December 16, 1997Circulation
Enhanced Myosin Light Chain Phosphorylations as a Central Mechanism for Coronary Artery Spasm in a Swine Model With Interleukin-1β
Why the study?
Does enhanced myosin light chain phosphorylation mediate coronary artery spasm in a swine model with interleukin-1beta?
Population
Swine model with interleukin-1beta applied chronically to porcine coronary arteries from the adventitia to…
Comparison
Intracoronary serotonin vs Control segment or simple endothelium removal
Design
Preclinical
Follow-up
2 weeks after operation
Authors
Discussion
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Member takes
Implication
Supports MLC phosphorylation in IL-1β swine spasm; leaves open human translation and therapeutic targeting.
Structured PICO
Does enhanced myosin light chain phosphorylation mediate coronary artery spasm in a swine model with interleukin-1beta?
P
Population
Swine model with interleukin-1beta (IL-1beta) applied chronically to porcine coronary arteries from the adventitia to induce an inflammatory/proliferative lesion
I
Intervention
Intracoronary serotonin (with or without fasudil, an inhibitor of protein kinases)
C
Comparator
Control segment (normal coronary artery) or simple endothelium removal
O
Outcome
Myosin light chain (MLC) phosphorylations (monophosphorylation and diphosphorylation) and coronary contractionssurrogate
Enhanced myosin light chain phosphorylations in vascular smooth muscle play a central role in the pathogenesis of coronary spasm in an IL-1beta swine model.
Cite This Study
Katsumata et al. (1997) studied this question.