| Autor: |
Ascer, Enrico, Mohan, Chittur, Gennaro, Mark, Cupo, Susan |
| Zdroj: |
Annals of Vascular Surgery; January 1992, Vol. 6 Issue: 1 p69-73, 5p |
| Abstrakt: |
Interleukin-1 and thromboxane are known to mediate the host response to sepsis, trauma, and myocardial ischemia. A well-established model of canine isolated gracilis muscle was used to evaluate whether cytokine (interleukin-1) played a role in skeletal muscle ischemia-reperfusion injury. Six adult mongrel dogs (25–30 kg) were subjected to six hours of muscle ischemia followed by reperfusion. Gracilis venous samples were collected pre-ischemia and at one hour of reperfusion. Systemic (arterial) blood samples were taken at one hour of reperfusion. Sera were analyzed for interleukin-1 by bioassay and thromboxane (B2) by radio-immunoassay. The gracilis muscle of the operated limb was harvested in all the animals for assessment of the percentage of muscle necrosis. This was found to be 56.2±14.8% by serial transections, nitroblue tetrazolium staining, and computerized planimetry. Interleukin-1 levels in the gracilis venous effluent increased from 21.88±7.13 units/ml during pre-ischemic baseline to 50.42±9.12 units/ml after six hours of ischemia followed by one hour of reperfusion (p<0.04). Thromboxane B2 levels were 2983±1083 pg/ml and 9483±2218 pg/ml at pre-ischemia and at one hour of reperfusion respectively (p<0.04). Systemic levels of both interleukin-1 and thromboxane B2 at one hour of reperfusion were 0 units/ml and 1584±520 pg/ml respectively, which were significantly lower than the one hour reperfusion gracilis venous effluent levels (p<0.04). This is the first report in which cytokines have been implicated in skeletal muscle ischemia-reperfusion injury. Modulation of interleukin-1 may impact positively on muscle necrosis and systemic manifestations of reperfusion injury. |
| Databáze: |
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