心包膜腔內注入 Neuropeptide Y以誘發缺氧心肌之血管新生–豬之動物實驗模式
Date Issued
2005
Date
2005
Author(s)
廖朝崧
DOI
932314B002222
Abstract
There are patients with coronary artery disease who suffered from severe and
diffuse narrowing or occlusion of their coronary arteries, in whom the conventional
revascularization procedures can not be applied. One potential strategy for these patients
is creation of new blood vessel channels in the region of ischemia, (therapeutic
angiogenesis). A number of potential angiogenic agents have been identified to enhance
the process of collateral development, but, to date, only two growth factors, fibroblastic growth factor (FGF) and vascular endothelial growth factor (VEGF), have been
clinically used in patients with refractory ischemia.
Neuropeptide Y (NPY) has been proved as one of the potent growth factors for
angiogenesis. The pericardial space may potentially serve as a drug delivery reservoir
which may render persistent effects of the administered therapeutic agents to the heart.
In this experiment, we tested the effects of NPY administered through pericardial
chamber on the angiogenesis of ischemic myocardium in a porcine myocardial
infarction model.
We performed experiments on 3 groups of pigs, the neuropeptide Y (NPY) group,
the control group, and the adhesion group. Acute myocardial infarction (AMI) was first
induced in all experimental pigs by occlusion of a coronary artery, left anterior
descending artery in most pigs. After 1-3 weeks, either drug administration (NPY or
minocyclin) or non-specific drug (saline) administration (control group) was performed.
The NPY group consisted of 10 pigs, in them NPY 0.5 mg in 5 ml sterile water was
administrated through a catheter into the pericardium. In the control group, 10 pigs,
after induction of AMI, only saline intrapericardial administration was applied. In the
adhesion group, 9 pigs, minocyclin was administrated into pericardial sac 1-2 weeks
after AMI to induce pericardial adhesion. Pigs were sacrificed 4-7 weeks after induction
of AMI and the hearts were measured grossly and examined microscopically.
In this study we found that administration of NPY did not induce new vessel
production in the myocardium near the infarction area. Yet, the administration of NPY
seemed to result in reduced heart weight, a beneficial effect. We also found that the wall
thickness of LV wall as well as the infarction size was not affected by the administration
of either NPY or minicyclin. Incidentally, we found that intrapericardial administration
of minicyclin could induce active new vessel growth in the myocardium near the
infarction area. This finding may be worthy of further studies.
Subjects
angiogenesis
collateral circulation
pericardial drug administration
coronary
artery disease
artery disease
myocardial ischemia
Publisher
臺北市：國立臺灣大學醫學院內科
Type
report
File(s)![Thumbnail Image]()
Loading...
Name
932314B002222.pdf
Size
1.19 MB
Format
Adobe PDF
Checksum
(MD5):df5cae3438ac8b1c730d2ce86fdf39a8