Objective： The present study was designed to determine if reactive oxygen species （ROS） in the paraventricular nucleus （PVN） were involved in modulating cardiac sympathetic afferent reflex （CSAR） in anesthetize...Objective： The present study was designed to determine if reactive oxygen species （ROS） in the paraventricular nucleus （PVN） were involved in modulating cardiac sympathetic afferent reflex （CSAR） in anesthetized rats. Methods： Malondialdehyde （MDA）, the end product of lipid peroxidation, in the PVN, was determined by thiobarbituric acid （TBA） spectrometric method. Renal sympathetic nerve activity （RSNA） and arterial pressure were recorded in sinoaortic-denervated and cervical-vagotomized rats. The CSAR was evaluated by the response of the RSNA evoked by epicardial application of bradykinin （BK, 0.4 9g）. Results： The MDA in the PVN was significantly increased after epicardial application of BK compared with control （2.0 ±0.3 vs 0.8 ±0.1 nmol/mg protein, P 〈 0.01）. Microinjection of a superoxide anion scavenger, tiron （20 nmol） into the PVN significantly inhibited the CSAR evoked by BK （12.3±1.9 vs4.2± 1.2%, P 〈0.01） and decreased MDA level （1.9±0.3 vs 0.6 ±0.1 nmol/mg protein, P 〈0.01） compared with control. Conclusion： The ROS in the PVN is involved in modulating the CSAR in rats.展开更多
Cardiac autonomic neuropathy(CAN) is a frequent chronic complication of diabetes mellitus with potentially life-threatening outcomes. CAN is caused by the impairment of the autonomic nerve fibers regulating heart rate...Cardiac autonomic neuropathy(CAN) is a frequent chronic complication of diabetes mellitus with potentially life-threatening outcomes. CAN is caused by the impairment of the autonomic nerve fibers regulating heart rate, cardiac output, myocardial contractility, cardiac electrophysiology and blood vessel constriction anddilatation. It causes a wide range of cardiac disorders, including resting tachycardia, arrhythmias, intraoperative cardiovascular instability, asymptomatic myocardial ischemia and infarction and increased rate of mortality after myocardial infarction. Etiological factors associated with autonomic neuropathy include insufficient glycemic control, a longer period since the onset of diabetes, increased age, female sex and greater body mass index. The most commonly used methods for the diagnosis of CAN are based upon the assessment of heart rate variability(the physiological variation in the time interval between heartbeats), as it is one of the first findings in both clinically asymptomatic and symptomatic patients. Clinical symptoms associated with CAN generally occur late in the disease process and include early fatigue and exhaustion during exercise, orthostatic hypotension, dizziness, presyncope and syncope. Treatment is based on early diagnosis, life style changes, optimization of glycemic control and management of cardiovascular risk factors. Medical therapies, including aldose reductase inhibitors, angiotensin-converting enzyme inhibitors, prostoglandin analogs and alpha-lipoic acid, have been found to be effective in randomized controlled trials. The following article includes the epidemiology, clinical findings and cardiovascular consequences, diagnosis, and approaches to prevention and treatment of CAN.展开更多
Cardiac autonomic neuropathy(CAN)is a serious complication of diabetes mellitus(DM)that is strongly associated with approximately five-fold increased risk of cardiovascular mortality.CAN manifests in a spectrum of thi...Cardiac autonomic neuropathy(CAN)is a serious complication of diabetes mellitus(DM)that is strongly associated with approximately five-fold increased risk of cardiovascular mortality.CAN manifests in a spectrum of things,ranging from resting tachycardia and fixed heart rate(HR)to development of"silent"myocardial infarction.Clinical correlates or risk markers for CAN are age,DM duration,glycemic control,hypertension,and dyslipidemia(DLP),development of other microvascular complications.Established risk factors for CAN are poor glycemic control in type 1 DM and a combination of hypertension,DLP,obesity,and unsatisfactory glycemic control in type 2DM.Symptomatic manifestations of CAN include sinus tachycardia,exercise intolerance,orthostatic hypotension(OH),abnormal blood pressure(BP)regulation,dizziness,presyncope and syncope,intraoperative cardiovascular instability,asymptomatic myocardial ischemia and infarction.Methods of CAN assessment in clinical practice include assessment of symptoms and signs,cardiovascular reflex tests based on HR and BP,short-term electrocardiography(ECG),QT interval prolongation,HR variability(24 h,classic24 h Holter ECG),ambulatory BP monitoring,HR turbulence,baroreflex sensitivity,muscle sympathetic nerve activity,catecholamine assessment and cardiovascular sympathetic tests,heart sympathetic imaging.Although it is common complication,the significance of CAN has not been fully appreciated and there are no unified treatment algorithms for today.Treatment is based on early diagnosis,life style changes,optimization of glycemic control and management of cardiovascular risk factors.Pathogenetic treatment of CAN includes:Balanced diet and physical activity;optimization of glycemic control;treatment of DLP;antioxidants,first of allα-lipoic acid(ALA),aldose reductase inhibitors,acetylL-carnitine;vitamins,first of all fat-soluble vitamin B1;correction of vascular endothelial dysfunction;prevention and treatment of thrombosis;in severe cases-treatment of OH.The promising methods include prescription of prostacyclin analogues,thromboxane A2 blockers and drugs that contribute into strengthening and/or normalization of Na^+,K^+-ATPase(phosphodiesterase inhibitor),ALA,dihomo-γ-linolenic acid(DGLA),ω-3 polyunsaturated fatty acids(ω-3 PUFAs),and the simultaneous prescription of ALA,ω-3 PUFAs and DGLA,but the future investigations are needed.Development of OH is associated with severe or advanced CAN and prescription of nonpharmacological and pharmacological,in the foreground midodrine and fludrocortisone acetate,treatment methods are necessary.展开更多
文摘Objective： The present study was designed to determine if reactive oxygen species （ROS） in the paraventricular nucleus （PVN） were involved in modulating cardiac sympathetic afferent reflex （CSAR） in anesthetized rats. Methods： Malondialdehyde （MDA）, the end product of lipid peroxidation, in the PVN, was determined by thiobarbituric acid （TBA） spectrometric method. Renal sympathetic nerve activity （RSNA） and arterial pressure were recorded in sinoaortic-denervated and cervical-vagotomized rats. The CSAR was evaluated by the response of the RSNA evoked by epicardial application of bradykinin （BK, 0.4 9g）. Results： The MDA in the PVN was significantly increased after epicardial application of BK compared with control （2.0 ±0.3 vs 0.8 ±0.1 nmol/mg protein, P 〈 0.01）. Microinjection of a superoxide anion scavenger, tiron （20 nmol） into the PVN significantly inhibited the CSAR evoked by BK （12.3±1.9 vs4.2± 1.2%, P 〈0.01） and decreased MDA level （1.9±0.3 vs 0.6 ±0.1 nmol/mg protein, P 〈0.01） compared with control. Conclusion： The ROS in the PVN is involved in modulating the CSAR in rats.
文摘Cardiac autonomic neuropathy(CAN) is a frequent chronic complication of diabetes mellitus with potentially life-threatening outcomes. CAN is caused by the impairment of the autonomic nerve fibers regulating heart rate, cardiac output, myocardial contractility, cardiac electrophysiology and blood vessel constriction anddilatation. It causes a wide range of cardiac disorders, including resting tachycardia, arrhythmias, intraoperative cardiovascular instability, asymptomatic myocardial ischemia and infarction and increased rate of mortality after myocardial infarction. Etiological factors associated with autonomic neuropathy include insufficient glycemic control, a longer period since the onset of diabetes, increased age, female sex and greater body mass index. The most commonly used methods for the diagnosis of CAN are based upon the assessment of heart rate variability(the physiological variation in the time interval between heartbeats), as it is one of the first findings in both clinically asymptomatic and symptomatic patients. Clinical symptoms associated with CAN generally occur late in the disease process and include early fatigue and exhaustion during exercise, orthostatic hypotension, dizziness, presyncope and syncope. Treatment is based on early diagnosis, life style changes, optimization of glycemic control and management of cardiovascular risk factors. Medical therapies, including aldose reductase inhibitors, angiotensin-converting enzyme inhibitors, prostoglandin analogs and alpha-lipoic acid, have been found to be effective in randomized controlled trials. The following article includes the epidemiology, clinical findings and cardiovascular consequences, diagnosis, and approaches to prevention and treatment of CAN.
文摘Cardiac autonomic neuropathy(CAN)is a serious complication of diabetes mellitus(DM)that is strongly associated with approximately five-fold increased risk of cardiovascular mortality.CAN manifests in a spectrum of things,ranging from resting tachycardia and fixed heart rate(HR)to development of"silent"myocardial infarction.Clinical correlates or risk markers for CAN are age,DM duration,glycemic control,hypertension,and dyslipidemia(DLP),development of other microvascular complications.Established risk factors for CAN are poor glycemic control in type 1 DM and a combination of hypertension,DLP,obesity,and unsatisfactory glycemic control in type 2DM.Symptomatic manifestations of CAN include sinus tachycardia,exercise intolerance,orthostatic hypotension(OH),abnormal blood pressure(BP)regulation,dizziness,presyncope and syncope,intraoperative cardiovascular instability,asymptomatic myocardial ischemia and infarction.Methods of CAN assessment in clinical practice include assessment of symptoms and signs,cardiovascular reflex tests based on HR and BP,short-term electrocardiography(ECG),QT interval prolongation,HR variability(24 h,classic24 h Holter ECG),ambulatory BP monitoring,HR turbulence,baroreflex sensitivity,muscle sympathetic nerve activity,catecholamine assessment and cardiovascular sympathetic tests,heart sympathetic imaging.Although it is common complication,the significance of CAN has not been fully appreciated and there are no unified treatment algorithms for today.Treatment is based on early diagnosis,life style changes,optimization of glycemic control and management of cardiovascular risk factors.Pathogenetic treatment of CAN includes:Balanced diet and physical activity;optimization of glycemic control;treatment of DLP;antioxidants,first of allα-lipoic acid(ALA),aldose reductase inhibitors,acetylL-carnitine;vitamins,first of all fat-soluble vitamin B1;correction of vascular endothelial dysfunction;prevention and treatment of thrombosis;in severe cases-treatment of OH.The promising methods include prescription of prostacyclin analogues,thromboxane A2 blockers and drugs that contribute into strengthening and/or normalization of Na^+,K^+-ATPase(phosphodiesterase inhibitor),ALA,dihomo-γ-linolenic acid(DGLA),ω-3 polyunsaturated fatty acids(ω-3 PUFAs),and the simultaneous prescription of ALA,ω-3 PUFAs and DGLA,but the future investigations are needed.Development of OH is associated with severe or advanced CAN and prescription of nonpharmacological and pharmacological,in the foreground midodrine and fludrocortisone acetate,treatment methods are necessary.
