial oxygen consumption. The VF instantly induced equilibration of left ventricular and aortic pressure and probably caused a relative underperfusion of the subendocardium. These factors all support persistence of VF.
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| 2. |
- Olsson, Annika, et al.
(författare)
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Marked increase of beta-amyloid(1-42) and amyloid precursor protein in ventricular cerebrospinal fluid after severe traumatic brain injury.
- 2004
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Ingår i: Journal of neurology. - 0340-5354. ; 251:7, s. 870
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Tidskriftsartikel (refereegranskat)abstract
- Severe traumatic brain injury (TBI) may result in widespread damage to axons, termed diffuse axonal injury. Alzheimer's disease (AD) is characterised by synaptic and axonal degeneration together with senile plaques (SP). SP are mainly composed of aggregated beta-amyloid (Abeta), which are peptides derived from the amyloid precursor protein (APP). Apart from TBI in itself being considered a risk factor for AD, severe head injury seems to initiate a cascade of molecular events that are also associated with AD. We have therefore analysed the 42 amino acid forms of Abeta (Abeta1-42) and two soluble forms of APP (alpha-sAPP and ss-sAPP) in ventricular cerebrospinal fluid (VCSF) and Abeta(1-42) in plasma from 28 patients in a serial samples 0-11 days after TBI. The levels of alpha-sAPP, ss-sAPP and Abeta(1-42) were determined using ELISA assays. After TBI, there was a significant stepwise increase in VCSF-Abeta(1-42) up to 1173 % from day 0-1 to day 5-6 and in VCSF-beta-sAPP up to 2033 % increase from day 0-1 to day 7-11. There was also a slight but significant increase of VCSF-beta-sAPP from day 0-1 to day 5-6 and day 7-11. By contrast, the plasma- Abeta(1-42) level is unchanged after injury. The marked increase in VCSFAbeta(1-42) implies that increased Abeta expression may occur as a secondary phenomenon after TBI with axonal damage. The unchanged level of plasma-Abeta(1-42) in contrast to the marked increase in VCSF-Abeta(1-42) after severe TBI, supports the suggestion that plasma Abeta(1-42) does not reflect Abeta metabolism in the central nervous system (CNS).
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