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- Schriefl, A. J., et al.
(författare)
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Remodeling of Intramural Thrombus and Collagen in an Ang-II Infusion ApoE-/- Model of Dissecting Aortic Aneurysms
- 2012
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Ingår i: Thrombosis Research. - : Elsevier BV. - 0049-3848 .- 1879-2472. ; 130:3, s. E139-E146
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Tidskriftsartikel (refereegranskat)abstract
- Fibrillar collagen endows the normal aortic wall with significant stiffness and strength and similarly plays important roles in many disease processes. For example, because of the marked loss of elastic fibers and functional smooth cells in aortic aneurysms, collagen plays a particularly important role in controlling the dilatation of these lesions and governing their rupture potential. Recent findings suggest further that collagen remodeling may also be fundamental to the intramural healing of arterial or aneurysmal dissections. To explore this possibility further, we identified and correlated regions of intramural thrombus and newly synthesized fibrillar collagen in a well-established mouse model of dissecting aortic aneurysms. Our findings suggest that intramural thrombus that is isolated from free-flowing blood creates a permissive environment for the synthesis of fibrillar collagen that, albeit initially less dense and organized, could protect that region of the dissected wall from subsequent expansion of the dissection or rupture. Moreover, alpha-smooth muscle actin positive cells appeared to be responsible for the newly produced collagen, which co-localized with significant production of glycosaminoglycans.
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- Aboab, J., et al.
(författare)
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CO2 elimination at varying inspiratory pause in acute lung injury
- 2007
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Ingår i: Clinical Physiology and Functional Imaging. - 1475-0961. ; 27:1, s. 2-6
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Tidskriftsartikel (refereegranskat)abstract
- Previous studies have indicated that, during mechanical ventilation, an inspiratory pause enhances gas exchange. This has been attributed to prolonged time during which fresh gas of the tidal volume is present in the respiratory zone and is available for distribution in the lung periphery. The mean distribution time of inspired gas (MDT) is the mean time during which fractions of fresh gas are present in the respiratory zone. All ventilators allow setting of pause time, T-P, which is a determinant of MDT. The objective of the present study was to test in patients the hypothesis that the volume of CO2 eliminated per breath, VTCO2, is correlated to the logarithm of MDT as previously found in animal models. Eleven patients with acute lung injury were studied. When T-P increased from 0% to 30%, MDT increased fourfold. A change of T-P from 10% to 0% reduced VTCO2 by 14%, while a change to 30% increased VTCO2 by 19%. The relationship between VTCO2 and MDT was in accordance with the logarithmic hypothesis. The change in VTCO2 reflected to equal extent changes in airway dead space and alveolar PCO2 read from the alveolar plateau of the single breath test for CO2. By varying T-P, effects are observed on VTCO2, airway dead space and alveolar PCO2. These effects depend on perfusion, gas distribution and diffusion in the lung periphery, which need to be further elucidated.
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- Andersson, Staffan, et al.
(författare)
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Assessment of autonomic nerve function in myotonic dystrophy
- 1990
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Ingår i: Journal of the Autonomic Nervous System. - : Elsevier BV. - 0165-1838 .- 1872-7476. ; 29:3, s. 187-192
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Tidskriftsartikel (refereegranskat)abstract
- The function of the autonomic nervous system was studied in 23 patients with myotonic dystrophy, from a defined population in northern Sweden with an extremely high prevalence of this disease. Heart rate variability tests showed only minor signs of parasympathetic dysfunction. Blood pressure and plasma noradrenaline measurements in recumbent and upright positions showed no signs of sympathetic neuropathy. Increased plasma levels of noradrenaline was an unexpected finding. Our study does not support the hypothesis that cardiac arrhythmias, orthostatic hypotension, gastrointestinal motility disturbances and urinary bladder dysfunction in myotonic dystrophy are caused by autonomic neuropathy, and we believe that these symptoms should rather be ascribed to a defective function of the target organs
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