TY - JOUR
T1 - Global left ventricular contractility in three models of hypertrophy evaluated with Emax
AU - Alyono, David
AU - Steves Ring, W.
AU - Crumbley, Arthur J.
AU - Schneider, Joseph R.
AU - O'Connor, Melody J.
AU - Parrish, Deborah
AU - Bache, Robert J.
AU - Anderson, Robert W.
N1 - Funding Information:
’ Supported by Grant HL 22 152 and HL 2 1872 from the National Heart, Lung and Blood Institute. ’ Dr. Alyono is the recipient of the National Research Service Award HL 06567 from the National Heart, Lung and Blood Institute, and the 1 lth American College of Surgeons Scholarship.
PY - 1984/7
Y1 - 1984/7
N2 - Using the load independent contractility index, end-systolic pressure-volume ratio (Emax), contractility of the hypertrophied left ventricle (LV) from three different models was evaluated in conscious, resting dogs. The experimental animals included 12 dogs with perinephritic hypertension (HYP) (aortic diastolic pressure 130 ± 5 mm Hg), 12 dogs who underwent aortic banding (AOB) at 6 to 8 weeks of age (resting aortic gradient 110 ± 15 mm Hg), and 12 dogs with chronic fluid overload from aortocaval fistula (ACF). These were compared with 12 normal dogs (CTL). LV dimension and pressure were measured with ultrasonic tranducers and micromanometers. All three models resulted in hypertrophy with significant (P < 0.01) increase in LV weight-to-body weight ratio (6.3 ± 0.4, 8.4 ± 0.5, 6.3 ± 0.4, respectively, vs 4.4 ± 0.1 g/kg). Cardiac output (6908 ± 740 vs 2424 ± 276 ml/min) and end-diastolic volume (118 ± 11 vs 50 ± 4 ml) were significantly (P < 0.01) increased in AOB (18 ± 1 vs 9 ± 2 mm Hg). dp/dtmax was not significantly different among all groups. Emax (CTL = 5.3 ± 0.4 mm Hg/ml) was not significantly changed in HYP (9.5 ± 2.1) but was significantly (P < 0.01) increased in AOB (14.1 ± 2.6), and significantly (P < 0.01) depressed in ACF (2.4 ± .03). Thus, LV hypertrophy from systemic hypertension (HYP) or proximal aortic hypertension (AOB) is, at least initially, associated with preservation of contractility and normal hemodynamic performance. However, LV contractility of hypertrophied heart from chronic fluid overload (ACF) was depressed, and the normal (or increased) hemodynamic performance (dp/dtmax, peak left ventricular pressure, cardiac output) appeared to be maintained by utilizing Starling preload reserves.
AB - Using the load independent contractility index, end-systolic pressure-volume ratio (Emax), contractility of the hypertrophied left ventricle (LV) from three different models was evaluated in conscious, resting dogs. The experimental animals included 12 dogs with perinephritic hypertension (HYP) (aortic diastolic pressure 130 ± 5 mm Hg), 12 dogs who underwent aortic banding (AOB) at 6 to 8 weeks of age (resting aortic gradient 110 ± 15 mm Hg), and 12 dogs with chronic fluid overload from aortocaval fistula (ACF). These were compared with 12 normal dogs (CTL). LV dimension and pressure were measured with ultrasonic tranducers and micromanometers. All three models resulted in hypertrophy with significant (P < 0.01) increase in LV weight-to-body weight ratio (6.3 ± 0.4, 8.4 ± 0.5, 6.3 ± 0.4, respectively, vs 4.4 ± 0.1 g/kg). Cardiac output (6908 ± 740 vs 2424 ± 276 ml/min) and end-diastolic volume (118 ± 11 vs 50 ± 4 ml) were significantly (P < 0.01) increased in AOB (18 ± 1 vs 9 ± 2 mm Hg). dp/dtmax was not significantly different among all groups. Emax (CTL = 5.3 ± 0.4 mm Hg/ml) was not significantly changed in HYP (9.5 ± 2.1) but was significantly (P < 0.01) increased in AOB (14.1 ± 2.6), and significantly (P < 0.01) depressed in ACF (2.4 ± .03). Thus, LV hypertrophy from systemic hypertension (HYP) or proximal aortic hypertension (AOB) is, at least initially, associated with preservation of contractility and normal hemodynamic performance. However, LV contractility of hypertrophied heart from chronic fluid overload (ACF) was depressed, and the normal (or increased) hemodynamic performance (dp/dtmax, peak left ventricular pressure, cardiac output) appeared to be maintained by utilizing Starling preload reserves.
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U2 - 10.1016/0022-4804(84)90160-4
DO - 10.1016/0022-4804(84)90160-4
M3 - Article
C2 - 6234433
AN - SCOPUS:0021250327
SN - 0022-4804
VL - 37
SP - 48
EP - 54
JO - Journal of Surgical Research
JF - Journal of Surgical Research
IS - 1
ER -