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12. A myocardial ischemia- and reperfusion-induced injury is mediated by reactive oxygen species released from blood platelets.

Author

Seligmann, Christian, Prechtl, Gerald, Kusus-Seligmann, Magda, and Daniel, Werner G.

Abstract

In recent experimental studies, blood platelets have been found to exhibit some cardiodepressive effects in ischemic and reperfused guinea pig hearts independent of thrombus formation. These effects seemed to be mediated by reactive oxygen species (ROS). However, the source of these ROS - platelets or heart - remained still unknown. Isolated, buffer-perfused and pressure-volume work performing guinea pig hearts were exposed to a low-flow ischemia (1 ml/min) of 30 min duration and reperfused at a constant flow of 5 ml/min. Human thrombocytes were administered as 1 min bolus (20 000 thrombocytes/µl perfusion buffer) in the 15th min of ischemia or in the 1st or 5th min of reperfusion in the presence of thrombin (0.3 U/ml perfusion buffer). Recovery of external heart work (REHW) was expressed as ratio between postischemic and preischemic EHW in percent. Intracoronary platelet retention (RET) was quantified as percent of platelets applied. In a second set of experiments, thrombocytes were incubated with 10 µM of the irreversible NADPH oxidase blocker diphenyliodonium chloride and washed twice, thereafter, and administered according to the same protocol as described above. Hearts exposed to ischemia and reperfusion in the presence of thrombin but without application of platelets served as controls. Controls without application of platelets did not reveal a severe compromisation of myocardial function (REHW 85.5 ± 1%). However, addition of platelets during ischemia or in the 1st or 5th min of reperfusion led to a significant reduction of REHW as compared with controls (REHW 62.4 ± 6, 53.9 ± 3, 40.5 ± 3, respectively). Application of platelets pretreated with diphenyliodonium chloride did not reveal any cardiodepressive effects being significantly different from controls without platelet application. Moreover, treatment of platelets with diphenyliodonium chloride did not significantly decrease intracoronary platelet retention. In conclusion, these results demonstrate that cardiodepressive effects of human thrombocytes in ischemic and reperfused guinea pig hearts are mediated by ROS released from thrombocytes and not the heart. [ABSTRACT FROM AUTHOR]

Published
2013
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13. Nitric Oxide Mitigates Leukocyte Adhesion and Vascular Leak After Myocardial Ischemia

Author

Kupatt, Christian, Zahler, Stefan, Seligmann, Christian, Massoudy, Parwis, Becker, Bernhard F., and Gerlach, Eckehart

Abstract

Tissue edema is a facet of ischemia/reperfusion injury in many organs, polymorphonuclear leukocytes (PMN) presumably playing a contributory role. We studied the intracoronary adhesion of PMN and its effect on vascular permeability during reperfusion in isolated guinea-pig hearts. After a global ischemia of 15 min duration, PMN (107) were infused into the coronary system during the first minute of reperfusion. PMN adhesion was measured as difference of applied PMN and those recovered in the effluent perfusate. Coronary permeability was assessed by measuring the rate of transudate formation (TF) on the epicardial surface, before as well as 5, 15 and 30 min after ischemia. Experiments were also performed in the presence of the NO-synthase inhibitor nitro-L-arginine (10μm) and the ACE-inhibitor ramiprilat (2μm), the latter known to enhance endogenous nitric oxide formation. Furthermore, the radical scavenger uric acid (0.5 mm) was applied either before and during ischemia or starting after PMN application. Ischemia/reperfusion increased coronary PMN adherence from 23±1% (basal) to 33±2%. Whereas ischemia alone did not influence TF (about 100μl/min during reperfusion), postischemic PMN infusion led to progressive TF. With nitro-L-arginine, PMN adhesion rose to 45±3%; TF increased to 212±30μl/min. In contrast, ramiprilat caused post-ischemic adhesion and TF to decline to basal values. In the presence of uric acid (UA) PMN adhesion declined to 26±2%, however, the subsequent increase in TF after withdrawal of UA was not markedly attenuated. On the other hand, infusion of UA after application of PMN caused a significant decrease of TF. The extracellular antioxidants SOD/catalase were without effect. As shown using luminol enhanced chemiluminescence, NO was able to scavenge oxygen free radicals released by activated PMN. These findings indicate that enhanced PMN adhesion in reperfusion leads to an increase in coronary permeability. Scavenging of oxygen free radicals with NO or UA appears to mitigate both, postischemic PMN adhesion and PMN-induced vascular injury, even after adhesion.

Published
1996
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14. ATRIAL FIBRILLATION.

Author

Seligmann, Christian, Hippisley-Cox, Julia, Coupland, Carol, Robson, John, and Brindle, Peter

Subjects
*ATRIAL fibrillation risk factors, *MEDICAL screening evaluation, *CARDIOVASCULAR diseases risk factors, *RHEUMATOID arthritis, STROKE risk factors
Abstract

A letter to the editor is presented regarding the identification of people at risk for stroke with pulse checking and electrocardiography.

Published
2012

16. [Dyspnea, what is the cause? Rhabdomyosarcoma].

Author

Seligmann C, Hackl T, and Menne J

Subjects
Diagnosis, Differential, Fatal Outcome, Female, Humans, Middle Aged, Coronary Angiography, Dyspnea etiology, Echocardiography, Heart Atria, Heart Neoplasms diagnosis, Rhabdomyosarcoma diagnosis
Published
2011

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