The Clinical Effect of High-Flow Oxygen Therapy through the Nose on Patients with Acute Left Heart Failure and Hypoxemia.

Objective: To evaluate the clinical efficacy of nasal high-flow oxygen therapy in patients with acute left heart failure and hypoxemia. Methods: From July 2016 to November 2018, patients with acute left heart failure complicated with hypoxemia treated in the Department of Critical Medicine of Yantai Affiliated Hospital of Binzhou Medical University were retrospectively observed (a total of 140 cases met the inclusion criteria). They were randomly divided into two groups, with 70 cases in each group. Patients were given continuous ECG monitoring, improved blood gas analysis test, and recorded HR, RR, map, SaO2, pH, PaO2, PaCO2, and Lac, perfect examination and color Doppler echocardiography, and record NT-proBNP and EF before and 24 hours after treatment. The effective rates of the two groups before and after oxygen therapy were detected. Results: There were 67 patients with high-flow oxygen therapy group improvement, 95.7% improvement rate, and 55 patients with general oxygen therapy group improvement rate. The treatment improvement rate was 78.6%. A total of 67 patients were treated with high-flow oxygen therapy. After high-flow oxygen therapy, HR (t = 18.8, P ≤ 0.05), RR (t = 19.7, P ≤ 0.05), MAP (t = 12.1, P ≤ 0.05), PaCO2 (t = 9.53, P ≤ 0.05), Lac (t = 8.69, P ≤ 0.05), and NT-proBNP (t = 7.03, P ≤ 0.05) were significantly lower than before. SaO2 (t = -12.4, P ≤ 0.05), pH (t = -12.2, P ≤ 0.05), PaO2 (t = -17.7, P ≤ 0.05), and EF (t = -13.4, P ≤ 0.05) were significantly higher than before. A total of 55 patients were in the general oxygen therapy group. After administration of ordinary oxygen therapy, HR (t = 18.2, P ≤ 0.05), RR (t = 10.8, P ≤ 0.05), MAP (t = 13.1, P ≤ 0.05), PaCO2 (t = 15.8, P ≤ 0.05), Lac (t = 7.1, P ≤ 0.05), and NT-proBNP (t = 10, P ≤ 0.05) were significantly lower than before. SaO2 (t = -15.5, P ≤ 0.05), pH (t = -4.5, P ≤ 0.05), PaO2 (t = -20, P ≤ 0.05), and EF value (t = -7.7, P ≤ 0.05) were significantly higher than before. Conclusion: High-flow oxygen therapy and general oxygen therapy have an obvious curative effect on patients with acute left heart failure and hypoxemia. Compared with the two, high-flow oxygen therapy is more effective. After high-flow oxygen therapy and general oxygen therapy in patients with acute left heart failure and hypoxia, HR, RR, MAP, SaO2, pH, PaO2, PaCO2, Lac, EF, and NT-proBNP value all improved, and the improvement of high-flow oxygen therapy was greater.

Short-term efficacy of ticagrelor in acute ST-segment elevation myocardial infarction patients undergoing an emergency percutaneous coronary intervention.

In total, 97 acute ST-segment elevation myocardial infarction (STEMI) patients who received an emergency percutaneous coronary intervention (PCI) were enrolled and divided into a ticagrelor group and a clopidogrel group. Thrombolysis in myocardial infarction (TIMI) blood flow and the corrected TIMI frame count (CTFC) were used to assess the blood perfusion of culprit vessels. Thromboelastography (TEG) was used to evaluate the antiplatelet effect of drugs. The results showed that the incidence of TIMI grade III blood flow in the ticagrelor group was significantly higher than that in the clopidogrel group. The CTFC in the anterior descending, circumflex, and right coronary arteries was statistically significantly lower in the ticagrelor group as compared with that in the clopidogrel group. At 2 h and 7 d postdrug treatment, the adenosine diphosphate-induced platelet inhibition rate (ADP%) in the ticagrelor group increased significantly as compared with that in the clopidogrel group, and the platelet aggregation rate of the ADP pathway (MAADP) decreased significantly in the ticagrelor group versus that in the clopidogrel group. In conclusion, ticagrelor significantly improved TIMI blood flow and had a better antiplatelet effect than clopidogrel in STEMI patients undergoing an emergency PCI.

Downregulation of NLRP2 inhibits HUVEC viability by inhibiting the MAPK signaling pathway.

Nucleotide­binding oligomerization domain (NOD)­like receptor proteins (NLRPs) are a subfamily of NOD­like receptors (NLRs) that mainly participate in innate immunity. Among the 14 NLRPs, studies on NLRP2 are few and mostly focus on its functions in reproduction and embryonic development. To the best of the authors' knowledge, there has been no research on the function of NLRP2 in human umbilical vein endothelial cells (HUVECs). The present study knockdown the expression of NLRP2 by transfecting a short interfering (si)RNA (siNLRP2) into HUVECs and investigating its effects on HUVECs. It was identified using a Cell Counting kit­8 assay that knockdown of NLRP2 can inhibit cell proliferation in HUVECs. The results of wound healing and Transwell assays indicated that migration and invasion were also suppressed by siNLRP2 transfection in HUVECs. Flow cytometry demonstrated that siNLRP2 induced cell cycle arrest and apoptosis in HUVECs. Western blot analysis revealed that the expression levels of cell cycle and apoptosis­associated proteins were markedly changed. In addition, knockdown of NLRP2 inhibited the mitogen­activated protein kinase (MAPK) signaling pathway by elevating extracellular signal­regulated kinase phosphorylation levels and reducing proto­oncogene serine/threonine­protein kinase expression. Taken together, it was concluded that NLRP2 served an important role in maintaining cell viability, proliferation and motility in HUVECs, mainly by promoting the MAPK signaling pathway.

Down-regulation of lncRNA OGFRP1 induces autophagy and growth inhibition by AKT/mTOR signaling pathway in HCAECs.

Long noncoding RNAs (lncRNAs) have been found to play important roles in nearly all biological processes. However, the functions of the majority of LncRNAs are not fully clear. Here we evaluated the function of lncRNA OGFRP1, which has not been previously annotated, in human coronary artery endothelial cells (HCAECs). First, we knocked down lncRNA OGFRP1 in HCAECs by using siRNA transfection. qRT-PCR results indicated that siRNA1 and siRNA3 both had potent interference efficiencies. Next, by using CCK8 assay and clone formation assay, we found that siRNA3 transfection induced growth inhibition in HCAECs. Cell migration and invasion were also found to be inhibited in OGFRP1 silenced cells. Moreover, siRNA1 transfection further verified the inhibitory effects of lncRNA OGFRP1 knockdown on the proliferation, migration and invasion of HCAECs. Flow cytometry detection demonstrated that OGFRP1 knockdown induced cell cycle arrest and apoptosis. Western blot assay indicated that p70S6K and CyclinD1 were down-regulated by knockdown of OGFRP1. The intrinsic apoptosis pathway was activated in lncRNA OGFRP1 silenced cells, including increased Bax and Active-caspase 3 and decreased Bcl2. The expression of autophagy markers LC3 and Beclin1 was increased and p62 decreased, all of which indicated that cell autophagy was promoted by down-regulation of lncRNA OGFRP1. Mechanistic studies showed that lncRNA OGFRP1 inhibited the AKT/mTOR signaling pathway, including increasing phosphorylation level of AKT, mTOR and GSK3ß. In conclusion, we find that down-regulation of lncRNA induces autophagy and inhibited the proliferation, migration and invasion by AKT/mTOR signaling pathway in HCAECs.

WITHDRAWN: Simvastatin prevents decreased SERCA2a activity in non-ischemic heart failure in rabbits via inhibition of ß-adrenergic signaling.

The Publisher regrets that this article is an accidental duplication of an article that has already been published, http://dx.doi.org/10.1016/j.biomag.2010.09.003. The duplicate article has therefore been withdrawn.

[Effects of valsartan on myocardial calcium/calmodulin-dependent protein kinase-II expression and activity in a rabbit model of heart failure].

OBJECTIVE: To investigate the effects of valsartan on myocardial expression and activity of calcium/calmodulin-dependent protein kinase-II (CaMK II) in a rabbit model of heart failure. METHODS: Rabbits were divided into sham-operated group, heart failure group (volume overload by aortic valve destruction induced aortic insufficiency plus pressure overload induced by abdominal aortic banding) and heart failure plus valsartan (20 mg x kg(-1) x d(-1), n = 9 each). Seven weeks later, echocardiography and hemodynamic examinations were performed and myocardial CaMK II expression and activity were detected by Western blot and CaMK II activity assay kit, respectively. RESULTS: Compared with the sham operated rabbits, left ventricular mass index [LVMI (3.61 +/- 0.09) g/kg vs. (1.32 +/- 0.06) g/kg, P<0.05] and end-diastolic pressure [LVEDP (23.00 +/- 2.37) mm Hg (1 mm Hg = 0.133 kPa) vs. (-1.50 +/- 0.5) mm Hg, P<0.05] were significantly increased while left ventricular shortening fractions [LVFS (17.38 +/- 3.13)% vs. (37.83 +/- 3.58)%, P<0.05] and ejection fraction [LVEF (38.50 +/- 6.07)% vs. (71.92 +/- 4. 56)%, P<0.05] were significantly decreased (all P<0.05) in heart failure rabbits, these changes could be significantly attenuated by valsartan treatment: LVMI [(2.07 +/- 0.14) g/kg vs. (3.61 +/- 0.09) g/kg, P<0.05], LVEDP [(2.17 +/- 0.72) mm Hg vs. (23.00 +/- 2.37) mm Hg, P<0.05], LVFS [(33.83 +/- 2.85)% vs. (17.38 +/- 3.13)%, P<0.05] and LVEF [(64.45 +/- 3.66)% vs. (38.50 +/- 6.07)%, P<0.05]. CaMK II expression (1.45 +/- 0.13 vs 0.89 +/- 0.05, 1.13 +/- 0.12, P<0.05) and activity [(3.54 +/- 0.17) pmol x min(-1) x microg(-1) vs. (2.18 +/- 0.13) pmol x min(-1) x microg(-1), (2.79 +/- 0.14) pmol x min(-1) x microg(-1), P<0.05] in heart failure rabbits were significantly increased than those sham operated rabbits which could be significantly attenuated by valsartan treatment. CONCLUSION: Valsartan improved cardiac function in heart failure rabbits probably via downregulating myocardial CaMK II expression and activity.

[Effects of valsartan on sarcoplasmic reticulum calcium adenosine triphosphatase, protein kinase A and protein phosphatase 1 alpha in a rabbit model of heart failure].

OBJECTIVE: To investigate the effects of valsartan on expressions of myocardial sarcoplasmic reticulum calcium adenosine triphosphatase (SERCA2), protein kinase A (PKA) and protein phosphatase 1 alpha (PP1alpha) in a rabbit model of heart failure. METHODS: Rabbits were divided into sham-operated group, heart failure group (volume overload by aortic valve destruction induced aortic insufficiency plus pressure overload induced by abdominal aortic banding) and heart failure plus valsartan (20 mgxkg(-1)xd(-1), n = 6 each). Seven weeks later, echocardiography examination was performed and SERCA2, PKA, PP1alpha protein and mRNA expressions were detected by Western blot and RT-PCR. RESULTS: Compared with the with sham operated rabbits, LVMI and LVEDP in heart failure rabbits were significantly increased while left ventricular shorten fraction (LVFS) and ejection fraction (EF) were significantly decreased (all P < 0.05), these changes could be significantly attenuated by valsartan treatment (all P < 0.05). SERCA2, PKA expressions at protein and mRNA levels were significantly downregulated and PP1alpha expressions significantly upregulated in heart failure rabbits than sham operated rabbits (all P < 0.05) and these changes could be significantly attenuated by valsartan (all P < 0.05). CONCLUSION: Valsartan improved cardiac function in volume and pressure overload induced heart failure rabbits possibly by upregulating expressions of myocardial SERCA2, PKA and downregulating expression of myocardial PP1alpha.