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  • 1
    Electronic Resource
    Electronic Resource
    Leiomyosarcoma of the pulmonary artery (1979)
    Springer
    Virchows Archiv 383 (1979), S. 207-216 
    Details
    ISSN: 1432-2307
    Keywords: Primary sarcoma of pulmonary artery ; Light-electron and immunofluorescence microscopy findings ; Myointimal cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A 25-year-old man with chest pain and shortness of breath was found to have a primary sarcoma of the pulmonary artery. On light- and electronmicroscopy and immunofluorescence microscopy the lesion was found to be composed of cells of smooth muscle origin. It was diagnosed as leiomyosarcoma. The cross and microscopic features of the tumor are described and the morphologic characteristics of previously reported vascular sarcomas are briefly reviewed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01200900
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  • 2
    Electronic Resource
    Electronic Resource
    Morphometry of intrarenal arteries in progressive sclerosis (1980)
    Springer
    Virchows Archiv 385 (1980), S. 351-359 
    Details
    ISSN: 1432-2307
    Keywords: Progressive sclerosis ; Morphometric investigation of intrarenal arteries ; Intimal thickening
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Vessels of known position in the vascular tree of the kidneys of two cases with a long history of progressive systemic sclerosis — one normotensive, one hypertensive — were examined morphometrically. Medial thickness, intimal thickness and the relative content of collagen and elastin in the vascular media were measured. Smooth muscle nuclei were counted in the arterial cross section. These morphometric data were compared with those obtained from two autopsy cases — one with a history of essential hypertension, one without any hypertensive history. The findings suggest that progressive sclerosis induces intimal thickening in all branches of the renal artery down to a distented diameter of 200 μm. In the case where progressive sclerosis was complicated by arterial hypertension increased medial thicknesses were found, similar to the findings in the case with a history of essential hypertension.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00432543
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Intracellular trapping of adenosine during myocardial ischemia by L-homocysteine (1986)
    Springer
    Basic research in cardiology 81 (1986), S. 267-275 
    Details
    ISSN: 1435-1803
    Keywords: adenosine ; myocardial ischemia ; L-homocysteine ; S-adenosyl-L-homocysteine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Experiments were carried out to test the hypothesis whether adenosine produced by ATP catabolism during ischemia can be trapped with L-homocysteine and be re-utilized during reperfusion. During intraatrial infusion of L-homocysteine (100 mg/kg/h), the ischemic accumulation of adenine nucleosides and oxypurines in dog myocardium was found to be less than 50% of that during control ischemia. A high proportion of adenosine was recovered as S-adenosyl-L-homocysteine. On reperfusion, S-adenosyl-L-homocysteine tissue content remained high. After 3 hours of reperfusion approximately 50% of the accumulated S-adenosyl-L-homocysteine were still found in the tissue. Infusion of L-homocysteine did not cause an accumulation of S-adenosyl-L-homocysteine in the nonischemic myocardial tissue. L-homocysteine treatment caused a further depletion of ATP during reperfusion after 30 minutes of ischemia, which can be interpreted as a toxic effect. We conclude that L-homocysteine is indeed able to trap adenosine produced by ATP breakdown, but the reaction is not readily reversible and is therefore not useful for quick restoration of postischemic ATP levels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01907409
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  • 4
    Electronic Resource
    Electronic Resource
    Influence of repetitive coronary occlusions on myocardial adenine nucleosides, high energy phosphates and ultrastructure (1987)
    Springer
    Basic research in cardiology 82 (1987), S. 557-565 
    Details
    ISSN: 1435-1803
    Keywords: repetitivecoronaryocclusions ; ultrastructure ; adenine nucleotide tissue content
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We compared the effects of repeated short periods of myocardial ischemia with those of permanent occlusion (canine open-chest) with regard to tissue content of adenine nucleotides, nucleosides, creatine phosphate, and ultrastructure. Coronary occlusion for 3 min followed by a reperfusion period of 7 min was repeated up to a cumulative occlusion time of either 45 or 90 min. After cumulative occlusions of 15, 30, 45, and 90 min, transmural needle biopsies were taken from the ischemic area to be analyzed for adenine nucleotides, nucleosides, creatine phosphate, and ultrastructural changes. At the end of each experiment, tetrazolium salt staining was used for macroscopic detection of myocardial necrosis. These data were obtained with those obtained from dogs with a permanent coronary occlusion of 45 and 90 min, respectively. After repeated coronary occlusions at a cumulative occlusion time of 45 min, macroscopic detection of necrosis was negative, and after 90 min of cumulative coronary occlusion, patchy subendocardial tissue necrosis was found in only one out of 13 dogs, whereas in the group with permanent coronary occlusion, small patchy subendocardial necrosis was found in 95% after 45 min, and after 90 min permanent coronary occlusion, large subendocardial necrotic areas spreading towards the epicardial layers were found in 90% of the hearts. Ultrastructural investigations showed only slight to moderate ischemic injury after 45 and 90 min intermittent coronary occlusion, whereas permanent coronary occlusion produced moderate to severe ischemic injury after 45 min; and 90 min permanent coronary occlusion produced irreversible ischemic injury in all subendocardial tissue samples and in 80% of the subepicardial tissue samples. ATP content was decreased significantly less during intermittent coronary occlusion compared with that during permanent coronary occlusion. AMP and nucleosides did accumulate during permanent occlusion but not with repetitive brief coronary occlusions. Our results show that intermittent reperfusion significantly delays ischemic injury in comparison with permanent coronary occlusion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01907226
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  • 5
    Electronic Resource
    Electronic Resource
    Influence of dipyridamole on infarct size and on cardiac nucleoside content following coronary occlusion in the dog (1985)
    Springer
    Basic research in cardiology 80 (1985), S. 682-692 
    Details
    ISSN: 1435-1803
    Keywords: dipyridamole ; infarct size ; cardiac nucleosides
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of 3 different doses (0.02, 0.1, 0.5 mg/kg/h) of dipyridamole on myocardial infarct size were evaluated in pentobarbital anesthetized open-chest dogs following sequential coronary occlusion of two medium sized coronary arteries in the same heart. The first coronary occlusion produced a control infarct, the other a test infarct under the influence of the drug. Dipyridamole infusion was started 10 min before the second occlusion at a rate of 0.02 (group A, n=9), 0.1 (group B, n=10) or 0.5 (group C, n=9) mg/kg/h respectively and continued to the end of reperfusion (90 min). Biopsy samples were obtained at the end of each occlusion period and at the end of the second reflow period. Infarct size was determined using post mortem angiography and pNBT staining. Control and treated infarct sizes, expressed as a percentage of the perfusion area, were 21.9±5.4% vs. 25.2±7.7% in group A (n=9), 21.8±7.3% vs. 18.3±5.2% in group B (n=9), and 22.3±7.7% vs. 16.2±4.8% in group C (n=8). There were no significant differences between control and treated infarct sizes in the 3 groups. After 90 min coronary occlusion tissue adenosine contents in the ischemic myocardium were significantly higher (42±7 nmol/gww in group C and 40±5 nmol/gww in group B) than those in the nonischemic myocardium, and dipyridamole enhanced these levels (395±6 nmol/gww in group C: p〈0.01, 55±10 nmol/gww in group B). Dipyridamole did not affect the tissue inosine levels in the ischemic myocardium after 90 min coronary occlusion. ATP and creatine phosphate levels were not affected by dipyridamole during ischemia or during reflow. The accumulated adenosine was not phosphorylated to AMP and on to ATP upon reperfusion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01907868
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    Paper (German National Licenses)
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