Why the study?
Does tetramethylpyrazine pretreatment reduce the incidence of arrhythmias and alter prostaglandin/thromboxane release in an ischemic rat heart model?
Does tetramethylpyrazine pretreatment reduce the incidence of arrhythmias and alter prostaglandin/thromboxane release in an ischemic rat heart model?
Tetramethylpyrazine pretreatment significantly reduces ischemia- and reperfusion-induced ventricular arrhythmias in a rat heart model, potentially mediated by favorable alterations in prostaglandin and thromboxane release.
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TMP pretreatment merits further arrhythmia research in models; leaves open any clinical translation from this Level 5 evidence.
Pretreatment with tetramethylpyrazine (TMP, 12 mg/kg/day), a drug originally derived from the rhizomes of Ligusticum wallichii, significantly reduced the incidence of ischemia-induced ventricular tachycardia (VT) and fibrillation (VF) from 100% and 50% of control hearts to 41% (p < 0.05) and 0% (p < 0.05), respectively, in the ischemic rat heart. TMP also diminished the incidence of reperfusion-induced VT and VF from 100% and 100% of control hearts to 33% (p < 0.05) and 41% (p < 0.05), respectively. Pretreatment with TMP produced a slight, but significant increase of 6-keto-PGF1 alpha and a decrease of TXB2 production during aerobic perfusion. Ischemia and reperfusion markedly increased the release of 6-keto-PGF1 alpha and TXB2. Pretreatment with TMP significantly enhanced the release of 6-keto-PGF1 alpha and diminished TXB2 outflow following left coronary artery occlusion and reperfusion.
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Feng et al. (1999) studied this question.
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