| Autor: |
P, Mondek, V, Sefránek, J, Tomka, I, Pechán, E, Silvanová, R, Nosál, R, Slysko |
| Rok vydání: |
2002 |
| Předmět: |
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| Zdroj: |
Rozhledy v chirurgii : mesicnik Ceskoslovenske chirurgicke spolecnosti. 81(5) |
| ISSN: |
0035-9351 |
| Popis: |
Surgical treatment of PAOD is related to iatrogenic ischaemia caused by arterial clamping and ischaemia which is result of natural development of the disease. The pathway of skeletal muscle reperfusion injury is complex and one of the most important factors related to injury is endothelial damage. The expected reason of endothelial damage is increased production of oxygen free radicals by prematurely activated PMN (polymorphonuclear) leukocytes (direct injury). Non-specific tissue injury is related to releasing of PMN elastase. Endothelial dysfunction, hypercoagulable state and microcirculation stasis are responsible for indirect injury and no-reflow fenomena.Observational pilot study.10 patients underwent surgery because of PAOD (all suffering from critical limb ischaemia). During reperfusion period in defined intervals following parameters were measured (samples were taken from ipsilateral femoral vein): PMN elastase, lactate, total antioxidant status, malondialdehyd, minerals, acid-base balance, blood count, APTT, prothrombin time, fibrinogen and HTI (heparin tolerance index).Patients with PAOD are threatened by hypercoagulable state with its clinical and surgical consequences. Maximal grade of local acidosis is reached 2 hours from the beginning of reperfusion. Tissue damage is expressed by maximum activity of PMN elastase 18-24 hours during reperfusion and represents non-specific tissue damage. Low total antioxidant status reveals high sensibility to oxygen free radicals. MDA does not achieve the pathological range in observed series.Our results confirmed inevitable importance of prevention of hypercoagulability, oxygen free radical tissue damage and PMN elastase activation to avoid of non-specific tissue damage. |
| Databáze: |
OpenAIRE |
| Externí odkaz: |
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