抄録
Recently it has experimentally and clinically become evident that spasm may occur in coronary arteries of some species of experimental animals and also of human. This study was attempted to elucidate if coronary spasm could be more easily induced in arteries which had been involved by organic diseases such as athero-sclerosis before drug-induction of spasm in experimental animals.
Swine had been pretreated with denuding of endothelium of left anterior descending branch of coronary arteries by brushing through coronary catheterization, and then fed with a high fat diet for 14 weeks at the longest. After coronary arteriosclerosis was proven to have been produced by a coronary angiography and ECG monitoring was set, methacholine was injected intramuscularly.
Among 9 swine in the experimental group with pre-existing coronary arteriosclerosis, 6 developed coronary arterial spasm, which was confirmed angiographically and in which ECG changes such as ST elevation in 4 animals or depression in 2. Spasm appeared in the period between 10 seconds to 20 minutes after the injection. In contrast, control group without the pretreatment to produce arteriosclerosis had 2 swine, which developed coronary spasm in 9 animals.
Coronary arterial spasm generally persisted from couples of minutes to over ten minutes. The animals to show ST elevation on ECG tended to develop stronger spastic changes on arteriography, while others to have ST depression had weaker lumen narrowing or localized spasm to certain focal segments.
Immunohistochemistry with use of anti-swine fibrinogen antibody revealed deposition of reaction products in subendothelial areas of intima, and also in cytoplasm of smooth muscle cells in the segments of the coronary arteries, where arteriosclerosis had been artificially produced. In the segments where spasm had been proven on angiography only very slight deposits of reaction product were demonstrated in subendothelial layer. This did not indicate intensified vascular permeability in those segments at one time spasm. Repeated arterial spasm may lead to accelerate vascular permeability, but further investigations would be needed to prove that.
This result of the experiment leads to a conclusion that preexistence of some organic diseases in coronary arteries may play a role in induction of coronary spasm by neurohumoral factors.
