DEVELOPMENT OF APPARATUS TO STUDY HEART IN VIVO
DEVELOPMENT OF APPARATUS TO STUDY HEART IN VIVO
批准号:
6123395
负责人:
STEVEN B LEICHTWEIS
金额:
$1.95万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
1998
资助国家:
美国
项目状态:
已结题
起止时间:
1998-09-15 至 1999-08-31
中文摘要
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英文摘要
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.
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