[Stimulation of adenosine A1 receptor attenuates angiotensin II induced myocardial hypertrophy in neonatal rats via the extracellular signal-regulated kinase signal pathways].

OBJECTIVE: To observe the impact of adenosine A1 receptor stimulation on extracellular signal-regulated kinase 1/2 (ERK1/2) signal pathways on angiotensin II (AngII) stimulated cardiomyocytes of neonatal rats in vitro. METHODS: Cardiomyocytes of neonatal rats were cultured in vitro. Cardiomyocytes hypertrophy was induced by AngII (0.1 µmol/L). The antihypertrophic effect of adenosine A1 receptor stimulation via adenosine A1 receptor agonist R-PIA (1 µmol/L) was observed in the presence or absence of ERK1/2 inhibitor 1, 4-Diamino-2, 3-dicyano-1, 4-bis(o-aminophenylmercapto) butadiene (U0126) 1 µmol/L, PKC inhibitor Ro-31-8220 (50 nmol/L), and pertussis toxin (PTX, 5 mg/L). The total protein content was assayed by the method of Lowry. The expression of mRNA of atrial natriuretic peptide (ANP) was determined by RT-PCR. [Ca(2+)]i was measured by confocal microscope using Fluo-3/AM as fluorescent indicator. The relative expression of ERK1/2 was determined by Western blot. RESULTS: Compared with normal control group, AngII induced significant cardiomyocyte hypertrophy. Compared with AngII group, R-PIA significantly inhibited AngII-induced increase of the protein content, cardiomyocytes volume and expression of ERK1/2, calcium ion fluorescence intensity, similar as U0126 and Ro-31-8220. The inhibitory effects on AngII induced cardiomyocytes hypertrophy of R-PIA were lost when preincubated with PTX. CONCLUSION: Adenosine A1 receptor can inhibit AngII induced cardiomyocyte hypertrophy through downregulating ERK signal pathways and reducing intracellular Ca(2+).

[Treatment of lactic acidosis with early continuous blood purification].

OBJECTIVE: To observe the therapeutic effect of early continuous blood purification (CBP) on lactic acidosis patients. METHODS: Using prospective randomized study method, 41 patients with lactic acidosis in intensive care unit (ICU) from January 2010 to April 2012 were randomly divided into CBP group (n=21) and control group (n=20). Among them, blood gas analysis, lactic acid, blood biochemistry were prospectively monitored at the time before treatment, 12, 24 and 72 hours after treatment. They were also evaluated with acute physiology and chronic health evaluation II (APACHEII) score, and length of stay in ICU and mortality in 28 days were recorded. RESULTS: Lactic acid level and APACHEII score were gradually decreased after treatment in both groups. Compared with control group, lactic acid at 12, 24 and 72 hours in CBP group was obviously lowered (12 hours: 8.23±3.94 mmol/L vs. 12.47±4.62 mmol/L, 24 hours: 4.46±1.57 mmol/L vs. 10.54±3.48 mmol/L, 72 hours: 2.69±1.03 mmol/L vs. 5.74±1.56 mmol/L, all P<0.01), while the APACHEII score at 12, 24 and 72 hours in CBP group was also significantly lowered (12 hours: 18.23±5.85 vs. 21.64±5.38, 24 hours: 16.49±4.62 vs. 20.61±5.71, 72 hours: 11.54±3.67 vs. 16.02±4.34, all P<0.05). Compared with control group, length of stay in ICU was also significantly shorter in CBP group (6.58±3.45 days vs. 11.65±4.94 days, P<0.05), and 28-day mortality was significantly lower in CBP group (23.8% vs. 45.0%, P<0.05). CONCLUSION: Early correction of lactic acidosis with CBP could reduce the mortality of lactic acidosis.