scholarly journals Isometric force development, isotonic shortening, and elasticity measurements from Ca2+-activated ventricular muscle of the guinea pig.

1978 ◽  
Vol 71 (4) ◽  
pp. 431-451 ◽  
Author(s):  
D W Maughan ◽  
E S Low ◽  
N R Alpert
1987 ◽  
Vol 253 (3) ◽  
pp. H645-H653
Author(s):  
O. N. Nwasokwa

Canine papillary muscle force-length-time relation (F-L-t) was investigated under pentobarbital sodium anesthesia. The time intervals taken from end diastole to any point (P) on the force-length plane was determined for isometric (t1) and isotonic (t2) systole and corrected for excitation contraction coupling duration. The ratio t1/t2, designated km, was approximately constant for widely scattered positions of P chosen systematically. The km in the 10 dogs ranged from 0.36 to 0.94 with means +/- SD of 0.66 +/- 0.16; km correlated negatively with muscle average cross-sectional area (r = -0.82; P less than 0.005). Assuming constancy of km, a general relationship was derived between (delta F/delta t)t1L, the rate of isometric force development at P; (delta L/delta t)t2F, the velocity of isotonic shortening at P; (delta F/delta L)(t1,t2)t, the stiffness; and (delta L/delta F)(t1,t2)t, the compliance of the myocardium (all taken at P) as follows (delta F/delta L)t1,t2t = -km(delta F/delta t)t1L/(delta L/delta t)t2F and (delta L/delta F)t1,t2t = -km-1(delta L/delta t)t2F/(delta F/delta t)t1t. The ratio of (delta F/delta t)t1L to (delta L/delta t)t2F defines functional proclivity and measures the differential propensity to force development relative to shortening. Thus myocardial stiffness or compliance determines functional proclivity by acting as an impedance-matching transformer that steps up or steps down force development of shortening as warranted by the loading conditions.


1984 ◽  
Vol 247 (1) ◽  
pp. H8-H16
Author(s):  
O. Nwasokwa ◽  
K. Sagawa ◽  
H. Suga

We studied the effect of intracycle (short-term) mechanical history on canine myocardial performance. Intracycle muscle force and/or length history was varied, and the resultant changes in end-systolic force-length relationship were analyzed. Antecedent isotonic shortening impaired, whereas isometric force development enhanced end-systolic myocardial performance. A history of shortening concurrent with force development produced an intermediate effect. We conclude that decreasing force or length impairs whereas increasing length or force enhances performance in the same cycle. Different combinations of antecedent force and length changes affect end-systolic performance by algebraic summation (superposition) of their disparate effects. Time measurements established that 1) total systolic time varied little with altered history, 2) isotonic shortening took longer than isometric contraction in reaching a point P in the force-length plane, and 3) less time was therefore available for contraction after P with antecedent isotonic shortening than with antecedent isometric force development. This history-dependent time differential accounts for the corresponding differential in performance.


1986 ◽  
Vol 250 (4) ◽  
pp. H612-H619 ◽  
Author(s):  
R. S. Moreland ◽  
T. C. Major ◽  
R. C. Webb

This study characterizes isometric force development in response to ouabain and K+-free solution in isolated aortic strips from spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats. SHR aortas were more sensitive to ouabain than those from WKY (threshold: SHR, 3.1 X 10(-5) M; WKY, 25.6 X 10(-5) M), and force development in response to 10(-3) M ouabain was greater in SHR (SHR, 586 +/- 51 mg; WKY, 245 +/- 24 mg). Monensin, a Na+ ionophore, potentiated contractile responses to ouabain, whereas amiloride, a Na+ channel blocker, and low Na+ solutions depressed contractile responses to ouabain. Contractile responses of SHR aortic strips to K+-free solution were faster than those of WKY aortic strips [time to half-maximal response (t1/2): SHR, 24 +/- 5 min; WKY, 47 +/- 4 min]. Maximal force development by aortic strips from SHR in response to K+-free solution was not different from that of WKY aortic strips (SHR, 808 +/- 34 mg; WKY, 750 +/- 37 mg). Monensin (10(-5) M) increased the rate of force development to K+-free solution to a greater extent in WKY aortic strips than in those from SHR (t1/2: SHR, 3 +/- 1 min; WKY, 4 +/- 2 min). Amiloride and low Na+ solution depressed contractile responses to K+-free solution in both SHR and WKY aortic strips. These observations demonstrate that SHR aortas are more responsive to ouabain and K+-free solution compared with WKY aortas. Contractile responses to ouabain and K+-free solution were sensitive to experimental interventions that alter transmembrane Na+ movements.(ABSTRACT TRUNCATED AT 250 WORDS)


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