Transmitral inflow pattern assessed by Doppler echocardiography in angiotensin II type 1A receptor knockout mice with myocardial infarction.
Many studies have suggested that the renin-angiotensin system plays an important role in the left ventricular (LV) remodeling and cardiac dysfunction that occurs after myocardial infarction (MI). Although angiotensin II type IA (AT1A) receptor knockout (KO) mice are reported to display less LV remodeling after MI, diastolic dysfunction has not been fully evaluated, so the present study measured transmitral inflow pattern in both AT1A receptor KO mice with MI (KO-MI) and wild type mice with MI (WT-MI). Cardiac geometry and function were examined by Doppler echocardiography and myocardial mRNA expression was determined by Northern blot analysis at 4 weeks after MI. The LV internal diastolic dimension of WT-MI was larger than that of the KO-MI (p<0.05). Marked increases in the E wave velocity and the ratio of the peak velocity of the E wave to the A wave were observed in the WT-MI (p<0.01). The deceleration rate of the E wave in KO-MI was lower than in WT-MI (p<0.05). mRNA expressions of ANP, BNP, collagen I and collagen III in the non-infarcted LV and RV of KO-MI were significantly lower than WT-MI. In conclusion, transmitral inflow abnormalities in KO-MI were attenuated compared with WT-MI.
Nakamura
Yasuhiro
Y
Department of Internal Medicine and Cardiology, Graduate School of Medicine, Osaka City University, Osaka, Japan.
Yoshiyama
Minoru
M
Omura
Takashi
T
Yoshida
Ken
K
Kim
Shokei
S
Takeuchi
Kazuhide
K
Iwao
Hiroshi
H
Yoshikawa
Junichi
J
D000818:Animals; D009320:Atrial Natriuretic Factor / Q000235:genetics; D024042:Collagen Type I / Q000235:genetics; D024061:Collagen Type III / Q000235:genetics; D003326:Coronary Circulation / Q000502:physiology*; D004195:Disease Models, Animal; D019560:Echocardiography, Three-Dimensional; D005786:Gene Expression Regulation; D006439:Hemodynamics; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D008943:Mitral Valve / Q000503:physiopathology*; D009203:Myocardial Infarction / Q000000981:diagnostic imaging / Q000235:genetics / Q000503:physiopathology*; D020097:Natriuretic Peptide, Brain / Q000235:genetics; D044140:Receptor, Angiotensin, Type 1; D011945:Receptors, Angiotensin / Q000172:deficiency* / Q000235:genetics / Q000502:physiology*; D014158:Transcription, Genetic
D024042:Collagen Type I; D024061:Collagen Type III; D044140:Receptor, Angiotensin, Type 1; D011945:Receptors, Angiotensin; D020097:Natriuretic Peptide, Brain; D009320:Atrial Natriuretic Factor