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  • 1
    Electronic Resource
    Electronic Resource
    Arrhythmias and infarction in the ischemic pig heart are not mediated by xanthine oxidase-derived free oxygen radicals (1987)
    Springer
    Basic research in cardiology 82 (1987), S. 493-505 
    Details
    ISSN: 1435-1803
    Keywords: Xanthine oxidase ; freeoxygen radicals ; myocardial ischemia ; reperfusion arrhythmias ; ventricular fibrillation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Xanthine oxidase activities of pig myocardium and blood during and following myocardial ischemia were measured using HPLC, and electrochemical detection of hypoxanthine, xanthine and uric acid. Myocardial ischemia was produced by occluding the anterior descending coronary artery two-thirds of the way from its origin. There was no accumulation of either xanthine orurate in the ischemic pig myocardium during occlusion periods of 90 min, but there was a substantial accumulation of hypoxanthine. Similarly, there was no increase in myocardial xanthine or urate during the 30 min reperfusion following coronary artery occlusion periods of 15, 30, 60 or 90 min. Following in vitro incubation at pH 8 of myocardial homogenates or blood with either hypoxanthine or xanthine and NAD, no urate production was detectable. In contrast, significant amounts of xanthine and/or urate were produced, following addition of xanthine oxidase to the reaction mixtures. Additional in vitro experiments showed that the following pig tissues were lacking xanthine oxidase activity: left and right atrial appendage, left and right ventricle, interventricular septum, anterior descending and circumflex coronary arteries, ascending aorta, lung, and blood. Large amounts of xanthine oxidase (9.3±1.8 SEM mU/g wet weight, n=7) were found in pig liver. In the ischemic pig heart, transmural infarction developed within 60 min of ischemia. Ventricular arrhythmias and fibrillation occured most frequently within 45 min of ischemia and within seconds after reperfusion. These results showed that the pig heart and blood were xanthine oxidase deficient, suggesting that xanthine oxidase-derived free oxygen radicals were not involved in the cytotoxic and arrhythmogenic effects brought about by myocardial ischemia and/or reperfusion in the pig.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01907097
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  • 2
    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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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Effect of adenosine and AICAR on ATP content and regional contractile function in reperfused canine myocardium (1985)
    Springer
    Basic research in cardiology 80 (1985), S. 445-458 
    Details
    ISSN: 1435-1803
    Keywords: AICAR ; adenosine ; ATP content ; contractile function
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We investigated whether the postischemic acceleration of adenosine triphosphate (ATP) synthesis by means of precursor infusion is beneficial for the contractile function of reperfused myocardium. A coronary artery was occluded for 45 min in 21 dogs to produce a marked but reversible ischemia. During the following 3 hours of reperfusion either adenosine (n=6) or AICAR (5-amino-imidazole-4-carboxamide-riboside) (n=6) was infused intracoronarily by a small transfemoral catheter positioned in the LAD. ATP repletion by adenosine was nearly 50% of the deficit caused by the previous ischemia, the effect of AICAR on steady-state tissue ATP concentration was insignificant. Regional systolic function of these both groups was compared to that of a control group (n=9) receiving only a saline infusion. We measured the regional function by subendocardially implanted ultrasound transducers using the transit time method. All three groups showed a reduction to about 25% of the initial segment shortening at the end of ischemia, followed by a quick recovery to half of the preocclusion segment shortening after reopening of the vessel. No further changes were observed in the control series during the 3 hours of reperfusion (50±10% SE segment shortening at the end). With adenosine infusion-in spite of the resulting considerable ATP elevation — no significant change of segmental contractile function occurred (44±5% SE segment shortening). Only the AICAR treated group differed from control. It produced a continuous deterioration during reflow resulting in a holosystolic bulging of −20%±10% SE at the end of 3 hours of reperfusion. Our results show that there is no correlation between different ATP tissue levels achieved by adenosine infusion and systolic function in reperfused myocardium after regional reversible ischemia. We hypothesize that reperfusion dyskinesia is caused by a failure of energy utilisation rather than of energy supply.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01908189
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    Paper (German National Licenses)
    Fulltext
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