Heart failure(HF)is a complex clinical syndrome characterized by the activation of at least several neurohumoral pathways that have a common role in maintaining cardiac output and adequate perfusion pressure of target...Heart failure(HF)is a complex clinical syndrome characterized by the activation of at least several neurohumoral pathways that have a common role in maintaining cardiac output and adequate perfusion pressure of target organs and tissues.The sympathetic nervous system(SNS)is upregulated in HF as evident in dysfunctional baroreceptor and chemoreceptor reflexes,circulating and neuronal catecholamine spillover,attenuated parasympathetic response,and augmented sympathetic outflow to the heart,kidneys and skeletal muscles.When these sympathoexcitatory effects on the cardiovascular system are sustained chronically they initiate the vicious circle of HF progression and become associated with cardiomyocyte apoptosis,maladaptive ventricular and vascular remodeling,arrhythmogenesis,and poor prognosis in patients with HF.These detrimental effects of SNS activity on outcomes in HF warrant adequate diagnostic and treatment modalities.Therefore,this review summarizes basic physiological concepts about the interaction of SNS with the cardiovascular system and highlights key pathophysiological mechanisms of SNS derangement in HF.Finally,special emphasis in this review is placed on the integrative and up-to-date overview of diagnostic modalities such as SNS imaging methods and novel laboratory biomarkers that could aid in the assessment of the degree of SNS activation and provide reliable prognostic information among patients with HF.展开更多
目的 分析不同病情程度子痫前期(preeclampsia, PE)孕妇血清脑啡肽酶(neprilysin)、儿茶酚抑素(catestatin)、分化型胚胎软骨发育基因1(split and hairy related protein-1,SHARP1)水平的变化及与心功能和妊娠结局的关系。方法 选取2020...目的 分析不同病情程度子痫前期(preeclampsia, PE)孕妇血清脑啡肽酶(neprilysin)、儿茶酚抑素(catestatin)、分化型胚胎软骨发育基因1(split and hairy related protein-1,SHARP1)水平的变化及与心功能和妊娠结局的关系。方法 选取2020年3月至2022年2月德州市妇女儿童医院收治的128例PE患者,分为轻度PE组(75例)与重度PE组(53例),另选取同期于本院产检的50例健康孕妇作为健康组。检测并比较3组血清脑啡肽酶、儿茶酚抑素、SHARP1水平,对轻、重度PE患者行超声心功能检查,比较两组左室射血分数(LVEF)、心脏指数(CI)、心输出量(CO)、舒张早期峰值速度(E)/舒张晚期峰值速度(A)参数,进行Pearson相关性分析及Logistic回归模型分析。结果 重度PE组血清脑啡肽酶水平高于健康组、轻度PE组,儿茶酚抑素、SHARP1水平低于健康组、轻度PE组(P<0.05)。轻度PE组血清脑啡肽酶水平高于健康组,儿茶酚抑素、SHARP1水平低于健康组(P<0.05)。重度PE组LVEF、CI、E/A低于轻度PE组,CO高于轻度PE组(P<0.05)。Pearson相关性分析结果显示,血清脑啡肽酶与LVEF、CI、E/A呈负相关,与CO呈正相关(P<0.05),儿茶酚抑素、SHARP1与LVEF、CI、E/A呈正相关,与CO呈负相关(P<0.05)。PE患者中良好妊娠结局102例,不良妊娠结局26例。良好妊娠结局和不良妊娠结局患者的血压、24 h尿蛋白、尿素氮(BUN)、血肌酐(Scr)、脑啡肽酶、儿茶酚抑素、SHARP1水平比较差异有统计学意义(P<0.05)。经Logistic回归分析显示,血压、24 h尿蛋白、BUN、Scr、脑啡肽酶、儿茶酚抑素、SHARP1水平为PE患者不良妊娠结局的影响因素(P<0.05)。结论 血清脑啡肽酶在PE患者中水平上升,儿茶酚抑素、SHARP1水平下降,与病情严重程度密切相关,是影响孕妇不良妊娠的危险因素,且与心功能受损有关。展开更多
Background Catestatin, a chromogranin A-derived peptide, is a potent antagonist of nicotine-evoked catecholamine release. We know that catecholamine plays an important role in cardiovascular remodeling induced by hype...Background Catestatin, a chromogranin A-derived peptide, is a potent antagonist of nicotine-evoked catecholamine release. We know that catecholamine plays an important role in cardiovascular remodeling induced by hypertension, therefore we hypothesized that catestatin would affect target-organ structure during hypertension. Methods Twelve spontaneously hypertensive rats （SHRs） were randomized to SHR control group and catestatin group, the normal control group was comprised of six healthy Wistar-Kyoto rats of the same age. Tail-cuff blood pressure and pulse rate were obtained at weeks 1, 4 and 8. At the end of the eight-week period, the heart, abdominal aorta and left kidney were excised and weighed, VG staining was done and the intima-media thickness of vessels and the collagen volume fraction were assessed by an image acquisition and analysis system. The proliferating cell nuclear antigen （PCNA） was observed by immunohistochemistry, and real time reverse transcription-polymerase chain reaction （RT-PCR） was used to detect the mRNA levels of proliferative genes including cyclin A, ki67 and PCNA in the abdominal aorta. Results All the parameters in SHR observed in the present study increased significantly compared to Wistar Kyoto rats （P 〈0.01 ）. With intervention with catestatin, the systolic blood pressure decreased slightly but it was not significantly different from the SHR control, the cardiac mass index and left ventricular mass index both decreased significantly, the collagen volume fraction decreased by nearly 30% in the heart, by 25% in vessels and by 10% in the kidney, and the intima-media thickness and expression of proliferative genes, including cyclin A, ki67 and PCNA, in the abdominal aorta also decreased significantly. Conclusions The present study indicated that catestatin could ameliorate proliferating changes of heart, kidney and vessels during hypertension, especially to the deposition of interstitial collagen. Blood pressure was not the main factor to mediate this effect, which展开更多
文摘Heart failure(HF)is a complex clinical syndrome characterized by the activation of at least several neurohumoral pathways that have a common role in maintaining cardiac output and adequate perfusion pressure of target organs and tissues.The sympathetic nervous system(SNS)is upregulated in HF as evident in dysfunctional baroreceptor and chemoreceptor reflexes,circulating and neuronal catecholamine spillover,attenuated parasympathetic response,and augmented sympathetic outflow to the heart,kidneys and skeletal muscles.When these sympathoexcitatory effects on the cardiovascular system are sustained chronically they initiate the vicious circle of HF progression and become associated with cardiomyocyte apoptosis,maladaptive ventricular and vascular remodeling,arrhythmogenesis,and poor prognosis in patients with HF.These detrimental effects of SNS activity on outcomes in HF warrant adequate diagnostic and treatment modalities.Therefore,this review summarizes basic physiological concepts about the interaction of SNS with the cardiovascular system and highlights key pathophysiological mechanisms of SNS derangement in HF.Finally,special emphasis in this review is placed on the integrative and up-to-date overview of diagnostic modalities such as SNS imaging methods and novel laboratory biomarkers that could aid in the assessment of the degree of SNS activation and provide reliable prognostic information among patients with HF.
文摘Background Catestatin, a chromogranin A-derived peptide, is a potent antagonist of nicotine-evoked catecholamine release. We know that catecholamine plays an important role in cardiovascular remodeling induced by hypertension, therefore we hypothesized that catestatin would affect target-organ structure during hypertension. Methods Twelve spontaneously hypertensive rats （SHRs） were randomized to SHR control group and catestatin group, the normal control group was comprised of six healthy Wistar-Kyoto rats of the same age. Tail-cuff blood pressure and pulse rate were obtained at weeks 1, 4 and 8. At the end of the eight-week period, the heart, abdominal aorta and left kidney were excised and weighed, VG staining was done and the intima-media thickness of vessels and the collagen volume fraction were assessed by an image acquisition and analysis system. The proliferating cell nuclear antigen （PCNA） was observed by immunohistochemistry, and real time reverse transcription-polymerase chain reaction （RT-PCR） was used to detect the mRNA levels of proliferative genes including cyclin A, ki67 and PCNA in the abdominal aorta. Results All the parameters in SHR observed in the present study increased significantly compared to Wistar Kyoto rats （P 〈0.01 ）. With intervention with catestatin, the systolic blood pressure decreased slightly but it was not significantly different from the SHR control, the cardiac mass index and left ventricular mass index both decreased significantly, the collagen volume fraction decreased by nearly 30% in the heart, by 25% in vessels and by 10% in the kidney, and the intima-media thickness and expression of proliferative genes, including cyclin A, ki67 and PCNA, in the abdominal aorta also decreased significantly. Conclusions The present study indicated that catestatin could ameliorate proliferating changes of heart, kidney and vessels during hypertension, especially to the deposition of interstitial collagen. Blood pressure was not the main factor to mediate this effect, which
