TY - JOUR
T1 - Time constant of isovolumic pressure fall
T2 - Determinants in the working left ventricle
AU - Frederiksen, J. W.
AU - Weiss, J. L.
AU - Weisfeldt, M. L.
PY - 1978
Y1 - 1978
N2 - The influence of hemodynamics and pharmacologic agents on the time course of isovolumic pressure fall was studied in the working dog, right-heart-bypass preparation. The time constant (T) was determined for the exponential portion of the left ventricular pressure (LVP) fall following maximum negative dP/dt. No significant changes in T occurred as a result of 1) variation in cardiac input between 1.5 and 4.0 l/min at constant peak LVP and heart rate (n = 8) or 2) variation in peak LVP between 85 ± 3 and 192 ± 3 mmHg at constant cardiac input and heart rate (n = 7). Abrupt changes in heart rate from 110 to 180 beats/min at constant stroke volume and peak LVP shortened T from 27 ± 4 to 23 ± 3 ms (P < 0.02). A significant increase in T occurred after administration of propranolol, whereas norepinephrine decreased T and acetylstrophanthidin after propranolol also decreased T. To attempt to dissociate possible effects of increased velocity of shortening on T from effects of increased inotropy per se, mean velocity of circumferential fiber shortening (V(CF)) was estimated in nine hearts. Lowering peak LVP from 160 ± 5 to 83 ± 3 mmHg resulted in an increase in mean V(CF) from 1.19 ± 0.27 to 1.54 ± 0.31 diam/s (circ/s) (P < 0.01); T did not change significantly, 42 ± 4 vs. 45 ± 4 ms (NS). Norepinephrine, in contrast, caused a similar increase in mean V(CF) from 1.59 ± 0.16 to 2.00 ± 0.22 diam/s (P < 0.05), but again T shortened, 36 ± 2 to 27 ± 2 ms (P < 0.01). Hence, in the working preparation, T appears independent of stroke volume, peak LVP, and fiber shortening velocity within broad physiological ranges. Large increases in heart rate result in small but significant shortening of T. T is altered by pharmacologic agents thought to influence the active cardiac relaxing system or the inotropic state or both.
AB - The influence of hemodynamics and pharmacologic agents on the time course of isovolumic pressure fall was studied in the working dog, right-heart-bypass preparation. The time constant (T) was determined for the exponential portion of the left ventricular pressure (LVP) fall following maximum negative dP/dt. No significant changes in T occurred as a result of 1) variation in cardiac input between 1.5 and 4.0 l/min at constant peak LVP and heart rate (n = 8) or 2) variation in peak LVP between 85 ± 3 and 192 ± 3 mmHg at constant cardiac input and heart rate (n = 7). Abrupt changes in heart rate from 110 to 180 beats/min at constant stroke volume and peak LVP shortened T from 27 ± 4 to 23 ± 3 ms (P < 0.02). A significant increase in T occurred after administration of propranolol, whereas norepinephrine decreased T and acetylstrophanthidin after propranolol also decreased T. To attempt to dissociate possible effects of increased velocity of shortening on T from effects of increased inotropy per se, mean velocity of circumferential fiber shortening (V(CF)) was estimated in nine hearts. Lowering peak LVP from 160 ± 5 to 83 ± 3 mmHg resulted in an increase in mean V(CF) from 1.19 ± 0.27 to 1.54 ± 0.31 diam/s (circ/s) (P < 0.01); T did not change significantly, 42 ± 4 vs. 45 ± 4 ms (NS). Norepinephrine, in contrast, caused a similar increase in mean V(CF) from 1.59 ± 0.16 to 2.00 ± 0.22 diam/s (P < 0.05), but again T shortened, 36 ± 2 to 27 ± 2 ms (P < 0.01). Hence, in the working preparation, T appears independent of stroke volume, peak LVP, and fiber shortening velocity within broad physiological ranges. Large increases in heart rate result in small but significant shortening of T. T is altered by pharmacologic agents thought to influence the active cardiac relaxing system or the inotropic state or both.
UR - http://www.scopus.com/inward/record.url?scp=0018157075&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0018157075&partnerID=8YFLogxK
U2 - 10.1152/ajpheart.1978.235.6.h701
DO - 10.1152/ajpheart.1978.235.6.h701
M3 - Article
C2 - 736158
AN - SCOPUS:0018157075
SN - 0363-6135
VL - 4
SP - H701-H706
JO - American Journal of Physiology
JF - American Journal of Physiology
IS - 6
ER -