DEVELOPMENT OF APPARATUS TO STUDY HEART IN VIVO

在体大鼠心脏的EPR血氧测定仪及大量有用数据 已经用过的离体心，有很多方面 这需要在体内进行研究。这些都是无法做到的 容易使用EPR等技术，因为运动问题 以及需要保持受控的生理状况，而 动物在光谱仪里。然而，我们现在已经参加了 关于PO2的初步技术发展和获得的有用数据 在一颗正常运转的心脏里。我们使用了体重在200-250之间的雄性Wistar大鼠 动物最初用低剂量的麻醉剂麻醉 戊巴比妥。然后放置一根管子，并施加正压 以异氟醚(1%)作为麻醉剂开始机械通气。一个 将聚乙烯导管置入右侧颈动脉 血压和周期性血气的连续监测 PO2(作为实验参数)和PCO2(TO)的测量 将其维持在生理范围内)。有一个意义重大的 开胸后血氧分压下降。保持血氧分压 在生理范围内，吸入空气中的氧气浓度 气体混合物需要增加到27%。放置了LiPc晶体 直接进入左心肌的中央。外部环路 为放置而开发了带有特殊塑料支架的谐振器 靠近心脏。这个支架包括一个支撑心脏的功能 在外环谐振器中的相同位置。预赛 数据显示，如果氧分压为14.2q2 mm Hg. 血液在90-95毫米汞柱的范围内(五只动物为一组)。之后 此对照测量左冠状动脉受压。在……里面 两个心脏的PO2降至零，而另外三个心脏的PO2下降到零 心肌血氧分压仅有轻度下降。我们的预赛 解释是冠状动脉压迫会导致非常严重的 局部缺血和晶体不在缺血区内。 三个实验。按压20min后再灌流。 在两颗心脏上进行了手术，这两颗心脏都完全恢复了 在20分钟内控制心肌血氧分压。具备以下技术能力 这些实验看起来似乎是合理的。

EPR oximetry of a rat heart in vivo While considerable useful data have been obtained using the isolated heart, there are many aspects which require studies in vivo. These have not been able to be done readily with techniques such as EPR because of the problems of motion and the need to maintain controlled physiological conditions while the animal is within the spectrometer. We now, however, have competed the initial technical developments and obtained useful data on the pO2 within a functioning heart. We used male Wistar rats weighing 200-250 g. Animals initially were anesthetized with a low dose of pentobarbital. and then a tube was placed and positive pressure ventilation started with isoflurane (1%) as the anesthetic. A polyethylene catheter was placed in the right carotid artery for continuos monitoring of blood pressure and periodic blood gas measurements of pO2 (as an experimental parameter) and pCO2 (to maintain it in the physiological range). There was a significant decrease in blood pO2 after the chest was opened. To keep blood pO2 in the physiological range the oxygen concentration in the inspiring gas mixture needed to be increased to 27%. LiPc crystals were placed directly into the middle of the left myocardium. An external loop resonator with a special plastic holder was developed for placement near the heart. This holder included a feature to support the heart at the same position in the external loop resonator. The preliminary data show that the myocardial pO2 = 14.2q2 mm Hg if oxygen tension in blood is in the range 90-95 mm Hg (in group of five animals). After this control measurement the left coronary artery was compressed. In two hearts myocardial pO2 dropped down to zero while in three others there was only a moderate decrease in myocardial pO2. Our preliminary interpretation is that the coronary artery compression causes a very local ischemia and crystals were not within the ischemic area in these three experiments. Reperfusion after 20 minutes compression was carried out in two hearts and these both had a full recovery to the control myocardial pO2 within 20 minutes. The technical capability to do the experiments seems reasonably established.