Catalpol,an iridoid glucoside isolated from Rehmannia glutinosa,has gained attention due to its potential use in treating cardio-cerebrovascular diseases(CVDs).This extensive review delves into recent studies on catal...Catalpol,an iridoid glucoside isolated from Rehmannia glutinosa,has gained attention due to its potential use in treating cardio-cerebrovascular diseases(CVDs).This extensive review delves into recent studies on catalpol's protective properties in relation to various CVDs,such as atherosclerosis,myocardial ischemia,infarction,cardiac hypertrophy,and heart failure.The review also explores the compound's anti-oxidant,anti-inflammatory,and anti-apoptotic characteristics,emphasizing the role of vital signaling pathways,including PGC-1a/TERT,PI3K/Akt,AMPK,Nrf2/HO-1,estrogen receptor(ER),Nox4/NF-kB,and GRP78/PERK.The article discusses emerging findings on catalpol's ability to alleviate diabetic cardiovascular complications,thrombosis,and other cardiovascular-related conditions.Although clinical studies specifically addressing catalpol's impact on CVDs are scarce,the compound's established safety and well-tolerated nature suggest that it could be a valuable treatment alternative for CVD patients.Further investigation into catalpol and related iridoid derivatives may unveil new opportunities for devising natural and efficacious CVD therapies.展开更多
Compared to antiarrhythmic drugs, implantable cardioverter defibrillator （ICD） leads to a more significant im- provement in preventing ventricular arrhythmia in heart failure patients. However, an important question...Compared to antiarrhythmic drugs, implantable cardioverter defibrillator （ICD） leads to a more significant im- provement in preventing ventricular arrhythmia in heart failure patients. However, an important question has been raised that how to select appropriate patients for ICD therapy. 1-123 metaiodobenzylguanidine （MIBG） planar and SPECT imaging have shown great potentials to predict ventricular arrhythmia in heart failure patients by as- sessing the abnormalities of the sympathetic nervous system. Clinical trials demonstrated that several parameters measured from 1-123 MIBG planar and SPECT imaging, such as heart-to-mediastinum ratio, washout rate, defect score, and innervation/perfusion mismatch, predicted ventricular arrhythmias in heart failure patients. This paper introduces the current practice of ICD therapy and reviews the technical background of 1-123 MIBG planar and SPECT imaging and their clinical data in predicting ventricular arrhythmia.展开更多
The present investigation is the continuation of our prior clinical studies on the content of parathyroid hormone (PTH), its paracrine analog, parathyroid hormone-related protein (PTHrP) and electrolytes in blood of p...The present investigation is the continuation of our prior clinical studies on the content of parathyroid hormone (PTH), its paracrine analog, parathyroid hormone-related protein (PTHrP) and electrolytes in blood of patients with heart failure. The results of these studies formed the basis for the nomination of the hypothesis on PTH and PTHrP compensatory-modulating effect on the contractile activity of heart. The objective of this study is to elucidate the mechanism of the compensatory-modulating effect of PTH on heart functional activity, which is realized by the study of effective doses of PTH by pharmacological analysis, using different inhibitors. The dose-dependent effect of PTH on the heart contraction rate and amplitude is studied on the frog isolated heart by the method of non-invasive registration of heart contractile activity. The method is based on the photoelectric principle of the reflected from the contractile object light ray transformation into an electric signaling. It is shown that the most effective dose that has positive chronotropic and inotropic effects on heart is 10–10 M hormone. To clarify the mechanism of PTH physiological dose action on the contractile activity of heart PTH 1-34 is combined with Ca-channel as well as phosphodiesterase blockers. The mentioned substances are applied based on the fact that PTH effect on target cells is mediated by secondary messengers, particularly calcium ions and cAMP. Based on the data obtained by combination of hormone with Verapamil (10–5 M) and Theophylline (10–4 M), we concluded on the involvement of calcium ions in the realization of chronotropic and cAMP in the inotropic effects on the heart.展开更多
Objective:Congenital heart disease(CHD)is caused by abnormal cardiac development,which is the most common congenital malformation at home and abroad.NKX2-5,GATA4 and ZIC3 have been shown to be associated with CHD.This...Objective:Congenital heart disease(CHD)is caused by abnormal cardiac development,which is the most common congenital malformation at home and abroad.NKX2-5,GATA4 and ZIC3 have been shown to be associated with CHD.This experiment explored the relationship between NKX2-5,GATA4 and ZIC3 gene mutations and sporadic CHD in Hainan Province.Methods:To collect 210 sporadic CHD patients in Hainan,the DNA of patients was extracted from blood,and the target gene fragments were amplified.Using high-resolution melting(HRM)and DNA sequencing technology,and we analyzed the sequences of NKX2-5,GATA4 and ZIC3 genes.Results:NKX2-5,GATA4 and ZIC3 genes were sequenced in 210 CHD patients,and seven gene mutations were found,including NKX2-5 heterozygous missense mutation(c.178G>T)and three heterozygous mutations in GATA4(c.677C>T,c.928A>G,c.1123G>A),three heterozygous mutations in ZIC3(c.19G>C,c.1255C>G,c.1348C>T),in which NKX2-5(c.178G>T),GATA4(c.1123G>A),and ZIC3(c.1255C>G,c.1348C>T)are new mutation sites.These gene mutations were predicted to be pathogenic mutations by bioinformatics software.Conclusion:Conclusion:Seven gene mutations were found in 210 patients,and it was the first report that the gene mutations of NKX2-5,GATA4 and ZIC3 in Hainan Province associated with the pathogenesis of CHD.展开更多
Objectives To study wheth- er change of BNP levels reflect the change of cardiac function and to investigate the short - term prognostic potential of BNP and QOL in patients with CHF. Methods 96 consecutive patients a...Objectives To study wheth- er change of BNP levels reflect the change of cardiac function and to investigate the short - term prognostic potential of BNP and QOL in patients with CHF. Methods 96 consecutive patients admittedwith CHF between September 2002 and January 2003 were stud- ied , upon entry the study, BNP levels were measured, Patients administered the disease - specificquality of life questionnaire Minnesota living with heart failure questionnaire (LiHFe) within 1 day. BNP levels and administering LiHFe were repeated three months later. Results BNP levels were increased proportional to the severity of cardiac function. Physical domain and total score of LiHFe were significantly correlated to the severity of CHF ( p < 0. 05 ). BNP levels were de- creased in improving group(p =0. 032) . In deteriora- ting group BNP levels increased (P = 0. 043 ) . Kaplan - meier analysis according to BNP level cutoff point 150 ng/1, the life curve of higher BNP level group was significantly lower than the lower group ( p = 0. 001 ) . In univariate logistic regression, NYHA class, BNP, LVEF, LVEDD, heart size, total score of LiHFe, phys- ical domain of LiHFe and the emotional domain of LiH- Fe were all significant prognostic factors of CHF ( p < 0. 05 for all). While in multiple regression, only BNP level( p = 0. 036) and the emotional domain of LiHFe ( p = 0. 025 ) were independent prognostic factors. Conclusions Change of BNP reflects the treatment efficacy of CHF. BNP and QOL are the two major short - time prognostic factors of the chronic heart failure patients.展开更多
Atrial fibrillation(AF)and prediabetes share common pathophysiological mechanisms with endothelial dysfunction and inflammation playing a key role.The resultant vicious cycle which sets in culminates in a higher ather...Atrial fibrillation(AF)and prediabetes share common pathophysiological mechanisms with endothelial dysfunction and inflammation playing a key role.The resultant vicious cycle which sets in culminates in a higher atherogenicity and thermogenicity of the vascular system resulting in increased major adverse cardiac or cerebrovascular event(MACCE)events.However,the same has not convincingly been verified in real-world settings.In the recent retrospective study by Desai et al amongst AF patients being admitted to hospitals following MACCE,prediabetes emerged as an independent risk factor for MACCE after adjusting for all confounding variables.However,certain questions like the role of metformin,quantifying the risk for MACCE amongst prediabetes compared to diabetes,the positive impact of reversion to normoglycemia remain unanswered.We provide our insights and give future directions for dedicated research in this area to clarify the exact relationship between the two.展开更多
Pathological myocardial hypertrophy is a common early clinical manifestation of heart failure,with noncoding RNAs exerting regulatory influence.However,the molecular function of circular RNAs(circRNAs)in the progressi...Pathological myocardial hypertrophy is a common early clinical manifestation of heart failure,with noncoding RNAs exerting regulatory influence.However,the molecular function of circular RNAs(circRNAs)in the progression from cardiac hypertrophy to heart failure remains unclear.To uncover functional circRNAs and identify the core circRNA signaling pathway in heart failure,we construct a global triple network(microRNA,circRNA,and mRNA)based on the competitive endogenous RNA(ceRNA)theory.We observe that cardiac hypertrophy-related circRNA(circRNA CHRC),within the ceRNA network,is down-regulated in both transverse aortic constriction mice and Ang-II--treated primary mouse cardiomyocytes.Silencing circRNA CHRC increases cross-sectional cell area,atrial natriuretic peptide,andβ-myosin heavy chain levels in primary mouse cardiomyocytes.Further screening shows that circRNA CHRC targets the miR-431-5p/KLF15 axis implicated in heart failure progression in vivo and in vitro.Immunoprecipitation with anti-Ago2-RNA confirms the interaction between circRNA CHRC and miR-431-5p,while miR-431-5p mimics reverse Klf15 activation caused by circRNA CHRC overexpression.In summary,circRNA CHRC attenuates cardiac hypertrophy via sponging miR-431-5p to maintain the normal level of Klf15 expression.展开更多
The present study was designed to make certain whether there exists adrenomedullin (ADM) in the rat central nervous system and evaluated the hemodynamic actions of intracerebroventricular administration (ICVA) of hum...The present study was designed to make certain whether there exists adrenomedullin (ADM) in the rat central nervous system and evaluated the hemodynamic actions of intracerebroventricular administration (ICVA) of human ADM[13-52]. By immunohistochemistry (ABC method),We found that there was a discrete localization of ADM-positive immunoreactivity in the rat central system including cerebral cortex,paraventricular tissues, hypothalamus, cerebella cortex, mesencephalon and medulla oblongata. By reverse transcription-polymerase chain reaction(RT-PCR) analysis, rat ADM mRNA was found to be expressed in rat brain. These above results of immunohistochemistry and RT-PCR suggest that ADM exists in the rat brain. We also found that centrally administered ADM[13-52]in a dose of 0.4 to 3. 2 nmol/kg provoked marked, prolonged and dosedependent increases in mean arterial blood pressure (MABP) and heart rate (HR). To clarify the mechanisms of the hemodynamic changes induced by centrally administered ADM [13-52]. the effect of centrally administered ADM [13-52] on renal sympathetic nerve activity (RSNA) was studied. The result showed that centrally administered ADM [13-52] ( 1. 6 nmol/kg) provoked a marked increase in RSNA .therefore .the increases in MABP and HR induced by centrally administered ADM [13-52]might be due to the stimulation of central sympathetic mechanism. In addtion,we also compared the relationship of activity and structure among the different fragments of ADM. In conclusion, ADMexists in the rat brain, and it may play an important role in the central control of cardiovascular system.展开更多
Fluctuations in autonomic cardiovascular regulation during exposure to high altitude may increase the risk of heart attack during waking and sleep. This study compared heart rate variability (HVR) and its components d...Fluctuations in autonomic cardiovascular regulation during exposure to high altitude may increase the risk of heart attack during waking and sleep. This study compared heart rate variability (HVR) and its components during sleep at low altitude and after 30 - 41 hours of acclimatization at high altitude (3480 m) in five mountain marathon runners controlled for diet, drugs, light-dark cycle and jet lag. In comparison to sea level, RR-intervals during sleep at high altitude decreased significantly (P 0.001). The significant increase in sympathetic autonomic cardiovascular modulation at high altitude protects against excessive oxygen deprivation during sleep. Increases in R-R intervals can require longer periods of acclimatization at3480 m to mitigate the effects of altitude/hypoxia on sympathetic tone, thus reducing cardiovascular distress at rest during waking and sleep and probably before during and after athletic performance at altitude.展开更多
Objective To investigate the effect of(-)-Stepholidine(SPD)on enhancing D1 receptor mediated contraction of cardiac muscle in isolated rat heart and to examine whether SPD has a direct effect on the heart dopamine D1 ...Objective To investigate the effect of(-)-Stepholidine(SPD)on enhancing D1 receptor mediated contraction of cardiac muscle in isolated rat heart and to examine whether SPD has a direct effect on the heart dopamine D1 receptors.SPD an active ingredient of the Chinese herb Stephania intermedia,binds to dopamine D1 and D2 like receptors.Biochemical,electrophysiological and behavioural experiments have provided strong evidence that SPD is both a D(1/5)agonist and a D(2/4)antagonist,which could indicate unique antipsychotic properties.Methods Normal adult rat working hearts were isolated by Langendorff technique.Results SPD significantly increased the cardiac muscle contraction in a dose-dependent manner.The selective D1 dopamine receptor antagonist SCH23390(1 μM)blocked the SPD induced heart contraction,however,neither the β-receptor antagonist propranolol(1 μM)nor the α1-receptor antagonist prazosin(1 μM)had any effect on blocking SPD induced heart contractions.Moreover,the L-type Ca2+ channel inhibitor nimodipine(1 μM)completely blocked the effect of SPD on cardiac muscle contraction.Conclusions SPD show the effect on enhancing contraction of isolated rat heart through activating L-type Ca2+ channel mediated by heart D1 receptors.展开更多
To study the variation and significance of plasma coagulation factor Ⅶ （FⅦ） in different kinds of ischemia heart disease （IHD） and examine its relation with plasma lipid and gene polymorphism. FⅦa was determine...To study the variation and significance of plasma coagulation factor Ⅶ （FⅦ） in different kinds of ischemia heart disease （IHD） and examine its relation with plasma lipid and gene polymorphism. FⅦa was determined with one stage clotting assay by using a recombinant soluble tissue factor （rsTF）. FⅦc was measured with one stage clotting assay. FⅦag was quantified with an enzyme-linked immunosorbent assay （ELISA）. Polymorphism was analyzed with PCR-urea-polyacrylamide gel electrophoresis. Our results showed that FⅦa in stable angina （SA）, unstable angina （UA）, obsolete and acute myocardial infraction （OMI, AMI） patients was higher than those of normal group with the differences being significant within any two groups. FⅦag in UA, OMI and AMI was higher than those in SA and normal groups. There were positive correlations between FⅦa and serum triglycerides, FⅦa and FⅦc, FⅦc and FⅦag. FⅦ-323 0/10 bp polymorphism analysis was performed in 60 patients and 0/10 bp polymorphism was found in 5 cases. FⅦc and FⅦag were much lower in cases of 0/10 bp groups than those in cases of 0/0 bp groups. It is concluded that there was activation of extrinsic coagulation pathway in every kind of IHD to different extent. FⅦa was the risk factor in the development of IHD, and more sensitive in reflecting the severity of cardiovacutar disease than FⅦc or FⅦag. FⅦa was higher in OMI, which may be one of the risk factors of re-infraction. Serum triglyceride may indirectly lead to the development of IHD by increasing the level of FⅦa, FⅦ-323 0/10 bp polymorphism was present in Chinese patients with IHD and it was correlated with the level of FⅦc, FⅦag in plasma. 10 bp allelomorphic gene was a protective factor against thrombogenesis.展开更多
基金supported by the National Natural Science Foundation of China(Grant Nos:.82070356 and 81770337)the Key Project of Hunan Provincial Science and Technology Innovation,China(Grant No.:2020SK1013)the Hunan Provincial Natural Science Foundation of China(Grant No.:2021JJ30033).
文摘Catalpol,an iridoid glucoside isolated from Rehmannia glutinosa,has gained attention due to its potential use in treating cardio-cerebrovascular diseases(CVDs).This extensive review delves into recent studies on catalpol's protective properties in relation to various CVDs,such as atherosclerosis,myocardial ischemia,infarction,cardiac hypertrophy,and heart failure.The review also explores the compound's anti-oxidant,anti-inflammatory,and anti-apoptotic characteristics,emphasizing the role of vital signaling pathways,including PGC-1a/TERT,PI3K/Akt,AMPK,Nrf2/HO-1,estrogen receptor(ER),Nox4/NF-kB,and GRP78/PERK.The article discusses emerging findings on catalpol's ability to alleviate diabetic cardiovascular complications,thrombosis,and other cardiovascular-related conditions.Although clinical studies specifically addressing catalpol's impact on CVDs are scarce,the compound's established safety and well-tolerated nature suggest that it could be a valuable treatment alternative for CVD patients.Further investigation into catalpol and related iridoid derivatives may unveil new opportunities for devising natural and efficacious CVD therapies.
文摘Compared to antiarrhythmic drugs, implantable cardioverter defibrillator （ICD） leads to a more significant im- provement in preventing ventricular arrhythmia in heart failure patients. However, an important question has been raised that how to select appropriate patients for ICD therapy. 1-123 metaiodobenzylguanidine （MIBG） planar and SPECT imaging have shown great potentials to predict ventricular arrhythmia in heart failure patients by as- sessing the abnormalities of the sympathetic nervous system. Clinical trials demonstrated that several parameters measured from 1-123 MIBG planar and SPECT imaging, such as heart-to-mediastinum ratio, washout rate, defect score, and innervation/perfusion mismatch, predicted ventricular arrhythmias in heart failure patients. This paper introduces the current practice of ICD therapy and reviews the technical background of 1-123 MIBG planar and SPECT imaging and their clinical data in predicting ventricular arrhythmia.
文摘The present investigation is the continuation of our prior clinical studies on the content of parathyroid hormone (PTH), its paracrine analog, parathyroid hormone-related protein (PTHrP) and electrolytes in blood of patients with heart failure. The results of these studies formed the basis for the nomination of the hypothesis on PTH and PTHrP compensatory-modulating effect on the contractile activity of heart. The objective of this study is to elucidate the mechanism of the compensatory-modulating effect of PTH on heart functional activity, which is realized by the study of effective doses of PTH by pharmacological analysis, using different inhibitors. The dose-dependent effect of PTH on the heart contraction rate and amplitude is studied on the frog isolated heart by the method of non-invasive registration of heart contractile activity. The method is based on the photoelectric principle of the reflected from the contractile object light ray transformation into an electric signaling. It is shown that the most effective dose that has positive chronotropic and inotropic effects on heart is 10–10 M hormone. To clarify the mechanism of PTH physiological dose action on the contractile activity of heart PTH 1-34 is combined with Ca-channel as well as phosphodiesterase blockers. The mentioned substances are applied based on the fact that PTH effect on target cells is mediated by secondary messengers, particularly calcium ions and cAMP. Based on the data obtained by combination of hormone with Verapamil (10–5 M) and Theophylline (10–4 M), we concluded on the involvement of calcium ions in the realization of chronotropic and cAMP in the inotropic effects on the heart.
基金Natural Science Foundation of Hainan Province(No.821RC562)Re-research Project of Hainan Province(No.ZDYF2022SHF2081)+1 种基金National Natural Science Foundation of China(No.81660224)Graduate Innovation Project of Hainan Province(No.Qhys2021-353)。
文摘Objective:Congenital heart disease(CHD)is caused by abnormal cardiac development,which is the most common congenital malformation at home and abroad.NKX2-5,GATA4 and ZIC3 have been shown to be associated with CHD.This experiment explored the relationship between NKX2-5,GATA4 and ZIC3 gene mutations and sporadic CHD in Hainan Province.Methods:To collect 210 sporadic CHD patients in Hainan,the DNA of patients was extracted from blood,and the target gene fragments were amplified.Using high-resolution melting(HRM)and DNA sequencing technology,and we analyzed the sequences of NKX2-5,GATA4 and ZIC3 genes.Results:NKX2-5,GATA4 and ZIC3 genes were sequenced in 210 CHD patients,and seven gene mutations were found,including NKX2-5 heterozygous missense mutation(c.178G>T)and three heterozygous mutations in GATA4(c.677C>T,c.928A>G,c.1123G>A),three heterozygous mutations in ZIC3(c.19G>C,c.1255C>G,c.1348C>T),in which NKX2-5(c.178G>T),GATA4(c.1123G>A),and ZIC3(c.1255C>G,c.1348C>T)are new mutation sites.These gene mutations were predicted to be pathogenic mutations by bioinformatics software.Conclusion:Conclusion:Seven gene mutations were found in 210 patients,and it was the first report that the gene mutations of NKX2-5,GATA4 and ZIC3 in Hainan Province associated with the pathogenesis of CHD.
文摘Objectives To study wheth- er change of BNP levels reflect the change of cardiac function and to investigate the short - term prognostic potential of BNP and QOL in patients with CHF. Methods 96 consecutive patients admittedwith CHF between September 2002 and January 2003 were stud- ied , upon entry the study, BNP levels were measured, Patients administered the disease - specificquality of life questionnaire Minnesota living with heart failure questionnaire (LiHFe) within 1 day. BNP levels and administering LiHFe were repeated three months later. Results BNP levels were increased proportional to the severity of cardiac function. Physical domain and total score of LiHFe were significantly correlated to the severity of CHF ( p < 0. 05 ). BNP levels were de- creased in improving group(p =0. 032) . In deteriora- ting group BNP levels increased (P = 0. 043 ) . Kaplan - meier analysis according to BNP level cutoff point 150 ng/1, the life curve of higher BNP level group was significantly lower than the lower group ( p = 0. 001 ) . In univariate logistic regression, NYHA class, BNP, LVEF, LVEDD, heart size, total score of LiHFe, phys- ical domain of LiHFe and the emotional domain of LiH- Fe were all significant prognostic factors of CHF ( p < 0. 05 for all). While in multiple regression, only BNP level( p = 0. 036) and the emotional domain of LiHFe ( p = 0. 025 ) were independent prognostic factors. Conclusions Change of BNP reflects the treatment efficacy of CHF. BNP and QOL are the two major short - time prognostic factors of the chronic heart failure patients.
文摘Atrial fibrillation(AF)and prediabetes share common pathophysiological mechanisms with endothelial dysfunction and inflammation playing a key role.The resultant vicious cycle which sets in culminates in a higher atherogenicity and thermogenicity of the vascular system resulting in increased major adverse cardiac or cerebrovascular event(MACCE)events.However,the same has not convincingly been verified in real-world settings.In the recent retrospective study by Desai et al amongst AF patients being admitted to hospitals following MACCE,prediabetes emerged as an independent risk factor for MACCE after adjusting for all confounding variables.However,certain questions like the role of metformin,quantifying the risk for MACCE amongst prediabetes compared to diabetes,the positive impact of reversion to normoglycemia remain unanswered.We provide our insights and give future directions for dedicated research in this area to clarify the exact relationship between the two.
基金supported by the National Natural Science Foundation of China(32071109,82070270,M-0048)the Shanghai Committee of Science and Technology(22ZR1463800,21ZR1467000)+1 种基金the Shanghai Jing'an District Discipline Construction Project(2021PY03)CAMS Innovation Fund for Medical Sciences(2019-I2M-5–053)。
文摘Pathological myocardial hypertrophy is a common early clinical manifestation of heart failure,with noncoding RNAs exerting regulatory influence.However,the molecular function of circular RNAs(circRNAs)in the progression from cardiac hypertrophy to heart failure remains unclear.To uncover functional circRNAs and identify the core circRNA signaling pathway in heart failure,we construct a global triple network(microRNA,circRNA,and mRNA)based on the competitive endogenous RNA(ceRNA)theory.We observe that cardiac hypertrophy-related circRNA(circRNA CHRC),within the ceRNA network,is down-regulated in both transverse aortic constriction mice and Ang-II--treated primary mouse cardiomyocytes.Silencing circRNA CHRC increases cross-sectional cell area,atrial natriuretic peptide,andβ-myosin heavy chain levels in primary mouse cardiomyocytes.Further screening shows that circRNA CHRC targets the miR-431-5p/KLF15 axis implicated in heart failure progression in vivo and in vitro.Immunoprecipitation with anti-Ago2-RNA confirms the interaction between circRNA CHRC and miR-431-5p,while miR-431-5p mimics reverse Klf15 activation caused by circRNA CHRC overexpression.In summary,circRNA CHRC attenuates cardiac hypertrophy via sponging miR-431-5p to maintain the normal level of Klf15 expression.
文摘The present study was designed to make certain whether there exists adrenomedullin (ADM) in the rat central nervous system and evaluated the hemodynamic actions of intracerebroventricular administration (ICVA) of human ADM[13-52]. By immunohistochemistry (ABC method),We found that there was a discrete localization of ADM-positive immunoreactivity in the rat central system including cerebral cortex,paraventricular tissues, hypothalamus, cerebella cortex, mesencephalon and medulla oblongata. By reverse transcription-polymerase chain reaction(RT-PCR) analysis, rat ADM mRNA was found to be expressed in rat brain. These above results of immunohistochemistry and RT-PCR suggest that ADM exists in the rat brain. We also found that centrally administered ADM[13-52]in a dose of 0.4 to 3. 2 nmol/kg provoked marked, prolonged and dosedependent increases in mean arterial blood pressure (MABP) and heart rate (HR). To clarify the mechanisms of the hemodynamic changes induced by centrally administered ADM [13-52]. the effect of centrally administered ADM [13-52] on renal sympathetic nerve activity (RSNA) was studied. The result showed that centrally administered ADM [13-52] ( 1. 6 nmol/kg) provoked a marked increase in RSNA .therefore .the increases in MABP and HR induced by centrally administered ADM [13-52]might be due to the stimulation of central sympathetic mechanism. In addtion,we also compared the relationship of activity and structure among the different fragments of ADM. In conclusion, ADMexists in the rat brain, and it may play an important role in the central control of cardiovascular system.
文摘Fluctuations in autonomic cardiovascular regulation during exposure to high altitude may increase the risk of heart attack during waking and sleep. This study compared heart rate variability (HVR) and its components during sleep at low altitude and after 30 - 41 hours of acclimatization at high altitude (3480 m) in five mountain marathon runners controlled for diet, drugs, light-dark cycle and jet lag. In comparison to sea level, RR-intervals during sleep at high altitude decreased significantly (P 0.001). The significant increase in sympathetic autonomic cardiovascular modulation at high altitude protects against excessive oxygen deprivation during sleep. Increases in R-R intervals can require longer periods of acclimatization at3480 m to mitigate the effects of altitude/hypoxia on sympathetic tone, thus reducing cardiovascular distress at rest during waking and sleep and probably before during and after athletic performance at altitude.
文摘Objective To investigate the effect of(-)-Stepholidine(SPD)on enhancing D1 receptor mediated contraction of cardiac muscle in isolated rat heart and to examine whether SPD has a direct effect on the heart dopamine D1 receptors.SPD an active ingredient of the Chinese herb Stephania intermedia,binds to dopamine D1 and D2 like receptors.Biochemical,electrophysiological and behavioural experiments have provided strong evidence that SPD is both a D(1/5)agonist and a D(2/4)antagonist,which could indicate unique antipsychotic properties.Methods Normal adult rat working hearts were isolated by Langendorff technique.Results SPD significantly increased the cardiac muscle contraction in a dose-dependent manner.The selective D1 dopamine receptor antagonist SCH23390(1 μM)blocked the SPD induced heart contraction,however,neither the β-receptor antagonist propranolol(1 μM)nor the α1-receptor antagonist prazosin(1 μM)had any effect on blocking SPD induced heart contractions.Moreover,the L-type Ca2+ channel inhibitor nimodipine(1 μM)completely blocked the effect of SPD on cardiac muscle contraction.Conclusions SPD show the effect on enhancing contraction of isolated rat heart through activating L-type Ca2+ channel mediated by heart D1 receptors.
文摘To study the variation and significance of plasma coagulation factor Ⅶ （FⅦ） in different kinds of ischemia heart disease （IHD） and examine its relation with plasma lipid and gene polymorphism. FⅦa was determined with one stage clotting assay by using a recombinant soluble tissue factor （rsTF）. FⅦc was measured with one stage clotting assay. FⅦag was quantified with an enzyme-linked immunosorbent assay （ELISA）. Polymorphism was analyzed with PCR-urea-polyacrylamide gel electrophoresis. Our results showed that FⅦa in stable angina （SA）, unstable angina （UA）, obsolete and acute myocardial infraction （OMI, AMI） patients was higher than those of normal group with the differences being significant within any two groups. FⅦag in UA, OMI and AMI was higher than those in SA and normal groups. There were positive correlations between FⅦa and serum triglycerides, FⅦa and FⅦc, FⅦc and FⅦag. FⅦ-323 0/10 bp polymorphism analysis was performed in 60 patients and 0/10 bp polymorphism was found in 5 cases. FⅦc and FⅦag were much lower in cases of 0/10 bp groups than those in cases of 0/0 bp groups. It is concluded that there was activation of extrinsic coagulation pathway in every kind of IHD to different extent. FⅦa was the risk factor in the development of IHD, and more sensitive in reflecting the severity of cardiovacutar disease than FⅦc or FⅦag. FⅦa was higher in OMI, which may be one of the risk factors of re-infraction. Serum triglyceride may indirectly lead to the development of IHD by increasing the level of FⅦa, FⅦ-323 0/10 bp polymorphism was present in Chinese patients with IHD and it was correlated with the level of FⅦc, FⅦag in plasma. 10 bp allelomorphic gene was a protective factor against thrombogenesis.
