• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

在离体灌注犬心模型中,在恒定平均主动脉压、冠状动脉灌注压和心率条件下,前负荷改变对缺血程度及缺血心肌功能的影响。

Effects of preload alteration on the degree of ischemia and function of ischemic myocardium under constant mean aortic pressure, coronary perfusion pressure and heart rate in isolated perfused canine heart.

作者信息

Satoh S, Maruyama Y, Ashikawa K, Isoyama S, Suzuki H, Watanabe J, Nishioka O, Ino-Oka E, Takishima T

出版信息

Jpn Circ J. 1986 Nov;50(11):1100-12. doi: 10.1253/jcj.50.1100.

DOI:10.1253/jcj.50.1100
PMID:3820524
Abstract

We examined the effects of preload alteration on global and regional (i.e., non-ischemic and ischemic areas) function in the presence of regional myocardial ischemia and on the degree of ischemia using 18 isolated, metabolically supported canine left ventricles. For this purpose, cardiac output (CO), systolic segment length change (SL), myocardial CO2 tension (PmCO2) and ST level of epicardial ECG were measured at 3 levels of left ventricular end-diastolic pressure (LVEDP), i.e., approximately 7 (low LVEDP), 11 (middle LVEDP), and 16 mmHg (high LVEDP) without and with left circumflex artery (LCx) stenosis under a constant mean aortic pressure (90 mmHg), mean coronary perfusion pressure (90 mmHg) and heart rate. In the Pre-ischemic stage, CO and SL increased significantly when LVEDP was elevated in a stepwise fashion by changing the height of the reservoir connected to the left atrium. There were no significant changes in PmCO2 or ST level. On the other hand, with LCx stenosis, CO did not show a subsequent increase at higher LVEDPs (i.e., from 796 +/- 103 ml/min at middle LVEDP to 931 +/- 153 ml/min at high LVEDP). Furthermore, there was no significant SL response in the LCx area following alterations of LVEDP, although there was considerable lengthening of end-diastolic length. Both increased PmCO2 and ST level of the LCx area, following LCx stenosis, further increased significantly with elevation of LVEDP. These results suggest the possibility that considerable elevation of LVEDP worsens the degree of ischemia and does not significantly augment ischemic regional myocardial function or global function, while mild elevation of preload improves or tends to improve simultaneously regional ischemic and global functions without aggravating the ischemic injury significantly. Therefore, we conclude that the preload level is quite important in managing ischemia induced myocardial dysfunction.

摘要

我们使用18个分离的、代谢支持的犬左心室,研究了在存在局部心肌缺血的情况下,前负荷改变对整体和局部(即非缺血区和缺血区)功能的影响以及对缺血程度的影响。为此,在恒定的平均主动脉压(90 mmHg)、平均冠状动脉灌注压(90 mmHg)和心率下,于左心室舒张末期压力(LVEDP)的3个水平,即大约7(低LVEDP)、11(中LVEDP)和16 mmHg(高LVEDP),在左旋支动脉(LCx)狭窄和无狭窄的情况下,测量心输出量(CO)、收缩期节段长度变化(SL)、心肌二氧化碳张力(PmCO2)和心外膜心电图的ST段水平。在缺血前期,通过改变连接左心房的贮液器高度使LVEDP逐步升高时,CO和SL显著增加。PmCO2或ST段水平无显著变化。另一方面,在LCx狭窄时,较高LVEDP水平下CO未出现后续增加(即从中LVEDP时的796±103 ml/min到高LVEDP时的931±153 ml/min)。此外,尽管舒张末期长度有相当程度的延长,但LVEDP改变后LCx区域无显著的SL反应。LCx狭窄后,LCx区域的PmCO2和ST段水平均升高,随着LVEDP升高进一步显著增加。这些结果提示,LVEDP显著升高可能会加重缺血程度,且不会显著增强缺血区域心肌功能或整体功能,而前负荷轻度升高可改善或倾向于同时改善局部缺血和整体功能,且不会显著加重缺血损伤。因此,我们得出结论,前负荷水平在处理缺血性心肌功能障碍中非常重要。

相似文献

1
Effects of preload alteration on the degree of ischemia and function of ischemic myocardium under constant mean aortic pressure, coronary perfusion pressure and heart rate in isolated perfused canine heart.在离体灌注犬心模型中,在恒定平均主动脉压、冠状动脉灌注压和心率条件下,前负荷改变对缺血程度及缺血心肌功能的影响。
Jpn Circ J. 1986 Nov;50(11):1100-12. doi: 10.1253/jcj.50.1100.
2
The changes in ECG ST segment and mechanical function of regional ischemic myocardium during afterload reduction in isolated dog hearts with coronary stenosis.冠状动脉狭窄的离体犬心在降低后负荷期间局部缺血心肌的心电图ST段变化及机械功能变化。
Jpn Circ J. 1986 Mar;50(3):248-57. doi: 10.1253/jcj.50.248.
3
The effect of heart rate and left ventricular end-diastolic pressure on the direction of ST segment displacement in acute ischemia.心率和左心室舒张末期压力对急性缺血时ST段移位方向的影响。
Tohoku J Exp Med. 1984 Sep;144(1):43-55. doi: 10.1620/tjem.144.43.
4
Pressure-length loop in the ischemic segment during left circumflex coronary artery stenosis and its modification by afterload reducing in excised perfused canine hearts.
Basic Res Cardiol. 1984 Mar-Apr;79(2):155-63. doi: 10.1007/BF01908302.
5
Effects of afterload elevation on the ischemic myocardium in isolated, paced canine heart with partial coronary stenosis.后负荷升高对部分冠状动脉狭窄的离体起搏犬心脏缺血心肌的影响。
Am J Cardiol. 1989 Mar 7;63(10):40E-44E. doi: 10.1016/0002-9149(89)90229-4.
6
Comparison of acute alterations in left ventricular relaxation and diastolic chamber stiffness induced by hypoxia and ischemia. Role of myocardial oxygen supply-demand imbalance.缺氧和缺血引起的左心室舒张及舒张期心室僵硬度急性改变的比较。心肌氧供需失衡的作用。
J Clin Invest. 1981 Jul;68(1):91-102. doi: 10.1172/jci110258.
7
Mechanisms of improving regional and global ventricular function by preload alterations during acute ischemia in the canine left ventricle.犬左心室急性缺血期间通过改变前负荷改善局部和整体心室功能的机制。
Circulation. 1985 Nov;72(5):1125-34. doi: 10.1161/01.cir.72.5.1125.
8
Effects of afterload reduction on global left ventricular and regional myocardial functions in the isolated canine heart with stenosis of a coronary arterial branch.后负荷降低对冠状动脉分支狭窄的离体犬心左心室整体及局部心肌功能的影响。
Circulation. 1983 Jan;67(1):139-47. doi: 10.1161/01.cir.67.1.139.
9
Regional ischemic ventricular dysfunction in myocardium supplied by a narrowed coronary artery with increasing halothane concentration in the dog.在犬体内,随着氟烷浓度升高,由狭窄冠状动脉供血的心肌区域出现缺血性心室功能障碍。
Anesthesiology. 1981 Oct;55(4):349-59. doi: 10.1097/00000542-198110000-00004.
10
The isolated working mouse heart: methodological considerations.离体工作小鼠心脏:方法学考量
Pflugers Arch. 1999 May;437(6):979-85. doi: 10.1007/s004240050870.

引用本文的文献

1
Mechanisms causing myocardial ischaemia.导致心肌缺血的机制。
Can J Anaesth. 1989 May;36(3 Pt 2):S31-4. doi: 10.1007/BF03005324.