Hearts of pressure-overload hypertrophy show an increased activation of intracardiac renin-angiotensin system which may contribute to ischemia and reperfusion injury. The purpose of this study is to evaluate whether t...Hearts of pressure-overload hypertrophy show an increased activation of intracardiac renin-angiotensin system which may contribute to ischemia and reperfusion injury. The purpose of this study is to evaluate whether the hypertrophied myocardium is more vulnerable to ischemia and reperfusion injury and to find out its relation to the cardiac renin-angiotensin system. Hypertrophied rat hearts induced by abdominal aortic banding for 6 weeks were subjected to 2 hours of hypothermic ischemic arrest followed by 30 minutes of reperfusion, and their cardiac function recovery was compared with that of sham-operated normal control hearts. The cardiac renin activity and angiotensin II content before ischemia and after reperfusion were determined. It was found that both the pre-ischemic renin activity and angiotensin II level were higher in hypertrophied myocardium than those in the control: ischemia and reperfusion injury increased both renin activity and angiotensin II content in the two groups, but the renin activity and angiotensin II level were further elevated after reperfusion in the hypertrophied hearts than those in the control hearts. Meanwhile, the cardiac function recovery after 30 minutes reperfusion in the hypertrophied hearts was poorer than that in the control. Correlation analysis revealed that there was a negative correlation between the cardiac output recovery and the myocardial angiotensin II content (r=-0.841), P<0.001), It is concluded that ischemia and reperfusion injury can activate cardiac renin-angiotensin system in isolated rat heart, which may be responsible for the increased susceptibility of the hypertrophied myocardium to ischemia and reperfusion injury.展开更多
The ESR signal of NO bound to hemoglobin was detected during the ischemia-reperfusion of myocardium with low temperature ESR technique, and the synergic effects of NO and oxygen free radicals in the injury of the proc...The ESR signal of NO bound to hemoglobin was detected during the ischemia-reperfusion of myocardium with low temperature ESR technique, and the synergic effects of NO and oxygen free radicals in the injury of the process were studied with this technique. Oxygen free radicals and NO bound to β-subunit of hemoglobin (β-NO complex) could be detected simultaneously in the ischemia-reperfused myocardium. Those signals could not be detected from the normal myocardium even in the presence of L-arginme. However, those signals could be detected and were dose-dependent with L-arginine in the ischemia-reperfused myocardiums and the signal could be suppressed with the inhibitor of NO synthetase, NG-nitro-L-arginine methylester (NAME). Measurement of the activities of lactate dehydrogenase (LDH) and creatine kinase (CK) in the coronary artery effluent of ischemia-reperfused heart showed that L-arginine at lower concentration (<1 mmol/L) could protect the heart from the ischemia-reperfusion injury but at higher concentration aggravate the injury. Addition of NAME to the reperfusion solution could also protect the myocardium. Addition of xanthine (X) ,'xanthine oxidase (XO) or Fe2+/H2O2 to the reperfusion solution increased the production of NO and oxygen free radicals and the ischemia-reperfused injury simultaneously. Addition of superoxide dismutase (SOD) and catalase decreased the production of NO and oxygen free radicals and the ischemia-reperfusion injury.展开更多
Advances in magnetic resonance(MR) and computed tomography(CT) imaging have improved visualization of acute and scar infarct.Over the past decade,there have been and continues to be many significant technical advancem...Advances in magnetic resonance(MR) and computed tomography(CT) imaging have improved visualization of acute and scar infarct.Over the past decade,there have been and continues to be many significant technical advancements in cardiac MR and multi-detector computed tomography(MDCT) technologies.The strength of MR imaging relies on a variety of pulse sequences and the ability to noninvasively provide information on myocardial structure,function and perfusion in a single imaging session.The recent technical developments may also allow CT technologies to rise to the forefront for evaluating clinical ischemic heart disease.Components of reperfusion injury including myocardial edema,hemorrhage,calcium deposition and microvascular obstruction(MO) have been demonstrated using MR and CT technologies.MR imaging can be used serially and noninvasively in assessing acute and chronic consequences of reperfusion injury because there is no radiation exposure or administration of radioactive materials.MDCT is better suited for assessing coronary artery stenosis and as an alternative technique for as-sessing viability in patients where MR imaging is contraindicated.Changes in left ventricular(LV) volumes and function measured on cine MR are directly related to infarct size measured on delayed contrast enhanced images.Recent MR studies found that transmural infarct,MO and peri-infarct zone are excellent predictors of poor post-infarct recovery and mortality.Recent MR studies provided ample evidence that growth factor genes and stem cells delivered locally have beneficial effects on myocardial viability,perfusion and function.The significance of deposited calcium in acute infarct detected on MDCT requires further studies.Cardiac MR and MDCT imaging have the potential for assessing reperfusion injury components and manifestations.展开更多
Background Endogenous nitric oxide and adenosine increase simultaneously to keep the balance of energy demand and supply when the oxygen supply is insufficient, which suggests that nitric oxide and adenosine might exe...Background Endogenous nitric oxide and adenosine increase simultaneously to keep the balance of energy demand and supply when the oxygen supply is insufficient, which suggests that nitric oxide and adenosine might exert a synergistic myoprotection during tissue hypoxia. In this study, we tested this hypothesis utilizing a canine model of prolonged global myocardial ischaemic reperfusion injury. Methods In this double blind, controlled study, the hearts of 24 anaesthetized mongrel dogs were arrested for 2 hours with aortic cross clamping and blood cardioplegia. The treatment groups were those supplemented with 2 mmol/L L-arginine （ARG）, supplemented with 1 mmol/L adenosine （ADO）, ARG ＋ ADO supplemented with both, and no supplementation （control） （n=6 in each group）. Haemodynamics, biochemical indices, adenosine triphosphate （ATP） content and myeloperoxidase activities of myocardium were determined to evaluate myocardial injury. Statistical comparison was performed by two way ANOVA. Results Although the requirements for inotropic supports were higher, the cardiac outputs were lower in control group than in ARG, ADO and the combination groups. Plasma cardiac troponin I levels were higher and the areas of hydropic changes were larger in control group than in ARG and ADO groups. Combination of arginine and adenosine provided further myoprotection with respect to better cardiac performance, lower release of cardiac troponin I, and smaller areas of hydropic changes compared with ARG and ADO groups. ATP content was higher, but myeloperoxidase activities of myocardium were significantly lower in the combination group than in control, ARG and ADO groups （P〈0.05）. Conclusions Combination of L-arginine and adenosine provides synergistic myoprotection in a canine model of global myocardial ischaemia. Thus, the combination is recommended when the heart is exposed to a prolonged ischaemia during cardiac surgery.展开更多
文摘Hearts of pressure-overload hypertrophy show an increased activation of intracardiac renin-angiotensin system which may contribute to ischemia and reperfusion injury. The purpose of this study is to evaluate whether the hypertrophied myocardium is more vulnerable to ischemia and reperfusion injury and to find out its relation to the cardiac renin-angiotensin system. Hypertrophied rat hearts induced by abdominal aortic banding for 6 weeks were subjected to 2 hours of hypothermic ischemic arrest followed by 30 minutes of reperfusion, and their cardiac function recovery was compared with that of sham-operated normal control hearts. The cardiac renin activity and angiotensin II content before ischemia and after reperfusion were determined. It was found that both the pre-ischemic renin activity and angiotensin II level were higher in hypertrophied myocardium than those in the control: ischemia and reperfusion injury increased both renin activity and angiotensin II content in the two groups, but the renin activity and angiotensin II level were further elevated after reperfusion in the hypertrophied hearts than those in the control hearts. Meanwhile, the cardiac function recovery after 30 minutes reperfusion in the hypertrophied hearts was poorer than that in the control. Correlation analysis revealed that there was a negative correlation between the cardiac output recovery and the myocardial angiotensin II content (r=-0.841), P<0.001), It is concluded that ischemia and reperfusion injury can activate cardiac renin-angiotensin system in isolated rat heart, which may be responsible for the increased susceptibility of the hypertrophied myocardium to ischemia and reperfusion injury.
基金Project supported by the National Natural Science Foundation of China.
文摘The ESR signal of NO bound to hemoglobin was detected during the ischemia-reperfusion of myocardium with low temperature ESR technique, and the synergic effects of NO and oxygen free radicals in the injury of the process were studied with this technique. Oxygen free radicals and NO bound to β-subunit of hemoglobin (β-NO complex) could be detected simultaneously in the ischemia-reperfused myocardium. Those signals could not be detected from the normal myocardium even in the presence of L-arginme. However, those signals could be detected and were dose-dependent with L-arginine in the ischemia-reperfused myocardiums and the signal could be suppressed with the inhibitor of NO synthetase, NG-nitro-L-arginine methylester (NAME). Measurement of the activities of lactate dehydrogenase (LDH) and creatine kinase (CK) in the coronary artery effluent of ischemia-reperfused heart showed that L-arginine at lower concentration (<1 mmol/L) could protect the heart from the ischemia-reperfusion injury but at higher concentration aggravate the injury. Addition of NAME to the reperfusion solution could also protect the myocardium. Addition of xanthine (X) ,'xanthine oxidase (XO) or Fe2+/H2O2 to the reperfusion solution increased the production of NO and oxygen free radicals and the ischemia-reperfused injury simultaneously. Addition of superoxide dismutase (SOD) and catalase decreased the production of NO and oxygen free radicals and the ischemia-reperfusion injury.
文摘Advances in magnetic resonance(MR) and computed tomography(CT) imaging have improved visualization of acute and scar infarct.Over the past decade,there have been and continues to be many significant technical advancements in cardiac MR and multi-detector computed tomography(MDCT) technologies.The strength of MR imaging relies on a variety of pulse sequences and the ability to noninvasively provide information on myocardial structure,function and perfusion in a single imaging session.The recent technical developments may also allow CT technologies to rise to the forefront for evaluating clinical ischemic heart disease.Components of reperfusion injury including myocardial edema,hemorrhage,calcium deposition and microvascular obstruction(MO) have been demonstrated using MR and CT technologies.MR imaging can be used serially and noninvasively in assessing acute and chronic consequences of reperfusion injury because there is no radiation exposure or administration of radioactive materials.MDCT is better suited for assessing coronary artery stenosis and as an alternative technique for as-sessing viability in patients where MR imaging is contraindicated.Changes in left ventricular(LV) volumes and function measured on cine MR are directly related to infarct size measured on delayed contrast enhanced images.Recent MR studies found that transmural infarct,MO and peri-infarct zone are excellent predictors of poor post-infarct recovery and mortality.Recent MR studies provided ample evidence that growth factor genes and stem cells delivered locally have beneficial effects on myocardial viability,perfusion and function.The significance of deposited calcium in acute infarct detected on MDCT requires further studies.Cardiac MR and MDCT imaging have the potential for assessing reperfusion injury components and manifestations.
基金This work was supported by the grants from the National Youth Natural Science Foundation of China(No.30400439)the "973" Program(No.2005CB522601)
文摘Background Endogenous nitric oxide and adenosine increase simultaneously to keep the balance of energy demand and supply when the oxygen supply is insufficient, which suggests that nitric oxide and adenosine might exert a synergistic myoprotection during tissue hypoxia. In this study, we tested this hypothesis utilizing a canine model of prolonged global myocardial ischaemic reperfusion injury. Methods In this double blind, controlled study, the hearts of 24 anaesthetized mongrel dogs were arrested for 2 hours with aortic cross clamping and blood cardioplegia. The treatment groups were those supplemented with 2 mmol/L L-arginine （ARG）, supplemented with 1 mmol/L adenosine （ADO）, ARG ＋ ADO supplemented with both, and no supplementation （control） （n=6 in each group）. Haemodynamics, biochemical indices, adenosine triphosphate （ATP） content and myeloperoxidase activities of myocardium were determined to evaluate myocardial injury. Statistical comparison was performed by two way ANOVA. Results Although the requirements for inotropic supports were higher, the cardiac outputs were lower in control group than in ARG, ADO and the combination groups. Plasma cardiac troponin I levels were higher and the areas of hydropic changes were larger in control group than in ARG and ADO groups. Combination of arginine and adenosine provided further myoprotection with respect to better cardiac performance, lower release of cardiac troponin I, and smaller areas of hydropic changes compared with ARG and ADO groups. ATP content was higher, but myeloperoxidase activities of myocardium were significantly lower in the combination group than in control, ARG and ADO groups （P〈0.05）. Conclusions Combination of L-arginine and adenosine provides synergistic myoprotection in a canine model of global myocardial ischaemia. Thus, the combination is recommended when the heart is exposed to a prolonged ischaemia during cardiac surgery.
