Comparative study on effects of puerarin and granulocyte colony-stimulating factor in treating acute myocardial infarction / 中国中西医结合杂志

<p><b>OBJECTIVE</b>To compare the effects of puerarin and granulocyte colony-stimulating factor (G-CSF) in treating acute myocardial infarction (AMI) and on the size of infarcted area and cytokines.</p><p><b>METHODS</b>Seventy-nine patients with anterior AMI were randomly divided into three groups, they were treated with conventional Western medical treatment, but to the puerarin group (PG) and the G-CSF group (GCG) puerarin and G-CSF was given additionally, respectively. The infarcted size, plasma G-CSF, matrix metalloproteinase-9 (MMP-9), serum interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) were detected before and after treatment.</p><p><b>RESULTS</b>The infarcted size was positively correlated to the levels of G-CSF, MMP-9, IL-6 and TNF-alpha before treatment ( r = 0.45, 0.42, 0.44 and 0.42, P<0.01 ). The infarcted size in the PG and the GCG decreased on the 28th day (P<0.01), the level of G-CSF, MMP-9, IL-6 and TNF-alpha in the PG on the 7th day all decreased (P<0.05), but these indexes in the GCG increased (P<0.05), while those in the control group were unchanged (P>0.05).</p><p><b>CONCLUSION</b>Puerarin and G-CSF are effective in decreasing infarcted size, but their effects on cytokines are different entirely.</p>

Effects of carvedilol on neurohormone and magnesium metabolism in patients with chronic heart failure / 中华心血管病杂志

<p><b>OBJECTIVE</b>To investigate the effects of carvedilol on neurohormone and magnesium metabolism in patients with chronic heart failure (CHF).</p><p><b>METHODS</b>Fifty-seven patients with CHF were divided into two groups randomly: received conventional treatment alone or combined with carvedilol for 8 weeks, respectively. Urine magnesium excretion (UME), plasma levels of magnesium (PMC), norepinephrine (NE), angiotensin-II (Ang-II), aldosterone (ALD), plasma renin activity (PRA) and peripheral monocyte magnesium content (MMC) were measured before and after treatments. Twenty-six health persons were selected as normal subjects.</p><p><b>RESULTS</b>There was a significant increase in UME and plasma concentrations of NE, ALD, Ang-II and PRA, and a significant decrease in MMC in patients with CHF, compared with the control group (P < 0.01). UME was positively correlated with ALD, Ang-II, PRA r = 0.41, 0.42, 0.38, respectively (P < 0.01). These parameters significantly improved after carvedilol (P < 0.05).</p><p><b>CONCLUSION</b>Carvedilol decreases significantly plasma concentrations of neurohormone and urine magnesium excretion, and increases cell magnesium content in patients with CHF.</p>

Study on the effect and mechanism of puerarin on the size of infarction in patients with acute myocardial infarction / 中国中西医结合杂志

<p><b>OBJECTIVE</b>To observe the effect of puerarin on infarction size, fatty acids metabolism, inflammatory response and atherosclerotic plaque stability in patients with acute myocardial infarction (AMI).</p><p><b>METHODS</b>Sixty-one patients with AMI were randomly divided into two groups, the control group (n = 30) and the treated group (n = 31). All were treated with conventional treatment, but to the treated group, puerarin injection was given additionally by injecting 500 mg per day for 2 weeks. Before and after treatment, blood levels of free fatty acids (FFA), matrix metalloproteinases-9 (MMP-9) and C-reactive protein (CRP) were assayed, and the size of infarction was determined by Ideker QRS scoring method.</p><p><b>RESULTS</b>Before treatment, the size of infarction was positively correlated to the levels of FFA, MMP-9 and CRP (r = 0.43, 0.42 and 0.39, respectively, all P<0.01). As compared with those before treatment, after treatment, the three parameters lowered by 30%, 41% and 23%, respectively and the size of infarction significantly reduced in the treated group (P<0.01), while in the control group, no significant change was found (P>0.05).</p><p><b>CONCLUSION</b>Puerarin treatment could significantly reduce the size of infarction in patients with AMI, the mechanism is possibly related with its effects in lowering plasma levels of FFA, inhibiting inflammation and stabilizing atherosclerotic plaque.</p>