Key result
Intravenous diltiazem significantly reduced the no-flow zone to left ventricular area ratio (5.6% vs 11.2%, p<0.01) and improved cardiac function in a rat model of coronary thrombotic microembolism.
Why the study?
Does intravenous diltiazem improve cardiac function and alleviate inflammatory responses and microvascular thrombotic injury in a rat model of coronary thrombotic microembolism?
Does intravenous diltiazem improve cardiac function and alleviate inflammatory responses and microvascular thrombotic injury in a rat model of coronary thrombotic microembolism?
Intravenous diltiazem attenuates microvascular thrombotic injury, inflammatory responses, and cardiac dysfunction in a rat model of coronary thrombotic microembolism, supporting its potential utility in managing microvascular spasm and no-reflow.
Diltiazem attenuated dysfunction in this rat CME model; leaves open any role in human microvascular embolism.
The aim of this study was to assess the feasibility of evaluating the therapeutic effects of intravenous diltiazem in a newly established rat model of coronary thrombotic microembolism (CME). CME was induced by injecting 0.199 ml saline containing 5 mg of automicrothrombotic particulates (~10 µm) into the aorta of Sprague Dawley rats. The injection was carried out over 10 sec using a tuberculin syringe with a 28‑gauge needle. The CME model rats were randomly divided into untreated (CME, n=38) and diltiazem‑treated (CME+DIL, n=38) groups. Diltiazem (1 mg/ml, 50 µg/min/kg) was intravenously injected using an infusion pump through the tail vein for 175 min, 5 min following the injection of the automicrothrombotic particulates. Hemodynamic measurements, echocardiography and pathohistological examinations were performed at various time-points (3 h, 24 h and 7 and 28 days) postoperatively. Arteriolar thrombosis, multifocal myocardial necrosis, inflammatory cell infiltration with markedly increased myocardial tumor necrosis factor α (TNF‑α) and interleukin-6 (IL‑6) expression, reduced left ventricular (LV) systolic function and increased plasma von Willebrand factor (vWF), endothelin-1 (ET-1) and serum c-troponin I (c-TnI) levels (indicating vascular endothelial injury and myocardial necrosis) were observed in the CME model rats. These pathological responses in CME rats were partly attenuated by intravenous diltiazem treatment. The present CME model is suitable for evaluating the therapeutic effects of intravenous diltiazem; intravenous diltiazem treatment significantly improved cardiac function through alleviating inflammatory responses and microvascular thrombotic injury in this rat model of CME.
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Bai et al. (2013) studied Coronary thrombotic microembolism (CME) (n=152). Intravenous diltiazem vs. Untreated (CME model without diltiazem) was evaluated on No-flow zone to left ventricular area ratio (NF/LV) at 3 hours postinjection (p=<0.01). Intravenous diltiazem significantly reduced the no-flow zone to left ventricular area ratio (5.6% vs 11.2%, p<0.01) and improved cardiac function in a rat model of coronary thrombotic microembolism.
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