TY - JOUR
T1 - Collateral function modified by glyceryl trinitrate and dipyridamole during coronary occlusion in conscious dogs
AU - Nabeyama, Shozo
AU - Tomoike, Hitonobu
AU - Hisano, Katashi
AU - Shimokawa, Hiroaki
AU - Inoue, Takeshi
AU - Yamamoto, Hideo
AU - Nakamura, Motoomi
N1 - Funding Information:
This project was supported in part by grants for Scientific Research and a grants for Developmental Scientific Research from the Ministry of Education, Science and Culture, Japan, and a research grant for cardiovascular disease from the Ministry of Health and Welfare, Japan.
PY - 1987/3
Y1 - 1987/3
N2 - Summary: The effects of glyceryl trinitrate and dipyridamole on induced ischaemia were studied in awake dogs during transient coronary occlusion before and after collateral development. Seventeen dogs were instrumented under sterile conditions with a miniature pressure gauge to measure left ventricular pressure, a cannula for aortic pressure, and pairs of piezoelectric crystals towards the subendocardium of the left ventricle for regional segment length measurements. A hydraulic cuff occluder and Doppler flow probe were placed around the left circumflex coronary artery. Collateral function was increased by repeated 2 min coronary occlusions at 32 min intervals for 2-9 days until regional wall motion returned to preocclusive values, despite the persistence of coronary occlusion. The effects of glyceryl trinitrate and dipyridamole were studied after the initial haemodynamic changes had subsided. Collateral function was quantified by integrating changes in end systolic length of the ischaemic area during coronary occlusion. Before collateral development the end systolic length area was 29.4(2.4) cm·s and was unchanged by glyceryl trinitrate or dipyridamole. After the development of collaterals the end systolic length area decreased from 4.1(1.1) to 2.2(1.0) cm·s (p<0.01) after glyceryl trinitrate and increased to 14.9(1.7) cm·s (p<0.01) after dipyridamole. Therefore, glyceryl trinitrate acted directly on collaterals and improved the induced ischaemia, whereas dipyridamole exaggerated the regional wall motion abnormality.
AB - Summary: The effects of glyceryl trinitrate and dipyridamole on induced ischaemia were studied in awake dogs during transient coronary occlusion before and after collateral development. Seventeen dogs were instrumented under sterile conditions with a miniature pressure gauge to measure left ventricular pressure, a cannula for aortic pressure, and pairs of piezoelectric crystals towards the subendocardium of the left ventricle for regional segment length measurements. A hydraulic cuff occluder and Doppler flow probe were placed around the left circumflex coronary artery. Collateral function was increased by repeated 2 min coronary occlusions at 32 min intervals for 2-9 days until regional wall motion returned to preocclusive values, despite the persistence of coronary occlusion. The effects of glyceryl trinitrate and dipyridamole were studied after the initial haemodynamic changes had subsided. Collateral function was quantified by integrating changes in end systolic length of the ischaemic area during coronary occlusion. Before collateral development the end systolic length area was 29.4(2.4) cm·s and was unchanged by glyceryl trinitrate or dipyridamole. After the development of collaterals the end systolic length area decreased from 4.1(1.1) to 2.2(1.0) cm·s (p<0.01) after glyceryl trinitrate and increased to 14.9(1.7) cm·s (p<0.01) after dipyridamole. Therefore, glyceryl trinitrate acted directly on collaterals and improved the induced ischaemia, whereas dipyridamole exaggerated the regional wall motion abnormality.
KW - Collateral function
KW - Dipyridamole
KW - Glyceryl trinitrate
KW - Myocardial ischaemia
KW - Regional wall motion
UR - http://www.scopus.com/inward/record.url?scp=85047677753&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85047677753&partnerID=8YFLogxK
U2 - 10.1093/cvr/21.3.177
DO - 10.1093/cvr/21.3.177
M3 - Article
C2 - 3115584
AN - SCOPUS:85047677753
VL - 21
SP - 177
EP - 187
JO - Cardiovascular Research
JF - Cardiovascular Research
SN - 0008-6363
IS - 3
ER -