目的探讨急性脑梗死患者治疗中急诊急救模式的应用效果。方法回顾性选取急性脑梗死患者100例,依据治疗方法分为急诊急救模式组和常规急诊治疗组,每组各50例。结果急诊急救模式组患者的急诊急救成功率高于常规急诊治疗组,从入院到急救医...目的探讨急性脑梗死患者治疗中急诊急救模式的应用效果。方法回顾性选取急性脑梗死患者100例,依据治疗方法分为急诊急救模式组和常规急诊治疗组,每组各50例。结果急诊急救模式组患者的急诊急救成功率高于常规急诊治疗组,从入院到急救医师接诊,时间短于常规急诊治疗组;从入院到开具CT报告,时间短于常规急诊治疗组;从入院到静脉溶栓,时间短于常规急诊治疗组;从入院到动脉成功置鞘,时间短于常规急诊治疗组;从置鞘到血管再通,时间短于常规急诊治疗组。美国国立卫生研究院卒中量表(National Institute of Health Stroke Scale,NIHSS)评分、改良爱丁堡-斯堪的纳维亚评分(Improved Edinburgh Scandinavian Score,CSS)评分均低于常规急诊治疗组,简易精神状态检查量表(Mini Mental Status Examination,MMSE)评分、改良Barthel指数量表(Modified Barthel Index,MBI)评分均高于常规急诊治疗组,差异均具有统计学意义(P<0.05)。急诊急救模式组患者的力气、手功能、交流、记忆与思维、参与、情绪、移动能力、日常生活能力评分均高于常规急诊治疗组(P<0.05),并发症发生率低于常规急诊治疗组(P<0.05)。结论急性脑梗死患者在救护中,急诊急救模式的应用效果优于常规急诊救护。展开更多
Acute myocardial infarction （AMI） is the leading cause of death and disability worldwide. Timely reperfusion is the standard of care and results in decreased infarct size, improving patient survival and prognosis. H...Acute myocardial infarction （AMI） is the leading cause of death and disability worldwide. Timely reperfusion is the standard of care and results in decreased infarct size, improving patient survival and prognosis. However, 25% of patients proceed to develop heart failure （HF） after myocardial infarction （MI） and 50% of these will die within five years. Since the size of the infarct is the major predictor of the outcome, including the development of HF, therapies to improve myocardial salvage have great potential. Over the past three decades, a number of stimuli have been discovered that activate endogenous cardioprotective pathways. In ischemic preconditioning （IPC） and ischemic postconditioning, ischemia within the heart initiates the protection. Brief reversible episodes of ischemia in vascular beds remote from the heart can also trigger cardioprotection when applied before, during, or immediately after myocardial ischemia-- known as remote ischemic pre-, per-, and post-conditioning, respectively. Although the mechanism of remote ischemic preconditioning （RIPC） has not yet been fully elucidated, many mechanistic components are shared with IPC. The discovery of RIPC led to research into the use of remote non-ischemic stimuli including nerve stimulation （spinal and vagal）, and electroacupuncture （EA）. We discovered and, with others, have elucidated mechanistic aspects of a non- ischemic phenomenon we termed remote preconditioning of trauma （RPCT）. RPCT operates via neural stimulation of skin sensory nerves and has similarities and differences to nerve stimulation and EA conducted at acupoints. We show herein that RPCT can be mimicked using electrical stimulation of the abdominal midline （EA-like treatment） and that this modality of activating cardioprotection is powerful as both a preconditioning and a postconditioning stimulus （when applied at reperfusion）. Investigations of these cardioprotective phenomena have led to a more integrative understanding of mechanisms related to cardioprotection, and in the last five to ten years, it has become clear that the mechanisms are similar, whether induced by ischemic or non-ischemic stimuli. Taking together much of the data in the literature, we propose that all of these cardioprotective ＂conditioning＂ phenomena represent activation from different entry points of a cardiac conditioning network that converges upon specific mediators and effectors of myocardial cell survival, including NF-KB, Stat3/5, protein kinase C, bradykinin, and the mitoKA^P channel. Nervous system pathways may represent a novel mechanism for initiating conditioning of the heart and other organs. IPC and RIPC have proven difficult to translate clinically, as they have associated risks and cannot be used in some patients. Because of this, the use of neural and nociceptive stimuli is emerging as a potential non-ischemic and non-traumatic means to initiate cardiac conditioning. Clinical relevance is underscored by the demonstration of postconditioning with one of these modalities, supporting the conclusion that the development of pharmaceuticals and electroceuticals for this purpose is an area ripe for clinical development.展开更多
文摘目的探讨急性脑梗死患者治疗中急诊急救模式的应用效果。方法回顾性选取急性脑梗死患者100例,依据治疗方法分为急诊急救模式组和常规急诊治疗组,每组各50例。结果急诊急救模式组患者的急诊急救成功率高于常规急诊治疗组,从入院到急救医师接诊,时间短于常规急诊治疗组;从入院到开具CT报告,时间短于常规急诊治疗组;从入院到静脉溶栓,时间短于常规急诊治疗组;从入院到动脉成功置鞘,时间短于常规急诊治疗组;从置鞘到血管再通,时间短于常规急诊治疗组。美国国立卫生研究院卒中量表(National Institute of Health Stroke Scale,NIHSS)评分、改良爱丁堡-斯堪的纳维亚评分(Improved Edinburgh Scandinavian Score,CSS)评分均低于常规急诊治疗组,简易精神状态检查量表(Mini Mental Status Examination,MMSE)评分、改良Barthel指数量表(Modified Barthel Index,MBI)评分均高于常规急诊治疗组,差异均具有统计学意义(P<0.05)。急诊急救模式组患者的力气、手功能、交流、记忆与思维、参与、情绪、移动能力、日常生活能力评分均高于常规急诊治疗组(P<0.05),并发症发生率低于常规急诊治疗组(P<0.05)。结论急性脑梗死患者在救护中,急诊急救模式的应用效果优于常规急诊救护。
基金supported by grants from the National Institutes of Health (NIHR01 HL091478) for W.Keith Jonesthe National Natural Science Foundation of China (81470425) for Xiaoping Ren
文摘Acute myocardial infarction （AMI） is the leading cause of death and disability worldwide. Timely reperfusion is the standard of care and results in decreased infarct size, improving patient survival and prognosis. However, 25% of patients proceed to develop heart failure （HF） after myocardial infarction （MI） and 50% of these will die within five years. Since the size of the infarct is the major predictor of the outcome, including the development of HF, therapies to improve myocardial salvage have great potential. Over the past three decades, a number of stimuli have been discovered that activate endogenous cardioprotective pathways. In ischemic preconditioning （IPC） and ischemic postconditioning, ischemia within the heart initiates the protection. Brief reversible episodes of ischemia in vascular beds remote from the heart can also trigger cardioprotection when applied before, during, or immediately after myocardial ischemia-- known as remote ischemic pre-, per-, and post-conditioning, respectively. Although the mechanism of remote ischemic preconditioning （RIPC） has not yet been fully elucidated, many mechanistic components are shared with IPC. The discovery of RIPC led to research into the use of remote non-ischemic stimuli including nerve stimulation （spinal and vagal）, and electroacupuncture （EA）. We discovered and, with others, have elucidated mechanistic aspects of a non- ischemic phenomenon we termed remote preconditioning of trauma （RPCT）. RPCT operates via neural stimulation of skin sensory nerves and has similarities and differences to nerve stimulation and EA conducted at acupoints. We show herein that RPCT can be mimicked using electrical stimulation of the abdominal midline （EA-like treatment） and that this modality of activating cardioprotection is powerful as both a preconditioning and a postconditioning stimulus （when applied at reperfusion）. Investigations of these cardioprotective phenomena have led to a more integrative understanding of mechanisms related to cardioprotection, and in the last five to ten years, it has become clear that the mechanisms are similar, whether induced by ischemic or non-ischemic stimuli. Taking together much of the data in the literature, we propose that all of these cardioprotective ＂conditioning＂ phenomena represent activation from different entry points of a cardiac conditioning network that converges upon specific mediators and effectors of myocardial cell survival, including NF-KB, Stat3/5, protein kinase C, bradykinin, and the mitoKA^P channel. Nervous system pathways may represent a novel mechanism for initiating conditioning of the heart and other organs. IPC and RIPC have proven difficult to translate clinically, as they have associated risks and cannot be used in some patients. Because of this, the use of neural and nociceptive stimuli is emerging as a potential non-ischemic and non-traumatic means to initiate cardiac conditioning. Clinical relevance is underscored by the demonstration of postconditioning with one of these modalities, supporting the conclusion that the development of pharmaceuticals and electroceuticals for this purpose is an area ripe for clinical development.
