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当向异氟烷麻醉的犬类给药一氧化二氮时,血流动力学控制可防止心肌缺血恶化。

Control of hemodynamics prevents worsening of myocardial ischemia when nitrous oxide is administered to isoflurane-anesthetized dogs.

作者信息

Nathan H J

机构信息

Department of Anesthesia, Ottawa Civic Hospital, University of Ottawa Heart Institute, Ontario, Canada.

出版信息

Anesthesiology. 1989 Nov;71(5):686-94. doi: 10.1097/00000542-198911000-00011.

DOI:10.1097/00000542-198911000-00011
PMID:2683872
Abstract

This study was designed to determine if nitrous oxide can worsen myocardial ischemia by directly affecting coronary tone in the absence of changes in myocardial oxygen consumption. Three anesthetics were compared in each animal: isoflurane 1.8% alone, isoflurane 1.4% with 50% nitrous oxide, and isoflurane 1.8% with 50% nitrous oxide. Heart rate, systolic aortic pressure and left atrial pressure were held constant during the three treatments. In 12 isoflurane-anesthetized dogs the chest was opened and the left anterior descending (LAD) coronary artery cannulated and perfused with an autoperfusion circuit. Systolic segment shortening was measured in the LAD circumflex regions of the heart with a sonomicrometer. Regional myocardial blood flow was measured with radioactive microspheres. Measurements were made during imposition of a stenosis on the perfusion circuit sufficient to decrease systolic shortening by 30-50%. The same stenosis was imposed three times in a randomized and balanced crossover design. When heart rate, blood pressure, and left atrial pressure were held constant, the substitution of 50% nitrous oxide for 0.4% isoflurane had no effect on myocardial blood flow or function in the ischemic or normal region. When nitrous oxide was added to 1.8% isoflurane, systolic shortening decreased by 35% in the ischemic and 27% in the normally perfused region, but myocardial blood flow was unaffected. The decrease in shortening was therefore not due to increased ischemia. The effects of nitrous oxide on ischemic myocardium can be explained by its well-known hemodynamic and direct myocardial actions. These results suggest that nitrous oxide does not have important direct effects on the coronary circulation.

摘要

本研究旨在确定在心肌耗氧量无变化的情况下,氧化亚氮是否会通过直接影响冠状动脉张力而加重心肌缺血。在每只动物身上比较了三种麻醉剂:单独使用1.8%异氟烷、1.4%异氟烷与50%氧化亚氮合用、1.8%异氟烷与50%氧化亚氮合用。在三种治疗过程中,心率、主动脉收缩压和左心房压力保持恒定。在12只接受异氟烷麻醉的狗身上,打开胸腔,将左前降支(LAD)冠状动脉插管,并通过自灌注回路进行灌注。用超声心动图仪测量心脏LAD回旋支区域的收缩节段缩短情况。用放射性微球测量局部心肌血流量。在灌注回路上施加足以使收缩节段缩短30 - 50%的狭窄时进行测量。以随机、平衡的交叉设计对相同的狭窄进行三次施加。当心率、血压和左心房压力保持恒定时,用50%氧化亚氮替代0.4%异氟烷对缺血或正常区域的心肌血流量或功能没有影响。当将氧化亚氮添加到1.8%异氟烷中时,缺血区域的收缩节段缩短减少了35%,正常灌注区域减少了27%,但心肌血流量未受影响。因此,缩短的减少并非由于缺血增加。氧化亚氮对缺血心肌的作用可以用其众所周知的血流动力学和直接心肌作用来解释。这些结果表明,氧化亚氮对冠状动脉循环没有重要的直接影响。

相似文献

1
Control of hemodynamics prevents worsening of myocardial ischemia when nitrous oxide is administered to isoflurane-anesthetized dogs.当向异氟烷麻醉的犬类给药一氧化二氮时,血流动力学控制可防止心肌缺血恶化。
Anesthesiology. 1989 Nov;71(5):686-94. doi: 10.1097/00000542-198911000-00011.
2
Nitrous oxide worsens myocardial ischemia in isoflurane-anesthetized dogs.氧化亚氮会使异氟烷麻醉犬的心肌缺血情况恶化。
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4
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Desflurane and isoflurane exert modest beneficial actions on left ventricular diastolic function during myocardial ischemia in dogs.地氟烷和异氟烷在犬心肌缺血期间对左心室舒张功能有适度的有益作用。
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Effect of isoflurane on the extent of myocardial necrosis and on systemic hemodynamics, regional myocardial blood flow, and regional myocardial metabolism in dogs after coronary artery occlusion.异氟烷对冠状动脉闭塞后犬心肌坏死范围、全身血流动力学、局部心肌血流量及局部心肌代谢的影响。
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Postsystolic shortening of canine left ventricle supplied by a stenotic coronary artery when nitrous oxide is added in the presence of narcotics.在麻醉状态下添加一氧化二氮时,由狭窄冠状动脉供血的犬左心室收缩后缩短。
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Regional and global myocardial function in the dog when nitrous oxide is added to halothane in the presence of critical coronary artery constriction.在冠状动脉严重收缩的情况下,将一氧化二氮添加到氟烷中时犬的局部和整体心肌功能。
Anesth Analg. 1986 May;65(5):431-6.

引用本文的文献

1
Nitrous oxide 1844-1990.一氧化二氮 1844 - 1990年
Can J Anaesth. 1990 Sep;37(6):603-7. doi: 10.1007/BF03006475.
2
Nitrous oxide does not worsen myocardial ischaemia following beta-receptor blockade in isoflurane anaesthetized dogs.
Can J Anaesth. 1991 Jul;38(5):640-7. doi: 10.1007/BF03008202.