Echocardiographic evaluation of pressure overload-induced cardiac remodeling in mice using different ultrasound machines / 南方医科大学学报

<p><b>OBJECTIVE</b>To compare the results of echocardiographic evaluation of pressure overload-induced cardiac remodeling in mice using different ultrasound machines.</p><p><b>METHODS</b>Eighteen C57 BL/6 mice were randomly divided into the sham-operated and the transverse aortic constriction (TAC) groups (n=9). Eight weeks after the operation, the cardiac function of TAC group was evaluated using Siemens ultrasonic instrument with 15L8 probe and the differences between the awake and anesthetized states were compared. The heart rate, left ventricular (LV) dimensions, systolic and diastolic functions were measured in both sham-operated and TAC groups using the Siemens ultrasonic instrument and a high-resolution ultrasonic imaging system for small animals (Vevo 770).</p><p><b>RESULTS</b>Compared with the mice in wakefulness, the anesthetized mice showed significantly decreased heart rate and LV fractional shortening (P<0.001) and markedly increased LV end diastolic diameter and LV end systolic diameter (P<0.05). Both machines sensitively detected the cardiac remodeling of TAC mice in comparison with the sham-operated group. Compared with Siemens machine, Vevo 770 provided a higher resolution of 2D and M mode echocardiography with clearer Doppler frequency image of the mitral valve flow for evaluation of the LV diastolic function.</p><p><b>CONCLUSION</b>Both machines are suitable for evaluating cardiac remodeling induced by pressure overload independent of anesthesia, though anesthesia depresses cardiac function. Vevo 770 is optimal to evaluate LV diastolic function in mice.</p>

Effects of dexmedetomidine hydrochloride on ERK1/2 activation in a rat model of ventilator-induced lung injury / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the effect of dexmedetomidine hydrochloride on inflammatory lung injury and phosphorylation of extracellular regulated protein (ERK1/2) in a rat model of ventilator-induced lung injury (VILI).</p><p><b>METHODS</b>Thirty-six adult male SD rats were randomized into 3 groups (n=12) to receive a 4-h standard ventilation (group C, with tidal volume of 8 ml/kg and respiratory rate of 90/min), high-tidal volume ventilation (group H, with tidal volume of 20 ml/kg and respiratory rate of 50 /min), and high-tidal volume ventilation plus 0.5 µg·kg(-1)·h(-1) dexmedetomidine infusion (group D), with the maintenance of a positive end expiratory pressure (PEEP) of 0 cmH(2)O. After mechanical ventilation the rats were sacrificed to collect the lung lavage liquid and lung tissue to examine the pulmonary inflammatory changes and tumor necrosis factor-α (TNF-α) expression as well as the expressions of ERK1/2 and p-ERK1/2.</p><p><b>RESULTS</b>Groups H and D showed obvious lung injury and significant elevations of the total protein, WBC, MPO, TNF-α, and ERK1/2 phosphorylation as compared with those of group C. The rats in group D showed milder lung pathologies with significantly lower levels of phosphorylation of ERK1/2 and TNF-α compared with those in group H.</p><p><b>CONCLUSION</b>Dexmedetomidine can significantly attenuate VILI, decrease the production of the inflammatory molecules, and inhibit the activation of ERK1/2, demonstrating a protective effect against VILI.</p>

Antihypertrophic effect of dihydropyridines calcium channel blockers is dependent on their potential of blocking N-type calcium channel / 南方医科大学学报

<p><b>OBJECTIVE</b>To compare the effects of amlodipine, benidipine and nifedipine on myocardial hypertrophy and evaluate the underlying mechanism.</p><p><b>METHODS</b>Myocardial hypertrophy model was created by transverse aortic constriction (TAC) in C57 BL/6 mice, and plasma catecholamine concentrations were measured 7 days after surgery to confirm the sympathetic activation. The 3 drugs were administered in TAC mice for 7 days and cardiac hypertrophy was evaluated according to the heart-to-body weight ratio (HW/BW). Effects of those drugs on the protein synthesis stimulated by phenylephrine in cultured neonatal cardiac myocytes were also examined.</p><p><b>RESULTS</b>HW/BW and plasma concentrations of catecholamine were significantly increased in TAC mice one week after surgery in comparison with to sham-operated mice. One week after TAC, the HW/BW ratio was significantly lower in the amolodipine but not nifedipine-treated group than in the TAC group. Administration of nifedipine via minipump infusion for one week did not decrease HW/BW ratio. Treatment with amlodpine or benidipine, but not nifedipine, decreased the neonatal rat myocyte protein synthesis induced by phenylephrine stimulation.</p><p><b>CONCLUSION</b>Antihypertrophic effect of DHEs on myocardium is dependent on their potential of blocking N-type calcium channel, and the underlying mechanism involves the sympathetic inhibition.</p>