Coronary blood flow after the regression of pressure-overload left ventricular hypertrophy. 1992

K Ishihara, and M R Zile, and M Nagatsu, and K Nakano, and M Tomita, and S Kanazawa, and L Clamp, and G DeFreyte, and B A Carabello
Ralph H. Johnson Department of Veterans Affairs Medical Center, Charleston, S.C.

Abnormal coronary blood flow (CBF) in long-standing left ventricular (LV) pressure-overload hypertrophy has been associated with ischemia and LV dysfunction. Thus, goals of therapy in pressure overload are not only the relief of the overload itself but also regression in hypertrophy and subsequent improvement in CBF. However, little is known about CBF in humans or in large mammals after the relief of pressure overload, when the hypertrophy has regressed. This study was performed to test the hypothesis that, even 6 months after the relief of pressure overload in the dog, CBF would still be abnormal. Three groups of dogs were studied: 1) normal control dogs (NL group), 2) dogs with LV pressure-overload hypertrophy (LVH group), and 3) dogs that had developed LV pressure-overload hypertrophy but in whom the pressure overload was relieved 6 months before the final study (LVH Reg group). CBF was studied in conscious dogs by use of the radiolabeled microsphere technique at rest, during rapid atrial pacing, and during maximum coronary vasodilation produced by adenosine infusion. The ratio of LV weight (g) to body weight (kg) (LVBW) was 4.2 +/- 0.3 in the NL group, 7.1 +/- 0.6 in the LVH group, and 7.7 +/- 0.5 in the LVH Reg group before pressure-overload relief (p = NS, LVH versus LVH Reg). Six months after removal of the pressure overload, the LVBW in the LVH Reg group had fallen to 5.5 +/- 0.3 (p < 0.05), but this LVBW was still greater than that in the NL group (p < 0.05). During rapid atrial pacing, endocardial and epicardial CBF rose significantly in NL dogs. However, during rapid atrial pacing, endocardial CBF fell from 1.18 +/- 0.22 to 0.7 +/- 0.20 ml/min per gram in the LVH group (p < 0.05) and did not rise in the LVH Reg group. During adenosine infusion, endocardial blood flow increased in NL dogs from 1.63 +/- 0.13 to 4.0 +/- 0.3 ml/min per gram and increased to a similar level in the LVH Reg group. Although CBF increased during adenosine infusion in the LVH group, the increase was less than that in the NL or LVH Reg group (p < 0.05). Minimum coronary vascular resistance was similar in NL dogs (14 +/- 2 units) and LVH Reg dogs (18 +/- 3 units, p = NS) but was significantly elevated (32 +/- 10 units) in LVH dogs (p < 0.05).(ABSTRACT TRUNCATED AT 400 WORDS)

UI MeSH Term Description Entries
D008955 Models, Cardiovascular Theoretical representations that simulate the behavior or activity of the cardiovascular system, processes, or phenomena; includes the use of mathematical equations, computers and other electronic equipment. Cardiovascular Model,Cardiovascular Models,Model, Cardiovascular
D001794 Blood Pressure PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS. Systolic Pressure,Diastolic Pressure,Pulse Pressure,Pressure, Blood,Pressure, Diastolic,Pressure, Pulse,Pressure, Systolic,Pressures, Systolic
D002304 Cardiac Pacing, Artificial Regulation of the rate of contraction of the heart muscles by an artificial pacemaker. Pacing, Cardiac, Artificial,Artificial Cardiac Pacing,Artificial Cardiac Pacings,Cardiac Pacings, Artificial,Pacing, Artificial Cardiac,Pacings, Artificial Cardiac
D003326 Coronary Circulation The circulation of blood through the CORONARY VESSELS of the HEART. Circulation, Coronary
D004285 Dogs The domestic dog, Canis familiaris, comprising about 400 breeds, of the carnivore family CANIDAE. They are worldwide in distribution and live in association with people. (Walker's Mammals of the World, 5th ed, p1065) Canis familiaris,Dog
D004452 Echocardiography Ultrasonic recording of the size, motion, and composition of the heart and surrounding tissues. The standard approach is transthoracic. Echocardiography, Contrast,Echocardiography, Cross-Sectional,Echocardiography, M-Mode,Echocardiography, Transthoracic,Echocardiography, Two-Dimensional,Transthoracic Echocardiography,2-D Echocardiography,2D Echocardiography,Contrast Echocardiography,Cross-Sectional Echocardiography,Echocardiography, 2-D,Echocardiography, 2D,M-Mode Echocardiography,Two-Dimensional Echocardiography,2 D Echocardiography,Cross Sectional Echocardiography,Echocardiography, 2 D,Echocardiography, Cross Sectional,Echocardiography, M Mode,Echocardiography, Two Dimensional,M Mode Echocardiography,Two Dimensional Echocardiography
D000241 Adenosine A nucleoside that is composed of ADENINE and D-RIBOSE. Adenosine or adenosine derivatives play many important biological roles in addition to being components of DNA and RNA. Adenosine itself is a neurotransmitter. Adenocard,Adenoscan
D000818 Animals Unicellular or multicellular, heterotrophic organisms, that have sensation and the power of voluntary movement. Under the older five kingdom paradigm, Animalia was one of the kingdoms. Under the modern three domain model, Animalia represents one of the many groups in the domain EUKARYOTA. Animal,Metazoa,Animalia
D013997 Time Factors Elements of limited time intervals, contributing to particular results or situations. Time Series,Factor, Time,Time Factor
D014655 Vascular Resistance The force that opposes the flow of BLOOD through a vascular bed. It is equal to the difference in BLOOD PRESSURE across the vascular bed divided by the CARDIAC OUTPUT. Peripheral Resistance,Total Peripheral Resistance,Pulmonary Vascular Resistance,Systemic Vascular Resistance,Peripheral Resistance, Total,Resistance, Peripheral,Resistance, Pulmonary Vascular,Resistance, Systemic Vascular,Resistance, Total Peripheral,Resistance, Vascular,Vascular Resistance, Pulmonary,Vascular Resistance, Systemic

Related Publications

K Ishihara, and M R Zile, and M Nagatsu, and K Nakano, and M Tomita, and S Kanazawa, and L Clamp, and G DeFreyte, and B A Carabello
June 2005, American journal of physiology. Heart and circulatory physiology,
K Ishihara, and M R Zile, and M Nagatsu, and K Nakano, and M Tomita, and S Kanazawa, and L Clamp, and G DeFreyte, and B A Carabello
March 1980, Cardiovascular research,
K Ishihara, and M R Zile, and M Nagatsu, and K Nakano, and M Tomita, and S Kanazawa, and L Clamp, and G DeFreyte, and B A Carabello
January 1996, Journal of molecular and cellular cardiology,
K Ishihara, and M R Zile, and M Nagatsu, and K Nakano, and M Tomita, and S Kanazawa, and L Clamp, and G DeFreyte, and B A Carabello
August 2017, Circulation,
K Ishihara, and M R Zile, and M Nagatsu, and K Nakano, and M Tomita, and S Kanazawa, and L Clamp, and G DeFreyte, and B A Carabello
January 1992, Cardiology,
K Ishihara, and M R Zile, and M Nagatsu, and K Nakano, and M Tomita, and S Kanazawa, and L Clamp, and G DeFreyte, and B A Carabello
June 1983, The American journal of cardiology,
K Ishihara, and M R Zile, and M Nagatsu, and K Nakano, and M Tomita, and S Kanazawa, and L Clamp, and G DeFreyte, and B A Carabello
October 1992, The American journal of physiology,
K Ishihara, and M R Zile, and M Nagatsu, and K Nakano, and M Tomita, and S Kanazawa, and L Clamp, and G DeFreyte, and B A Carabello
July 1978, Circulation research,
K Ishihara, and M R Zile, and M Nagatsu, and K Nakano, and M Tomita, and S Kanazawa, and L Clamp, and G DeFreyte, and B A Carabello
April 2012, Journal of molecular and cellular cardiology,
K Ishihara, and M R Zile, and M Nagatsu, and K Nakano, and M Tomita, and S Kanazawa, and L Clamp, and G DeFreyte, and B A Carabello
June 1983, Chest,
Copied contents to your clipboard!