Effects of intravenous fluorocarbons during and without oxygen enhancement on acute myocardial ischemic injury assessed by measurement of intramyocardial gas tensions.
Effects of intravenous fluorocarbons during and without oxygen enhancement on acute myocardial ischemic injury assessed by measurement of intramyocardial gas tensions.
复制标题
通过测量心肌内气体张力评估静脉内氟碳化合物在强化供氧期间和不强化期间对急性心肌缺血损伤的影响。
DOI：
10.1016/0002-8703(82)90561-0
复制
发表时间：
1982
影响因子：
4.8
通讯作者：
Braunwald,E
中科院分区：
文献类型：
--
作者：
Rude,RE;Glogar,D;Khuri,SF;Kloner,RA;Karaffa,S;Muller,JE;ClarkJr,LC;Braunwald,E
碳氟化合物（含氟有机化合物，其中O2和CO2是高度可溶的）已被证明是血液气体运输功能的有效替代品。为了研究氟碳化合物对急性局部心肌缺血的影响，我们比较了在麻醉的狗中，在缺血心肌中放置质谱探针的配对暂时冠状动脉闭塞（CAO）引起的心肌内pCO 2（ΔPm CO2）升高和心肌内pO 2（最低点PmO 2）下降。在方案A（n = 7）中，在第一次CAO期间仅用100%O2通气并接受氟碳化合物（全氟化合物，PFC）40 ml/kg静脉注射，在第二次CAO前加入O2：Δ PmCO 2从32.8 ± 4.7降至23.3 ± 3.9 mm Hg第二次CAO的最低点PmO 2（21.6 ± 7.4 mm Hg）高于第一次（9.4 ± 3.9 mm Hg，p< 0.05）。在方案B中的6只犬中，也用100% O2通气，在第二次闭塞前输注40 ml/kg生理盐水，但这并没有改变对CAO的反应。因此，PFC产生的体积膨胀程度并没有减少100%O2通气犬的缺血。随后的研究进行，以确定是否循环PFCs改善急性缺血性损伤的狗与环境空气通风。在方案C中的8只犬中，PFC给药后Δ PmCO 2降低;然而，PFC未改变最低PmO 2;在方案D中的7只犬中，仅接受生理盐水的CAO之间，心肌气体张力无差异。在任何实验组中，CAO之间的中央缺血区的心肌血流量没有变化。我们的结论是，循环PFCs减少急性局部心肌缺血期间，无论是100%O2或环境空气通气，PFC-O2治疗增加心肌O2的可用性在中央缺血区。PFC-O2和PFC给药减少缺血性损伤的机制可能是多因素的，结合了增加O2供应和减少心肌O2需求的因素。
Fluorocarbons (fluorinated organic compounds in which O2and CO2are highly soluble) have been shown to be effective substitutes for the gas transport functions of blood. In order to investigate the effects of fluorocarbons on acute regional myocardial ischemia, we compared the rise of intramyocardial pCO2(ΔPm CO2) and the decline in intramyocardial pO2(nadir PmO2) produced by paired, temporary coronary artery occlusions (CAO) in anesthetized dogs instrumented with mass spectrometer probes positioned in ischemic myocardium. In protocol A (n = 7) dogs were ventilated with 100% O2alone during the first CAO and received fluorocarbons (perfluorochemicals, PFC) 40 ml/kg intravenously in addition to O2before a second CAO: ΔPmCO2fell from 32.8 ± 4.7 to 23.3 ± 3.9 mm Hg (p< 0.05) and the nadir PmO2was higher during the second CAO (21.6 ± 7.4 mm Hg) than during the first (9.4 ± 3.9 mm Hg,p< 0.05). In six dogs in protocol B also ventilated with 100% O2, 40 ml/kg normal saline was infused before the second occlusion, but this did not alter the response to CAO. Thus the degree of volume expansion produced by PFCs did not reduce ischemia in dogs ventilated with 100% O2. Subsequent studies were undertaken to determine whether circulating PFCs ameliorated acute ischemic injury in dogs ventilated with ambient air. In eight dogs in protocol C, ΔPmCO2was decreased after PFC administration; however, nadir PmO2s were not altered by PFC; in seven dogs in protocol D receiving only normal saline between CAOs, there were no differences in myocardial gas tension. There were no changes in myocardial blood flow to the central ischemic zone between CAOs in any experimental group. We conclude that circulating PFCs reduce acute regional myocardial ischemia during ventilation with either 100% O2or ambient air, and that PFC-O2treatment augments myocardial O2availability in the central ischemic zone. The mechanisms by which PFC-O2and PFC administration reduce ischemic injury are likely multifactorial, combining elements of enhanced O2supply and decreased myocardial O2demand.