Effects of short-acting β-adrenergic blocker on B-type natriuretic peptide at early stage of postresuscitation in rabbits

Postresuscitation myocardial dysfunction is reversible heart failure and B-type natriuretic peptide （BNP） is a biochemical marker of ventricular disorders secreted from ventricle, which can be used to assess the status of left ventricular function. This study investigated the effect of β-adrenergic blocker on concentration of BNP and cardiac function after cardiopulmonary resuscitation in rabbits.

β-Receptor blocker enhances the anabolic effect of PTH after osteoporotic fracture

The autonomic nervous system plays a crucial role in regulating bone metabolism,with sympathetic activation stimulating bone resorption and inhibiting bone formation.We found that fractures lead to increased sympathetic tone,enhanced osteoclast resorption,decreased osteoblast formation,and thus hastened systemic bone loss in ovariectomized(OVX)mice.However,the combined administration of parathyroid hormone(PTH)and theβ-receptor blocker propranolol dramatically promoted systemic bone formation and osteoporotic fracture healing in OVX mice.The effect of this treatment is superior to that of treatment with PTH or propranolol alone.In vitro,the sympathetic neurotransmitter norepinephrine(NE)suppressed PTH-induced osteoblast differentiation and mineralization,which was rescued by propranolol.Moreover,NE decreased the PTH-induced expression of Runx2 but enhanced the expression of Rankl and the effect of PTH-stimulated osteoblasts on osteoclastic differentiation,whereas these effects were reversed by propranolol.Furthermore,PTH increased the expression of the circadian clock gene Bmal1,which was inhibited by NE-βAR signaling.Bmal1 knockdown blocked the rescue effect of propranolol on the NE-induced decrease in PTHstimulated osteoblast differentiation.Taken together,these results suggest that propranolol enhances the anabolic effect of PTH in preventing systemic bone loss following osteoporotic fracture by blocking the negative effects of sympathetic signaling on PTH anabolism.

Treatment of Helicobacter pylori with potassium competitive acid blockers:A systematic review and meta-analysis

BACKGROUND Helicobacter pylori(H.pylori)infects over half the global population,causing gastrointestinal diseases like dyspepsia,gastritis,duodenitis,peptic ulcers,GMALT lymphoma,and gastric adenocarcinoma.Eradicating H.pylori is crucial for treating and preventing these conditions.While conventional proton pump inhibitor(PPI)-based triple therapy is effective,there’s growing interest in longer acid suppression therapies.Potassium competitive acid blocker(P-CAB)triple and dual therapy are new regimens for H.pylori eradication.Initially used in Asian populations,vonoprazan(VPZ)has been recently Food and Drug Administration-approved for H.pylori eradication.AIM To assess the efficacy of regimens containing P-CABs in eradicating H.pylori infection.METHODS This study,following PRISMA 2020 guidelines,conducted a systematic review and meta-analysis by searching MEDLINE and Scopus libraries for randomized clinical trials(RCTs)or observational studies with the following command:[("Helicobacter pylori"OR"H pylori")AND("Treatment"OR"Therapy"OR"Eradication")AND("Vonaprazan"OR"Potassium-Competitive Acid Blocker"OR"P-CAB"OR"PCAB"OR"Revaprazan"OR"Linaprazan"OR"Soraprazan"OR"Tegoprazan")].Studies comparing the efficacy of P-CABs-based treatment to classical PPIs in eradicating H.pylori were included.Exclusion criteria included case reports,case series,unpublished trials,or conference abstracts.Data variables encompassed age,diagnosis method,sample sizes,study duration,intervention and control,and H.pylori eradication method were gathered by two independent reviewers.Meta-analysis was performed in R software,and forest plots were generated.RESULTS A total of 256 references were initially retrieved through the search command.Ultimately,fifteen studies(7 RCTs,7 retrospective observational studies,and 1 comparative unique study)were included,comparing P-CAB triple therapy to PPI triple therapy.The intention-to-treat analysis involved 8049 patients,with 4471 in the P-CAB intervention group and 3578 in the PPI control group across these studies.The analysis revealed a significant difference in H.pylori eradication between VPZ triple therapy and PPI triple therapy in both RCTs and observational studies[risk ratio(RR)=1.17,95%confidence interval(CI):1.11-1.22,P<0.0001]and(RR=1.13,95%CI:1.09-1.17,P<0.0001],respectively.However,no significant difference was found between tegoprazan(TPZ)triple therapy and PPI triple therapy in both RCTs and observational studies(RR=1.04,95%CI:0.93-1.16,P=0.5)and(RR=1.03,95%CI:0.97-1.10,P=0.3),respectively.CONCLUSION VPZ-based triple therapy outperformed conventional PPI-based triple therapy in eradicating H.pylori,positioning it as a highly effective first-line regimen.Additionally,TPZ-based triple therapy was non-inferior to classical PPI triple therapy.

Use of Beta-Blocker in Acute ST-Elevation Myocardial Infarction

This paper reported beta-blocker use in 21 STEMI patients over four years. The patients were between 50 - 65 years of age presenting with anterior, lateral, and inferior STEMI (ST-Elevation Myocardial Infarction). Seven of the patients were female, and 14 were male. They presented to an emergency room of a rural hospital that did not provide emergency percutaneous coronary angioplasty/stenting (PTCA/stenting). The hospital is about 70 minutes from a facility that provided PTCA/ stenting—all the patients presented with typical angina chest pain with ST elevation. They are hemodynamic stable. Most patients received Lopressor 35 mg IVP, with one receiving 115 mg in a 5 mg increment. They were chest pain-free and hemodynamically before leaving the ER for the transfer for PTCA/stent. The results demonstrated that beta-blockers are effective in relieving pain in STEMI patients. Further study is needed to determine its efficacy, safety, and how to use it.

SNP Identification in α_(2A)-Adrenergic Receptor Gene in Chinese and the Effect on Gene Expression

Objective: To scan single nucleotide polymorphism ( SNP ) in Chinese alpha-2Aadrenergic receptor (α_(2A)-AR) gene and study the effects of the SNP on the gene expression.Methods: The complete sequence of α_(2A)-AR gene was analyzed with automated DNA sequencer to scanSNPs. Genomic DNA was extracted from whole blood and a 239 bp fragment containing the G/Cpolymorphism was amplified with PCR using a pair of. specific primers. PCR-RFLP was used to performthe genotyping of the SNP at the site-1 296 bp of the people in the North of China. Electrophoresismobility shift assay ( EMSA ) was used to study the binding of the 390 bp fragments (- 1 414-1 025bp) with G or C at the site-1 296 bp and nuclear extracts . Results: In our study, two SNPs werefound in α_(2A)-AR gene. Allele frequencies of the SNP at the site-1 296 bp were 0.61 and 0.39 forG and C , and the genotype frequencies were 0.34 , 0.54 and 0.13 for GG, GC and CC respectively fromthe people in the North of China. In the EMSA, a specific binding appeared in the complex ofnuclear extracts and DNA with C at-1 296 bp . Conclusion: Two SNPs exist in α_(2A)-AR gene from thepeople in the North of China , and DNA fragment with allele C of the SNP at the site-1 296 bp couldbind with a specific protein, which could influence the gene expression.

Regulation of bone metabolism mediated byβ-adrenergic receptor and its clinical application

Recent studies have confirmed thatβ-adrenergic receptors(β-ARs)are expressed on the surface of osteoblasts and osteoclasts,and that the sympathetic nervous system can regulate bone metabolism by activating them.β-AR blockers(BBs)are commonly used in the treatment of cardiovascular diseases in the elderly.It is important to investigate whether BBs have a beneficial effect on bone metabolism in the treatment of cardiovascular diseases,so as to expand their clinical application.This article reviews the effects of BB on bone metabolism and the progress of clinical research.

Developmental changes in functional expression andβ-adrenergic regulation of If in the heart of mouse embryo

The hyperpolarization-activated current (If) plays an important role in determining the spontaneous rate of cardiac pacemaker cells. The automatic rhythmicity also exists in working cells of embryonic heart, therefore we studied developmental changes in functional expression and β-adrenergic regulation of Iy in embryonic mouse heart. The expression of If is high in early developmental stage (EDS) (10.5 d after coitus) ventricular myocytes, low in intermediate developmental stage (IDS) (13.5 d) atrial or ventricular myocytes and even lower in late developmental stage (LDS) (16.5 d) atrial or ventricular myocytes, indicating that these cells of the EDS embryonic heart have some properties of pacemaker cells.β-adrenergic agonist isoproterenol (ISO) stimulates If in LDS but not in EDS cardiomyocytes, indicating that the β-adrenergic regulation of If is not mature in EDS embryonic heart. But forskolin (a direct activator of adenylate cyclase) and 8-Br-cAMP (a membrane-permeable analogue of cAMP) increase the amplitude of If in EDS cells, indicating that adenylate cyclase and cAMP function fairly well at early stage of development. Furthermore, the results demonstrate that If is modulated by phosphorylation via cAMP dependent PKA both in EDS and LDS cells.

Effects ofβ_2-Adrenergic Antagonist on Cytosolic Ca^(2+) in Ventricular Myocytes from Infarcted Rat Heart

Objectives To investigate the effects of β2-adrenergic antagonist on cytosolic Ca^2 ＋ （[Ca^2＋ ]i） in ventricular myocytes from infarcted rat heart. Methods A ligature was placed around left anterior descending coronary artery of rat hearts. Rats in the control group were sham-operated. Cardiomyocytes were dissociated at two, four, eight weeks after myocardial infarction （MI） and [Ca^2＋]i was measured via fura-2 fluorescence. The response of cardiomyocytes to isoproterenol in presence or absence of betal-adrenergic antagonist atenolol, beta2-adrenergic antagonist ICI118, 551 or non-selective β1, 2- adrenergic antagonists propranolol was examined. Results The followings were found that ICI 118, 551 had no significant effects on the rise of [Ca^2＋]i induced by isoproterenol in normal ventricular myocytes （P 〉 0.05）, ICI118, 551 only significantly attenuated the rise of [Ca^2＋]i induced by isoproterenol at four weeks and eight weeks after MI （24.5%±5.7% vs 57.8% ± 13.2%, P〈 0.01; 12.2%±7.9% vs 44.6%±11.3%, P〈 0.01）. Atenolol had suppressive effects only in the control group and the post-MI group of two weeks （P 〈 0.05）, and propranolol had suppressive effects in the control and all the three post-MI groups （P 〈 0.01）. Conclusions Beta2-adrenergic antagonist ICI118, 551 may exert negative effects on Ca^2＋ overload initiated by sympathetic stimulation after MI.

Inhibition of central sympathetic nervous tone improves cardiomyocyte contraction by increasing the response of beta 2-adrenergic receptor in aged rats

In the present study,selective β1-adrenergic receptor antagonist CGP20712A and selective β2-adrenergic receptor antagonist ICI 118551 were administered to isolated cardiomyocytes from young （4-6 months）,aged （18-20 months）,and clonidine-pretreated aged （18-20 months） Sprague-Dawley rats.Cardiomyocyte contraction amplitude was measured to assess cardiomyocyte response to the β-adrenergic receptor agonist,isoprenaline.CGP20712A reduced cardiomyocyte contraction amplitude in young and aged groups and significantly reduced contraction amplitude in cells from young rats.ICI 118551 had no effect on cardiomyocyte contraction amplitude in young rats,but significantly decreased contraction amplitude in the aged groups,in particular in the clonidine-pretreated aged rats.Results demonstrated that reduced central sympathetic tone improved cardiomyocyte contraction in aged rats by improving the response of β2-adrenergic receptor to isoprenaline.

Gene transfer of a β_2-adrenergic receptor kinase inhibitor up-regulates the level of β_2-adrenergic receptor and cAMP in the asthmatic murine lung

Objective： To investigate the effects of gene transfer of a β-adrenergic receptor（β-AR） kinase inhibitor（β ARIct） on pulmonary β2-adrenergic receptor and cAMP following β2-AR agonist treatment in asthmatic mice, and to analyze the relationship between the routes of gene delivery and the changes of β2AR and cAMP. Methods： BALB/c mice were sensitized and challenged by ovalbumin to establish the asthmatic model treated with βAR agonist （salbutamol injected intramuscularly）. The plasmid with the expression of βARKct was constructed and βARKct gene transfer was performed through intravenous injection or intratracheal instillation in asthmatic mice. The gene expression was measured with Western blot analysis, and the changes of pulmonary β-AR and cAMP evaluated by Radioimmunoassay. Results： The expression of tranfered βARKct gene was detectable in lungs and it was expressed more in the lungs of the mice receiving intratracheally plasmid than those receiving intravenously. The levels of βAR and cAMP were upregulated after using plasmid-βARKct to the asthmatic mice treated with βAR agonist. Conclusion： Our results indicated that there were down-regulation of βAR and cAMP in asthmatic mice treated with βAR agonist. Gene transfer of βARKct could inhibit the extent of the down-regulation of βAR and cAMP. The route of gene delivery could also affect the degree of up-regulation of βAR and cAMP. Gene transfer βARKct may provide a novel approach to the therapeutic strategy for asthma.

Effects of Propranolol on β-Adrenergic Receptor ofExperimental Acute Myocardial Infarction in Rats

By using receptor autoradiography to observe the distribution and density of receptors, the effects of propranolol, a β-blocker, on β-adrenergic receptor of experimental acute myocardial infarction (AMI) were studied. One week after ligation of proximate left anterior descend (LAD) coronary artery, [3H] DHA binding sites were markedly decreased in both infarctregion and non-infarct region. After treatment of propranolol (100μg/kg), the [3H] DHA binding sites were obviously increased in the infarct region, and they were further decreased in the non-infarct region. The ratio of [3H] DHA binding sites of the infarct region to non-infarct region was from 0. 24 at LAD ligation to 0. 87 after propranolol treatment, which was close to 0. 97 of control group (sham operation). The results indicated that the propranolol acted directly on myocardial β-adrenergic through the receptor regulation of the balance of β-receptors between the infarct region and non-infarct region, and improvement of the myocardial consonation and contraction synergism, thereby protecting the heart affected by AMI.

Genetic variations of beta 2-adrenergic receptor gene are associated with essential hypertension in Xinjiang Kazakans

Objective The aims of the present study were to investigate the associations of 46 A〉G, 79 C〉G, 491 C〉T and 659 C〉G genetic variants of the human beta 2-adrenergic receptor （β2-AR）, ADRB2, gene with essential hypertension （EH） in Xinjiang Kazakans population.Methods A gender-matched case-control （271 hypertensive cases and 267 normotensive controls） study was used to investigate the associations of the four variations in the coding region of ADRB2 with EH. The genotypes of the variants were identified by the polymerase chain reaction and restriction fragment length polymorphism （PCR-RFLP） methods. Results 46 A〉G, 79 C〉G and 659 C〉G polymorphisms were common in the Kazakan population, but 491 C〉T was a mutation （frequency ofT allele was only 0.003） and only found in EH group. The fxequency distributions of genotypes and alleles for 659 C〉G between the EH and control groups was significantly different （P〈0.05）, while those for 46 A〉G and 79 C〉G polymorphisms were not statistically different. Logistic regression analysis suggested that the G allele of 659 C〉G polymorphism was a risk factor for hypertension （minor allele vs common homo; odds ratio, 13.240, 95% CI, 4.052-43.274; P〈0.05）. Covariance analysis showed that systolic and diastolic blood pressure levels in GG＋CG group of 659 C〉G were significantly higher than those in the CC group, but no significant difference of blood pressure were found between common homo and minor allele for 46 A〉G and 79C〉G polymorphisms. Haplotype analysis showed that two hyplotypes, HI： 46A-79C-491C-523C（48%）and H5：46A-79C-491C-659G, were associated with EH.Conelusion ADRB2 genetic variants may play independent roles in the molecular genetic mechanism of EH in Xinjiang Kazakans population （d Geriatr Cardio12010; 7：52-57）.

Beta-adrenergic receptor polymorphisms: A basis for pharmacogenetics

Aims: Polymorphisms of the β-adrenergic receptor, the frequency of which may differ in ethnic groups, alters β-receptor function. The aim of this study was to elucidate the frequency of β1 and β2-adrenergic receptor polymorphisms in healthy Greeks and to compare with those of Caucasian European (Euro) and African American (AA) origin. Methods: Ninety-nine individuals with a median age of 63 without clinical evidence of any disease were studied. Blood samples were obtained and common β1 and β2-adrenergic receptor polymorphisms that change the en-coded amino acid were determined by pyrosequencing. Results: The most common β1-adrenergic receptor polymorphism in Greeks is nucleotide substitution cytosine for guanine at position 1165 (1165 C/G) resulting in amino acid substitution arginine for glycine at position 389 (389 Arg/Gly) with a minor allele frequency of 28% (Euro 27%, AA 42%);this polymorphism increases the sensitivity of the β1-receptor. The most common β2-adrenergic receptor polymorphism in Greeks is the nucleotide substitution guanine for adenine at position 46 (46 G/A) resulting in amino acid substitution glycine for arginine at position 16 (16 Gly/Arg) with a minor allele frequency of 38% (Euro 41%, AA 50%);this polymerphism facilitates receptor down-regulation during chronic adrenergic stimulation. Conclusion: The most common β1 and β2-adrenergic receptor polymorphisms in the Greek population are similar to those of other European ancestry, and less common than in those of African origin indicating variability in ethnic groups. This information provides insight into common polymorphisms that may assist in optimizing β-antagonist and agonist therapy.

Activation of β_2-Adrenergic Receptor Induced by Three Catecholamine Agonists:a Docking and Molecular Dynamics Study

We studied the activation of β2-adrenergic receptor（β2AR） by norepinephrine, epinephrine and isoprote- renol using docking and molecular dynamics（MD） simulation. The simulation was done on the assumption that β2AR was surrounded with explicit water and infinite lipid bilayer membrane at body temperature. So the result should be close to that under the physiological conditions. We calculated the structure of binding sites in β2AR for the three ac- tivators. We also simulated the change of the conformation ofβ2AR in the transmembrane regions（TMs）, in the mo- lecular switches, and in the conserved DRY（Aspartic acid, Arginine and Tyrosine） motif. This study provides detailed information concerning the structure ofβ2AR during activation process.

Impact of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers on the mortality in sepsis: A meta-analysis

BACKGROUND The effect of angiotensin-converting enzyme inhibitors(ACEIs)or angiotensin receptor blockers(ARBs)on the mortality of patients with sepsis is not well characterized.AIM To elucidate the association between prior ACEI or ARB exposure and mortality in sepsis.METHODS The PubMed,EMBASE,Web of Science,and Cochrane Library databases were searched for all studies of premorbid ACEI or ARB use and sepsis mortality until November 302019.Two reviewers independently assessed,selected,and ab-stracted data from studies reporting ACEIs or ARBs,sepsis,and mortality.The primary extracted data consisted of premorbid ACEI or ARB exposure,mortality,and general patient data.Two reviewers independently assessed the risk of bias and quality of evidence.RESULTS A total of six studies comprising 281238 patients with sepsis,including 49799 cases with premorbid ACEI or ARB exposure were eligible for analysis.Pre-morbid ACEIs or ARBs exposure decreased the 30-d mortality in patients with sepsis.Moreover,the use of ACEIs or ARBs was associated with approximately a 6%decreased risk of 30-d mortality.CONCLUSION The results of this systematic review suggest that ACEI or ARB exposure prior to sepsis may be associated with reduced mortality.Further high-quality cohort studies and molecular mechanism experiments are required to confirm our results.

Association between Depression, Pressure Pain Sensitivity, Stress and Autonomous Nervous System Function in Stable Ischemic Heart Disease: Impact of Beta-Adrenergic Receptor Blockade

Background: Depression and ischemic heart disease (IHD) are associated with persistent stress and autonomic nervous system (ANS) dysfunction. The former can be measured by pressure pain sensitivity (PPS) of the sternum, and the latter by the PPS and systolic blood pressure (SBP) response to a tilt table test (TTT). Beta-blocker treatment reduces the efferent beta-adrenergic ANS function, and thus, the physiological stress response. Objective: To test the effect of beta-blockers on changes in depression score in patients with IHD, as well as the influence on persistent stress and ANS dysfunction. Methods: Three months of non-pharmacological intervention aiming at reducing PPS and depression score in patients with stable IHD. Beta-blocker users (N = 102) were compared with non-users (N = 75), with respect to signs of depression measured by the Major Depressive Inventory questionnaire (MDI), resting PPS, and PPS and SBP response to TTT. Results: MDI score decreased 30% in non-users (p = 0.005) compared to 4% (p > 0.1) among users (between-group p = 0.003;effect size = 0.4). Resting PPS decreased in both the groups. Among most vulnerable patients with MDI ≥ 15, reductions in MDI score and resting PPS score correlated in non-users, only (r = 0.69, p = 0.007). Reduction in resting PPS correlated with an increase in PPS and SBP response to TTT. Conclusions: Stress intervention in patients with IHD was anti-depressive in non-users, only. Similarly, the association between the reduction in depression, reduction in persistent stress, and restoration of ANS dysfunction was only seen in non-users, suggesting a central role of beta-adrenergic receptors in the association between these factors.

厄贝沙坦通过调节NLRP3表达在糖尿病肾病大鼠中的保护作用

目的 观察糖尿病肾病大鼠中NLRP3(NOD-like receptor protein 3)的表达,并在沉默NLRP3和以血管紧张素受体抑制剂(ARB)厄贝沙坦干预后观察NLRP3及炎症和纤维化因子的表达变化,探讨厄贝沙坦对糖尿病肾病大鼠的保护作用。方法 雄性SD大鼠随机分成5组:对照(Control)组、模型(Model)组、空载(Model+Blank)组、NLRP3沉默(Model+NLRP3 Sh)组、ARB(Model+ARB)组,分别在糖尿病肾病模型建立后8周、12周处死大鼠并收集肾脏组织。实时荧光定量PCR检测NLRP3、半胱氨酸天冬氨酸蛋白酶-1(Caspase-1)、核因子κB(NF-κB)P65和波形蛋白(Vimentin)的mRNA表达水平;Western blot检测NLRP3、P65、热休克蛋白47(heat shock protein 47,HSP47)和Vimentin的蛋白表达水平;免疫荧光法观察NLRP3、Caspase-1和Vimentin的表达;PAS、PASM和Masson染色观察肾脏病理改变。结果 与对照组比较,模型组及空载组NLRP3、Caspase-1、P65和Vimentin mRNA的表达升高(均P<0.05),NLRP3、Caspase-1、P65、HSP47和Vimentin的蛋白表达升高(均P<0.05)。与模型组及空载组相比,NLRP3沉默组及ARB组的上述指标表达均下调(均P<0.05),模型组与空载组以上指标之间差异无统计学意义。病理染色结果显示NLRP3沉默和厄贝沙坦干预可减轻糖尿病肾病大鼠肾脏损害,减轻肾小球肥大、肾小球硬化、系膜扩张、间质纤维化。结论 糖尿病肾病大鼠肾脏NLRP3信号通路被激活,且炎性和纤维化因子表达上调。厄贝沙坦可阻断NLRP3信号通路,减轻肾脏损害。天然免疫受体NLRP3可能成为治疗糖尿病肾病的新靶点。

氟比洛芬酯对胸腔镜右肺叶切除术患者单肺通气期间肺功能的影响

目的观察氟比洛芬酯对胸腔镜右肺叶切除术患者采用封堵器行单肺通气期间肺氧合功能、呼吸力学及肺部并发症的影响。方法选择择期全麻下行胸腔镜右肺叶切除术采用封堵器行单肺通气的患者60例,男25例,女35例,年龄35~64岁,BMI 18~28 kg/m^(2),ASAⅠ或Ⅱ级。采用随机数字表法将患者分为两组:氟比洛芬酯组(F组)和对照组(C组),每组30例。F组在麻醉诱导前15 min静注氟比洛芬酯1.0 mg/kg,C组不予处理。于麻醉诱导前20 min(T_(0))、单肺通气30 min(T_(1))、单肺通气60 min(T_(2))、双肺通气15 min(T_(3))时抽取桡动脉血行血气分析,计算氧合指数(OI)并记录SpO_(2)。记录T_(1)、T_(2)时的气道峰压(Ppeak)、气道平台压(Pplat)、肺动态顺应性(Cdyn)和无效腔气量与潮气量之比(V_(D)/V_(T))。记录单肺通气期间低氧血症发生情况、补救例数、术后转ICU例数、术后72 h内肺不张、急性肺损伤和肺炎发生情况。结果与C组比较,F组T_(1)时SpO_(2)、T_(1)—T_(3)时PaO_(2)和OI、T_(1)、T_(2)时Cdyn明显升高(P<0.05);T_(1)、T_(2)时Ppeak和V_(D)/V_(T)、T_(2)时Pplat明显降低(P<0.05)。两组无一例单肺通气期间发生低氧血症和补救、术后转入ICU、术后72 h内发生肺不张、急性肺损伤和肺炎。结论对胸腔镜右肺叶切除术采用封堵器行单肺通气的患者,麻醉诱导前静注氟比洛芬酯有助于改善单肺通气期间肺氧合功能,优化呼吸力学参数。

预先单肺通气联合呼吸暂停对支气管封堵器用于胸腔镜手术单肺通气时肺萎陷的影响

目的 探讨预先单肺通气(OLV)联合呼吸暂停对支气管封堵器(BB)用于胸腔镜手术行OLV时肺萎陷的影响。方法 选择择期行胸腔镜下左肺段或肺叶切除术的患者75例,随机分为预先OLV组(A组)、呼吸暂停组(B组)和预先OLV联合呼吸暂停组(C组),每组25例。记录3组打开胸膜到肺完全萎陷的时间、外科医生满意度、进胸前准备时间、OLV时间、手术时间和OLV开始至胸膜打开后20 min内低氧血症[经皮动脉血氧饱和度(SpO_(2))<90%]的发生情况;记录3组胸膜腔开放即刻(T_0)、胸膜腔开放后1 min (T_1)、5 min (T_2)、10 min (T_3)和20 min (T_4)的肺萎陷评分(LCS)。结果 与A组和B组比较,C组肺完全萎陷时间明显缩短,外科医生满意度明显提高,差异均有统计学意义(P <0.05),A组和B组肺完全萎陷时间和外科医生满意度比较,差异均无统计学意义(P> 0.05);与A组比较,B组T0时点LCS低于A组,而在T_1时点,则明显高于A组,C组T_(1)、T_(2)、T_(3)和T_(4)时点LCS明显高于A组和B组,差异均有统计学意义(P <0.05);C组T2时点SpO_(2)明显低于A组和B组,差异有统计学意义(P <0.05)。结论 对于用BB行OLV的胸腔镜手术患者,预先使用OLV联合呼吸暂停,可以改善非通气侧肺的肺萎陷效果,缩短了肺完全萎陷时间,提高了外科医生满意度,且OLV的早期LCS更高,但仍需监测OLV期间的SpO_(2)。

真实世界中伊伐布雷定在急性心肌梗死住院患者中使用状况的单中心回顾性分析

目的 分析本中心急性心肌梗死住院患者伊伐布雷定的使用状况。方法 回顾性分析2019年1月至2020年4月天津市人民医院1 021例急性心肌梗死住院患者的临床资料,连续选取其中100例资料完整的使用伊伐布雷定、合用或未合用美托洛尔缓释片的患者作为观察组,另外连续选取同期100例使用美托洛尔缓释片、未使用伊伐布雷定的患者作为对照组。比较两组患者的基线特征、治疗前后心率、收缩压和舒张压变化;分析观察组伊伐布雷定的使用原因;描述观察组伊伐布雷定和美托洛尔缓释片的剂量调整情况;记录观察组中与伊伐布雷定相关的不良反应。结果 两组患者的前壁心肌梗死和非ST段抬高型心肌梗死比例、Killip心功能分级Ⅰ和Ⅱ级比例、治疗前心率、收缩压和舒张压、治疗前左心室射血分数、主动脉内球囊反搏植入比例、肌酸激酶峰值和B型利钠肽峰值比较,差异均有统计学意义(均为P<0.01)。对照组治疗前后心率、收缩压和舒张压变化均有统计学差异(均为P<0.001);观察组治疗前后心率变化有统计学差异(P<0.001),收缩压和舒张压变化无统计学差异(均为P>0.05)。观察组使用伊伐布雷定的主要原因为医生担心患者血压偏低或心功能不能耐受β受体阻滞剂。观察组初始有89例(89.0%)患者合用了美托洛尔缓释片,伊伐布雷定和美托洛尔缓释片的剂量呈“此消彼长”的变化,未出现与伊伐布雷定相关的严重不良反应。结论 本中心的数据表明,在临床实践中伊伐布雷定通常用于心率偏快、血压偏低、合并心功能不全的急性心肌梗死患者,特别是前壁心肌梗死患者。通过与β受体阻滞剂联合使用,调整剂量,可以安全、有效地控制急性心肌梗死患者住院期间心率。