Disassociation Between Left Ventricular Mechanical and Electrical Properties in Ischemic Rat Heart After G-CSF Treatment

Abstract

Both early and delayed administrations of G-CSF can improve electrophysiological properties after myocardial ischemia, but have no beneficial effects on LV mechanical remodeling.

Neutrophil extracellular traps in ischemia-reperfusion injury-induced myocardial no-reflow: therapeutic potential of DNase-based reperfusion strategy

“…Long-term LV functional analysis. Two-dimensional (2D) echocardiographic measurements were performed on postoperation day 45, as previously described (36,62). The rats were anesthetized, and transthoracic echocardiography of the LV was performed (Vivid7, GE Medical System, Horton, Norway).…”

Modulation of Mononuclear Phagocyte Inflammatory Response by Liposome-Encapsulated Voltage Gated Sodium Channel Inhibitor Ameliorates Myocardial Ischemia/Reperfusion Injury in Rats

“…Myocardial I/R injury was induced as previously described in our lab [29]. Briefly, rats were anesthetized with pentobarbital sodium (40 mg/kg ip) and submitted to artificial ventilation (75 strokes/min, tidal volume 8 mL/kg) using a volume-controlled rodent respirator (Harvard Apparatus, USA).…”

“…After echocardiographic measurement, the rats were anesthetized with intraperitoneal pentobarbital sodium (40 mg/kg) for invasive hemodynamics using a 2F high fidelity microtip pressure catheter (SPR-320, Millar Instruments, USA) to measure systolic and diastolic blood pressures (SBP and DBP), left ventricular end diastolic pressure (LVEDP), left ventricular end systolic pressure (LVESP), maximal slope of systolic pressure increment (+ dP/dt max ), and maximal slope of diastolic pressure decrement (- dP / dt min ) as previously described [29,32]. …”

Granulocyte Colony Stimulating Factor in the Treatment of Cardiac Ischemic Disease. A Decade has Passed: Is it Time to Give Up?

“…Moreover, myocardial remodeling causes sympathetic hyperinnervation and consequently arrhythmic events [46]. Liu and co-workers [4] present data that indicate that G-CSF-treated hearts had improved electrophysiological outcomes and less inducible ventricular arrhythmias during programmed ventricular stimulation, although the mechanism remains unclear and needs further investigation. Possible mechanisms are through increasing Cx43 expression as shown by Kuhlmann et al (2006) [47] and Baldo (2008) [48], or stabilization of the Cx43 protein via Wnt signaling cascade [49].…”

“…In the present issue of Cardiovascular Drugs and Therapy Liu et al point out a distinct effect of G-CSF after myocardial infarction (MI): a disassociation between left ventricular mechanical and electrical properties in ischemic rat heart after G-CSF treatment [4]. For this purpose, the authors treated ischemic rats with subcutaneous G-CSF injections (100 μg/kg/d for five consecutive days) 1 h or 24 h after infarction.…”