Mitophagy in intracerebral hemorrhage:a new target for therapeutic intervention

Intracerebral hemorrhage is a life-threatening condition with a high fatality rate and severe sequelae.However,there is currently no treatment available for intracerebral hemorrhage,unlike for other stroke subtypes.Recent studies have indicated that mitochondrial dysfunction and mitophagy likely relate to the pathophysiology of intracerebral hemorrhage.Mitophagy,or selective autophagy of mitochondria,is an essential pathway to preserve mitochondrial homeostasis by clearing up damaged mitochondria.Mitophagy markedly contributes to the reduction of secondary brain injury caused by mitochondrial dysfunction after intracerebral hemorrhage.This review provides an overview of the mitochondrial dysfunction that occurs after intracerebral hemorrhage and the underlying mechanisms regarding how mitophagy regulates it,and discusses the new direction of therapeutic strategies targeting mitophagy for intracerebral hemorrhage,aiming to determine the close connection between mitophagy and intracerebral hemorrhage and identify new therapies to modulate mitophagy after intracerebral hemorrhage.In conclusion,although only a small number of drugs modulating mitophagy in intracerebral hemorrhage have been found thus far,most of which are in the preclinical stage and require further investigation,mitophagy is still a very valid and promising therapeutic target for intracerebral hemorrhage in the long run.

Knockdown of NADPH oxidase 4 reduces mitochondrial oxidative stress and neuronal pyroptosis following intracerebral hemorrhage

Intracerebral hemorrhage is often accompanied by oxidative stress induced by reactive oxygen species,which causes abnormal mitochondrial function and secondary reactive oxygen species generation.This creates a vicious cycle leading to reactive oxygen species accumulation,resulting in progression of the pathological process.Therefore,breaking the cycle to inhibit reactive oxygen species accumulation is critical for reducing neuronal death after intracerebral hemorrhage.Our previous study found that increased expression of nicotinamide adenine dinucleotide phosphate oxidase 4(NADPH oxidase 4,NOX4)led to neuronal apoptosis and damage to the blood-brain barrier after intracerebral hemorrhage.The purpose of this study was to investigate the role of NOX4 in the circle involving the neuronal tolerance to oxidative stress,mitochondrial reactive oxygen species and modes of neuronal death other than apoptosis after intracerebral hemorrhage.We found that NOX4 knockdown by adeno-associated virus(AAV-NOX4)in rats enhanced neuronal tolerance to oxidative stress,enabling them to better resist the oxidative stress caused by intracerebral hemorrhage.Knockdown of NOX4 also reduced the production of reactive oxygen species in the mitochondria,relieved mitochondrial damage,prevented secondary reactive oxygen species accumulation,reduced neuronal pyroptosis and contributed to relieving secondary brain injury after intracerebral hemorrhage in rats.Finally,we used a mitochondria-targeted superoxide dismutase mimetic to explore the relationship between reactive oxygen species and NOX4.The mitochondria-targeted superoxide dismutase mimetic inhibited the expression of NOX4 and neuronal pyroptosis,which is similar to the effect of AAV-NOX4.This indicates that NOX4 is likely to be an important target for inhibiting mitochondrial reactive oxygen species production,and NOX4 inhibitors can be used to alleviate oxidative stress response induced by intracerebral hemorrhage.

Preventive and therapeutic effect of simvastatin on secondary inflammatory damage of rats with cerebral hemorrhage

Objective:To investigate the preventive and therapeutic effect and mechanism of simvastatin on secondary inflammatory damage of rats with cerebral hemorrhage.Methods:Sixty SD rat aged 9-12 weeks were chosen and divided into the control group,model group and simvastatintreated group randomly with 20 rats in each group.Rats in the model group and simvastatintreated group were infused with autologous fresh uncoagulated blood to the right brain tissue of the basal ganglia to build the cerebral hemorrhage model,while rats in the control group were treated with the same amount of normal saline.Then,rats in the simvastatin-treated group were given a gavage of 3 mg/kg of simvastatin once a day after modeling.Rats in the three groups were given nerve dysfunction score(NDS) and wet-dry weighting method was used to detect the brain water content(BWC) of brain tissues around the lesion of the rats.Then Nissl staining was conducted and the undamaged neurons were counted.Immunohistochemical SP method was applied to count the number of NF-d the immuno fluorκB,TLR4 and IL-1escence method wasβ positive cells in brain tissues around the lesions,an employed to determine the expression levels of NF-κB,TLR4 and IL-1me points were aβ proteins.Results:The NDS results of the simvastatin-treated group at all till significantly higher than those of the model group(P < 0.05);the BWC values of the simvastatin-treated group at all time points were all significantly lower than those of the model group at the same periods(P < 0.05);the number of the undamaged neurons around the lesions of the simvastatin-treated group at all time points were all significantly higher than those of the model group(P < 0.05);seven days after treatment,the number of the NF-κB,TLR4 and IL-1β positive cells in brain tissues around the lesions of the simvastatin-treated group were all significantly lower than those of the model group(P < 0.05),and its expression levels of NF-ower than those of the model group(κB,TLR4 and IL-1P < 0.05).Conclusioβ protein were also significantly lns:Simvastatin can inhibit the expressions of NF-κB,TLR4 and IL-1β proteins in rats with cerebral hemorrhage,and protect neurons and reduce secondary inflammatory damages by down-regulating the above protein-mediated inflammatory responses.

Expression of yeast silencing information regulator 2 in secondary injury of intracerebral hemorrhage

Objective:to investigate the expression of yeast silencing information regulator 2(Sirt2)in the secondary injury of intracerebral hemorrhage(ICH).Methods:twelve Sprague Dawley(SD)rats were randomly divided into a sham group and an ICH group,with six rats in each group.A rat model of ICH was established by injecting collagenase type IV into the right striatum of the rats.The expression of Sirt2 was measured by Western blot and immunohistochemistry after ICH.Result:the behavioral score of the ICH rats was the lowest at 48 h after the operation;therefore the rats at 48 h after surgery were selected as the model rats.The expression of Sirt2 was significantly higher in the striatal tissue of the ICH rats compared with the sham group(P<0.05).Conclusion:the expression of Sirt2 around hematoma in ICH rats decreases,and Sirt2 is expected to become a new target for ICH treatment.

Perihematoma Damage at Different Time Points in Experimental Intracerebral Hemorrhage

The damage degree of neurons in perilesion at different time points was observed in order to explore the optimal operation occasion. Piglet lobar hematomas were produced by pressure-controlled infusions of 2.5 mL autonomous blood into the right frontal hemispheric white matter over 15 min, and the metabolic changes were ambulatorily detected with MRS at 3rd, 12th, 24th and 48th h after hematoma induction. Brain tissues of perihematoma were also obtained at different time points. The transcription level of Bax gene was detected by in situ hybridization and apoptosis by TUNEL technique, and the pathologic change of neurons was observed under an electron microscope. The results showed that the number of Bax positive cells reached the peak at 24 h （79.00± 4.243/5 fields）. There was no significant difference in A values between 3 h and 6 h, 12 h （P〉 0. 05）, but there significant difference between 24 h and 3 h, 6 h, 12 h （P〈0. 05）. The number of apoptotic cells reached the peak at 24 h （P〈0. 001）, and there was no significant difference between 3 h and 6 h （P=0. 999）. The area of the apoptotic cells showed no significant difference between 3 h and 6 h or among 3 h, 6 h and 6 h （P〉0.05）. Lac peak mainly occurred at 24 h and 48 h, while on the healthy side, no Lac peak was detectable. The ratio of NAA/Cr presented a descent tendency, but there was no significant difference among the groups before 12 h （P〉0. 05）, there was very significant difference between 3, 6 and 24, 48 h （P〈0. 01）. Under electronic microscopy, the neuronal damage surrounding hematoma in 3 to 6 h was milder than in 24 h to 48 h. It was concluded that the secondary apoptosis, damage and metabolic disturbance of the neurons surround- ing hematoma was milder in 3-6 h in acute intracerebral hemorrhage, while obviously aggravated in 24-48 h. An effective intervention is needed to reduce secondary damage as soon as possible.

Oxidized low-density lipoprotein receptor 1:a novel potential therapeutic target for intracerebral hemorrhage

Oxidized low-density lipoprotein receptor 1(OLR1)is upregulated in neurons and participates in hypertension-induced neuronal apoptosis.OLR1 deletion exerts protective effects on cerebral damage induced by hypertensive-induced stroke.Therefore,OLR1 is likely involved in the progress of intracerebral hemorrhage.In this study,we examined the potential role of OLR1 in intracerebral hemorrhage using a rat model.OLR1 small interfering RNA(10μL;50 pmol/μL)was injected into the right basal ganglia to knock down OLR1.Twenty-four hours later,0.5 U collagenase type VII was injected to induce intracerebral hemorrhage.We found that knockdown of OLR1 attenuated neurological behavior impairment in rats with intracerebral hemorrhage and reduced hematoma,neuron loss,inflammatory reaction,and oxidative stress in rat brain tissue.We also found that silencing of OLR1 suppressed ferroptosis induced by intracerebral hemorrhage and the p38 signaling pathway.Therefore,silencing OLR1 exhibits protective effects against secondary injury of intracerebral hemorrhage.These findings suggest that OLR1 may be a novel potential therapeutic target for intracerebral hemorrhage.

Incidence of Hemorrhage after ENT Procedures and Seasonal Variation: A Retrospective Study and Literature Review

Background: Ear, nose, throat procedures are the most performed procedures for adults and children per year. Doctors might have noticed that at certain times of the year, there would be an increase in admissions of post tonsillectomy bleeding or epistaxis after nasal surgeries. Objectives: To determine whether a correlation exists between season and the rate of hemorrhage presentation after ear, nose, throat procedures. Methods: A 12-year retrospective review from January of 2003 to June of 2015, involving 1032 patients who developed secondary hemorrhage following ear, nose, throat related surgeries. We analyzed the presentation of hemorrhage in relation to the month of admission. Meteorological data were obtained from the Meteorological directorate of Bahrain. Results: Post-Operative Hemorrhage occurred in (1032) patients. The season and air temperature had a significant influence on secondary post-tonsillectomy hemorrhage and post-septoplasty epistaxis according to the age with a significant increase in their rate during the summer months (p < 0.05). Conclusion: The incidence of hemorrhage showed monthly and seasonal variations. This is clearly a multi-factorial problem. However, in patients at high risk of bleeding, consideration should be given to performing surgeries at a time of year of lower rates.

靶向抑制铁死亡在脑出血后继发性脑损伤治疗中的作用研究进展

脑出血后继发性脑损伤(SBI-ICH)可导致神经元的不可逆损伤。研究表明,细胞铁死亡可以介导脑出血后神经元死亡的病理过程,而抑制铁死亡能够有效地减少SBI-ICH。作者综述了铁死亡参与SBI-ICH的发病机制及药物靶向抑制铁死亡在SBI-ICH防治方面应用的研究进展,以期为脑出血防治方法的探索提供帮助。

铁死亡的发生机制及其在脑出血中的作用与相关药物治疗研究进展

铁死亡是一种新发现的、铁依赖性的非凋亡性细胞死亡方式,参与多种疾病的病理过程。脑出血是一种高发病率、高死亡率、高致残率的疾病,是神经科常见的急危重症,预后不良,极大地威胁人类的健康。脑出血引起的脑组织原发性损伤与细胞毒性、神经炎症、氧化应激等相关的继发性损伤是导致其预后不良的主要原因,其中,脑出血后继发性脑损伤是目前临床治疗的难点。研究表明,铁死亡与脑出血后继发性脑损伤的过程密切相关。深入研究脑出血后铁死亡的发生机制及其药物治疗的前景,将为脑出血后继发性脑损伤的诊治提供新思路和新靶点。

转录因子p53与脑出血铁死亡的研究进展

脑出血是死亡率最高的脑卒中亚型,占脑血管疾病的35%,具有高致残、致死率。铁死亡是一种铁依赖性非凋亡细胞死亡模式,近年来发现在脑卒中存在铁死亡现象。p53作为一种转录因子,p53表达不足的情况下可以促进铁死亡的发生;此外,通过各种代谢途径p53能够在存在铁死亡诱导剂(如谷胱甘肽过氧化酶4抑制剂或高水平的活性氧)的情况下抑制铁死亡。p53作为典型和非典型铁死亡途径的关键调节因子参与铁死亡的调节。本文就p53与脑出血后铁死亡脑损伤关系的研究进展进行综述。

自发性脑出血继发脑室出血预后相关危险因素的Meta分析

目的 了解中国自发性脑出血继发脑室出血人群预后相关的影响因素。方法 检索PubMed、Embase、Cochrane Library、万方、中国知网、维普数据库中有关自发性脑出血继发脑室出血病例预后分析的队列研究,检索时限为从1990年1月1日—2023年6月18日,最终共纳入11项非随机病例对照研究,共计944例自发性脑出血继发脑室出血患者,包括583例预后良好和361例预后不良的患者。采用Newcastle-Ottawa量表评估质量,RevMan 5.4.0软件进行Meta分析。结果 患者发病时意识障碍(OR=7.38,95%CI=4.91~11.09,P<0.00001)、年龄(OR=2.66,95%CI=1.57~4.51,P=0.0003)、出血量(OR=8.45,95%CI=4.95~14.41,P<0.00001)、出血部位(OR=10.18,95%CI=3.43~30.20,P<0.0001)、入院血糖(OR=5.76,95%CI=2.87~11.54,P<0.00001)、中线有无移位(OR=4.67,95%CI=2.50~8.72,P<0.00001)、破入脑室的部位(OR=3.80,95%CI=2.38~6.08,P<0.00001)、范围(OR=0.18,95%CI=0.08~0.40,P<0.0001)和程度(OR=9.34,95%CI=5.10~17.13,P<0.00001)、瞳孔改变(OR=191.67,95%CI=36.44~1008.04,P<0.00001)、脑膜刺激征(OR=9.76,95%CI=4.09~23.25,P<0.00001)、治疗方案(OR=0.31,95%CI=0.15~0.64,P=0.02)、脑室铸型(OR=8.01,95%CI=3.09~20.76,P<0.0001)是继发脑室出血患者预后不良的危险因素。结论 发病时意识障碍、年龄>70岁、出血量≥20 ml、脑干出血、入院时血糖值高、中线有移位、3、4脑室受累、破入脑室范围广、双瞳孔不等大、有脑膜刺激征、脑室铸型、采用内科治疗方案是发生SIVH预后不良的危险因素,能够为SIVH预防决策的制定提供循证依据。

脑出血后神经炎症反应相关生物标志物的研究进展

脑出血(ICH)是一种常见且严重的脑血管疾病,病死率和致残率均较高。ICH的病理、生理机制极其复杂,神经炎症反应在ICH的病理、生理变化过程中起重要作用,参与ICH后早期继发性脑损伤和脑损伤后续修复。ICH引起的神经炎症反应涉及多种炎症细胞激活、炎症细胞因子释放,在此过程中许多与ICH后神经炎症反应相关的生物标志物被广泛研究,动态监测炎症反应相关生物标志物水平有助于判断ICH的病情严重程度及预后评估,早期进行干预治疗可降低患者病死率和致残率。

Management of cerebral amyloid angiopathy and atrial fibrillation:We are still far from precision medicine

The use of anticoagulation therapy could prove to be controversial when trying to balance ischemic stroke and intracranial bleeding risks in patients with concurrent cerebral amyloid angiopathy(CAA)and atrial fibrillation(AF).In fact,CAA is an age-related cerebral vasculopathy that predisposes patients to intracerebral hemorrhage.Nevertheless,many AF patients require oral systemic dose-adjusted warfarin,direct oral anticoagulants(such as factor Xa inhibitors)or direct thrombin inhibitors to control often associated with cardioembolic stroke risk.The prevalence of both CAA and AF is expected to rise,due to the aging of the population.This clinical dilemma is becoming increasingly common.In patients with coexisting AF and CAA,the risks/benefits profile of anticoagulant therapy must be assessed for each patient individually due to the lack of a clear-cut consensus with regard to its risks in scientific literature.This review aims to provide an overview of the management of patients with concomitant AF and CAA and proposes the implementation of a risk-based decision-making algorithm.

白藜芦醇单用或与miR-27b激动剂联合应用对脑出血大鼠脑组织继发性病理损伤的防治作用观察

目的观察白藜芦醇(Res)单用或与miR-27b激动剂联合应用对脑出血(ICH)大鼠脑组织继发性病理损伤的防治作用。方法将180只雄性SD大鼠随机分为假手术组、ICH组、Res组、Res+miR-27b agomir组、NC组,每组36只。ICH组、Res组、Res+miR-27b agomir组以及NC组大鼠采用胶原酶注射尾状核法制备ICH模型。Res组、Res+miR-27b agomir组、NC组大鼠在造模前连续7 d腹腔注射Res,假手术组及ICH组采注射等体积DMSO。Res+miR-27b agomir组大鼠在造模前3 d将miR-27b激动剂miR-27b agomir注入大鼠右侧脑室,NC组大鼠注射agomir阴性对照试剂,假手术组、ICH组、Res组注射等量生理盐水。各组大鼠造模成功后继续喂养24 h,使用mNSS评分量表评估神经功能。各组大鼠处死后取脑组织,采用TUNEL法测算脑组织神经细胞凋亡率,采用ELISA法检测大鼠脑组织炎症因子、氧化应激相关因子,采用qRT-PCR法检测大鼠脑组织中miR-27b、核因子相关因子2(Nrf2)mRNA,采用Western Blotting法检测大鼠脑组织中Nrf2/ARE信号通路相关蛋白Nrf2、血红素加氧酶(HO-1)、醌氧化还原酶1(Nqo1)。结果假手术组大鼠mNSS评分、脑组织神经细胞凋亡率和TNF-α、IL-1β、MDA表达水平均低于其余各组(P均<0.05),SOD活力均高于其余各组(P均<0.05);ICH组大鼠mNSS评分、脑组织神经细胞凋亡率和TNF-α、IL-1β、MDA表达水平均高于其余各组(P均<0.05),SOD活力均低于其余各组(P均<0.05);且Res+miR-27b agomir组大鼠mNSS评分、脑组织神经细胞凋亡率和TNF-α、IL-1β、MDA表达水平均高于Res组和NC组(P均<0.05),SOD活力均低于Res组和NC组(P均<0.05)。与假手术组相比,ICH组、Res组、Res+miR-27b agomir组、NC组大鼠脑组织中miR-27b相对表达量均降低,Nrf2mRNA和蛋白、HO-1蛋白、NQO1蛋白相对表达量均升高(P均<0.05);与ICH组相比,Res组、Res+miR-27b agomir组、NC组大鼠脑组织中miR-27b相对表达量均降低,Nrf2 mRNA和蛋白、HO-1蛋白、NQO1蛋白相对表达量均升高(P均<0.05);与Res+miR-27b agomir组相比,Res组、NC组大鼠脑组织中miR-27b相对表达量均降低,Nrf2 mRNA和蛋白、HO-1蛋白、NQO1蛋白相对表达量均升高(P均<0.05)。结论Res单用或联合miR-27b激动剂可对ICH大鼠脑组织继发性病理损伤起防治作用,其防治作用可能与激活Nrf2/ARE信号通路有关。

沉默转录激活因子4抑制脑出血后神经元坏死性凋亡的体外实验

背景:脑出血介导的神经元坏死性凋亡是继发性脑损伤的重要原因。转录激活因子4(activating transcription factor 4,ATF4)是转录激活因子家族成员之一,在脑出血后的继发性脑损伤中扮演重要角色。然而,ATF4在脑出血后的神经元坏死性凋亡中的机制有待明确。目的:探索沉默ATF4基因对脑出血后神经元坏死性凋亡的影响。方法:共同培养HT-22小鼠海马神经元细胞系和BV-2小鼠小胶质细胞系,利用氯化血红素刺激神经元构建脑出血体外模型。在0-100μmol/L区间设置氯化血红素干预细胞的浓度梯度,通过MTT实验评估氯化血红素处理24 h后对神经元细胞活力的影响。然后将共培养细胞分为4组:空白对照组不加任何干预,对照组加入50μmol/L氯化血红素处理,其余2组在加入氯化血红素48 h前分别用阴性对照小干扰RNA(NC siRNA)、ATF4小干扰RNA(ATF4 siRNA)干预细胞,再用50μmol/L氯化血红素处理细胞24 h后,利用PI/Hoechst染色检测神经元坏死性凋亡情况,Western blot检测ATF4、RIP3、MLKL的蛋白表达,双重免疫荧光染色定位于神经元,观察神经元坏死性凋亡的发生程度及ATF4的调控作用。结果与结论:①50μmol/L氯化血红素可以较大程度诱导神经元坏死性凋亡;②对照组和NC siRNA组的PI+/Hoechst+细胞数量高于空白对照组(P<0.0001),ATF4 siRNA组PI+/Hoechst+细胞数量低于对照组(P<0.0001);③与对照组相比,ATF4 siRNA组在抑制ATF4蛋白表达(P<0.001)的同时,也抑制了RIP3、MLKL蛋白表达(P<0.001);④通过对神经元荧光染色定位,与对照组相比,ATF4 siRNA组的RIP3、MLKL蛋白表达明显降低(P<0.0001);⑤结果表明,通过沉默ATF4基因可以直接或间接抑制脑出血后神经元坏死性凋亡相关基因的表达,起到缓解继发性脑损伤的作用。

中国脑血管病临床管理指南(第2版)(节选)——第5章脑出血临床管理

自发性脑出血是卒中的一种严重亚型,在中国卒中患者中占23.4%,以急性发病、病情迅速变化以及高致死和致残率为显著特点。鉴于管理脑出血所面临的紧迫和复杂挑战,本指南旨在为其临床处理提供系统性和全面性的推荐意见。本章节覆盖了从脑出血院前评估、医疗干预到二级预防和康复的各个关键环节。在具体推荐方面,本指南根据不同的证据等级,为早期诊断、影像学评估、急性期干预、内科和重症监护、外科干预以及二级预防策略提供了指导,旨在全面提升自发性脑出血诊疗的科学性和系统管理质量。

硫代半乳糖苷通过抑制半乳糖凝集素-8的糖结合活性改善脑出血继发性脑损伤

目的探讨小鼠脑出血后半乳糖凝集素-8(Galectins-8)对脑出血急性期脑损伤程度的影响。方法采用胶原酶注入法建立小鼠脑出血模型,制作冰冻切片,采用免疫荧光染色观察血肿周围免疫炎症细胞表达情况,干湿质量法检测脑组织含水量,劳克坚牢蓝/焦油紫(LFB/CV)染色观察CH急性期脑组织的血肿体积、脑肿胀程度。结果脑出血后硫代半乳糖苷抑制Galectins-8的糖结合活性,可显著减少血肿周围活化的小胶质细胞及浸润的中性粒细胞数量(Iba1:t=2.904,P=0.0272;MPO:t=3.503,P=0.0128),抑制脑血肿体积扩大(t=2.486,P=0.0486),减轻脑水肿(t=5.369,P=0.0126),从而改善脑出血后的继发性脑损伤。结论脑出血后Galectins-8一定程度上加重了继发性脑损伤的程度,可能成为治疗脑出血新的潜在治疗靶点。

脑出血后小胶质细胞极化及其相关炎症信号通路对继发性脑损伤的影响

脑出血是一种由脑实质血管破裂引起的严重疾病,目前尚无有效的治疗方法。研究表明炎症反应在脑出血继发性脑损伤中发挥了重要作用。在出血部位,小胶质细胞被迅速招募并激活,且在促炎型与抑炎型之间动态转变,不同的信号通路可以改变小胶质细胞极化的状态,从而对脑损伤起到调控作用,这提示了小胶质细胞在脑出血继发脑损伤的病理过程中具有复杂的作用机制。促炎型小胶质细胞释放的各种炎症因子介导神经细胞和神经组织的炎症损伤;抑炎型小胶质细胞释放趋化因子、脑源性神经营养因子、抗炎介质等诱导小胶质细胞向病变方向迁移,吞噬有害分子和细胞碎片,减轻炎症损伤,促进炎症消退、组织修复及神经再生。然而,目前对于小胶质细胞极化在脑出血后的动态变化及机制尚未完全阐明,故对参与脑出血小胶质细胞极化的相关调控分子以及信号通路的研究已引起了广泛关注,有望成为脑出血治疗的潜在靶点。

自发性脑出血后继发性脑损伤的影像学研究进展

在自发性脑出血所致原发性损伤的最佳治疗方法尚存争议的情况下,继发性脑损伤带来的影响越来越得到重视。继发性脑损伤是自发性脑出血后必然发生的病理生理过程,诸多研究表明继发性脑损伤对预后有着显著影响。影像学手段是临床研究中用于评估继发性脑损伤最常用的手段,不同的影像学方法均可对明确继发性脑损伤与预后的关系提供一定帮助。本文对继发性脑损伤各种影像学评估方法的研究现状展开综述,希望从中获取继发性脑损伤准确预测方法的新思路。

麦角新碱联合卡贝缩宫素预防二次剖宫产产后出血的效果研究

目的:探讨麦角新碱联合卡贝缩宫素预防二次剖宫产产后出血的效果及对患者凝血功能、肾素-血管紧张素-醛固酮系统(RAAS)、不良反应的影响。方法:选取2020年3月-2021年3月华润武钢总医院接诊的88例二次剖宫产产妇作为本次研究对象,按照随机数字表法将其分为观察组和对照组,各44例。对照组的产后出血预防方案为卡贝缩宫素,观察组的方案为麦角新碱联合卡贝缩宫素。对两组的产后出血情况、凝血指标、RAAS及不良反应进行分析和研究。结果:(1)产后2、24 h,观察组的出血量低于对照组,且产后出血发生率低于对照组,差异均有统计学意义(P<0.05)。(2)产前,两组各项凝血功能指标比较,差异均无统计学意义(P>0.05);产后24 h,两组的凝血酶时间(TT)与产前比较,差异无统计学意义(P>0.05);两组的凝血酶原时间(PT)和活化部分凝血活酶时间(APTT)较产前延长(P<0.05),但是两组间的PT、APTT、TT指标比较,差异无统计学意义(P>0.05)。(3)产后24 h,观察组的血浆血管紧张素Ⅰ(AngⅠ)、血管紧张素Ⅱ(AngⅡ)和肾素活性(PRA)水平明显低于对照组,差异有统计学意义(P<0.05)。(4)观察组的不良反应发生率低于对照组,差异有统计学意义(P<0.05)。结论:麦角新碱联合卡贝缩宫素可有效降低二次剖宫产产后出血的发生率,在改善凝血功能的同时有效地抑制RAAS的异常状态,且安全性较高,值得临床应用和推广。