Intracellular Ca2+ transients in the cat papillary muscle

1982 ◽  
Vol 60 (4) ◽  
pp. 524-528 ◽  
Author(s):  
J. P. Morgan ◽  
J. R. Blinks

Intracellular Ca2+ transients in cat papillary muscles were detected with the calcium-sensitive bioluminescent protein aequorin and correlated with tension development. The effects of a variety of inotropic interventions are interpreted in terms of their probable effects on Ca2+ entry, Ca2+ release, Ca2+ sequestration, and the Ca2+ -sensitivity of the contractile apparatus. In contrast to results reported in dog Purkyně strands, the aequorin signals in cat papillary muscles appear to be dominated by release of Ca2+ from intracellular stores.

1979 ◽  
Vol 237 (3) ◽  
pp. H293-H298
Author(s):  
I. Palacios ◽  
K. Sagar ◽  
W. J. Powell

It has been previously established that hyperthyroid myocardium exhibits increased performance under well-oxygenated conditions. To date, it is not known whether hyperthyroid cardiac muscle can maintain this increased performance during hypoxia. The responses of isolated right ventricular papillary muscles from hyperthyroid and euthyroid kittens to hypoxia were compared under isometric conditions at 31 degrees C. Under well-oxygenated conditions, the hyperthyroid cardiac muscle exhibited both an increased contractility and an accelerated rate of relaxation. A similar degree of acute hypoxic stress for 15 min resulted in a greater decrease in contractility in the hyperthyroid compared with the euthyroid papillary muscle as indicated by a greater fall in both peak tension development (2.2 +/- 0.25 from 4.2 +/- 0.2 vs. 0.9 +/- 0.15 from 3.2 +/- 0.4 g/mm2, P less than 0.01) and +dT/dt (12.9 +/- 2.3 from 25 +/- 3 vs. 4.0 +/- 0.6 from 14 +/- 1 g-s-1-mm-2, P less than 0.01). In addition, compared with the euthyroid data, hypoxia resulted in impaired myocardial relaxation in the hyperthyroid cardiac muscle. Thus, the hyperthyroid compared with the euthyroid papillary muscle exhibits both a greater decrease in contractility and an impairment of myocardial relaxation during hypoxia, indicating a greater susceptibility to a given hypoxic stress.


1986 ◽  
Vol 250 (2) ◽  
pp. H208-H212 ◽  
Author(s):  
J. E. Carter ◽  
I. Palacios ◽  
W. H. Frist ◽  
S. Rosenthal ◽  
J. B. Newell ◽  
...  

Hypoxia has been demonstrated to cause impairment of myocardial relaxation. This impairment of relaxation is particularly pronounced during early reoxygenation. This study was undertaken in 24 isometric cat papillary muscles at 38 degrees C to determine if nifedipine can influence the impairment of relaxation produced during reoxygenation following hypoxia. A dose of nifedipine was chosen that produced only a minimal depression of peak systolic tension and no change in the half time to relaxation (RT 1/2) under well-oxygenated conditions. Thirty minutes of hypoxia were produced in 12 muscles, and systolic tension decreased by the same amount in muscles treated or not treated with nifedipine. During early hypoxia in the absence of nifedipine, RT1/2 was significantly prolonged (P less than 0.01) from 104 +/- 7 to 126 +/- 9 ms. After pretreatment with nifedipine, the change in RT1/2 with hypoxia was not significant. More striking was the near abolition of the marked impairment of relaxation seen during early reoxygenation (238 +/- 33 ms without nifedipine and 128 +/- 8 ms with nifedipine, P less than 0.01). These data establish that, although nifedipine only minimally attenuates the relaxation impairment early during hypoxia, this agent can substantially reduce the impairment of relaxation produced by early reoxygenation.


1977 ◽  
Vol 233 (5) ◽  
pp. H613-H616 ◽  
Author(s):  
L. L. Huntsman ◽  
S. R. Day ◽  
D. K. Stewart

Microspheres infused into the coronary microcirculation were used as markers to define segments within isolated cat papillary muscles. Video recording and analysis provided measurements of the variations of segment lengths as the muscles contracted at lengths of 76–100% Lmax. In all muscles, segments in the center region were found to shorten during muscle isometric contraction while those in the end regions lengthened. Central shortening was typically 10–15%. In the passive state, segment lengths varied directly with muscle length over a broad range characterized by low force. Segments in the center region, however, displayed an abrupt transition to high stiffness at a certain length while end regions continued to stretch. Force-length relationships obtained for the presumably healthy center segment are significantly different from those obtained for the whole muscle. These results suggest that there may be major difficulties with the interpretation of mechanical measurements on papillary muscles unless contractile inhomogeneity is eliminated or taken into account.


1986 ◽  
Vol 87 (2) ◽  
pp. 223-242 ◽  
Author(s):  
D T Yue ◽  
E Marban ◽  
W G Wier

To determine features of the steady state [Ca2+]-tension relationship in intact heart, we measured steady force and intracellular [Ca2+] ([Ca2+]i) in tetanized ferret papillary muscles. [Ca2+]i was estimated from the luminescence emitted by muscles that had been microinjected with aequorin, a Ca2+-sensitive, bioluminescent protein. We found that by raising extracellular [Ca2+] and/or by exposing muscles to the Ca2+ channel agonist Bay K 8644, tension development could be varied from rest to an apparently saturating level, at which increases in [Ca2+]i produced no further rise in force. 95% of maximal Ca2+-activated force was reached at a [Ca2+]i of 0.85 +/- 0.06 microM (mean +/- SEM; n = 7), which suggests that the sensitivity of the myofilaments to [Ca2+]i is far greater than anticipated from studies of skinned heart preparations (or from previous studies using Ca2+-sensitive microelectrodes in intact heart). Our finding that maximal force was reached by approximately 1 microM also allowed us to calculate that the steady state [Ca2+]i-tension relationship, as it might be observed in intact muscle, should be steep (Hill coefficient of greater than 4), which is consistent with the Hill coefficient estimated from the entire [Ca2+]i-tension relationship derived from families of variably activated tetani (6.08 +/- 0.68; n = 7). Finally, with regard to whether steady state measurements can be applied directly toward understanding physiological contractions, we found that the relation between steady force and [Ca2+]i obtained during tetani was steeper than that between peak force and peak [Ca2+]i observed during physiological twitches.


1962 ◽  
Vol 203 (1) ◽  
pp. 206-208
Author(s):  
Arthur L. Bassett ◽  
Brian F. Hoffman

Isolated cat papillary muscles were used to demonstrate the effects of temperatures up to 48 C on resting length and amplitude of isotonic contraction. Progressive heating caused an initial increase and then a marked decrease in resting length; the shortening was irreversible in most instances. Progressive heating caused a decrease and then an increase in amplitude of contraction. Maintained high temperature caused a subsequent decrease in contraction. The permanence of these changes depended on the maximum temperature reached and the duration of exposure. Ouabain and epinephrine failed to influence the contracture caused by high temperature.


1972 ◽  
Vol 50 (1) ◽  
pp. 37-44 ◽  
Author(s):  
E. C. Vos ◽  
G. B. Frank

A brief exposure (about 10–30 s) of a frog's toe muscle or a small bundle of fibers from the semi-tendinosus muscle to just subthreshold potassium concentrations potentiated contractures subsequently produced by exposing the muscles to a potassium concentration slightly above the threshold. The contractures thus potentiated had greater maximum tensions, and greater rates of tension development and relaxation than control contractures elicited by the same final potassium concentration. The resistance to stretch (R.T.S.) in the first few seconds of the potentiated contractures was about twice that of control contractures. Maximum potentiation occurred with preexposures of about 30 s; longer preexposures led to a decrease of potentiation and eventually to a depression of the contracture. The potentiation was not immediately abolished when the muscle was reexposed to Ringer solution but persisted for 2 min or longer (the 'washout effect'). It was concluded that exposing a muscle to low subcontracture threshold concentrations of potassium for a few seconds primes the intracellular contractile apparatus, probably by causing an increased sarcoplasmic concentration of Ca2+ ions, resulting in a potentiation of subsequently induced submaximal potassium contractures. The increase in metabolism (or 'Solandt effect') seen under these conditions is temporally related to the decline and eventual loss of the potentiation and is probably a reflection of active processes involved in reducing the sarcoplasmic concentration of Ca2+ ions.


2021 ◽  
Vol 8 (31) ◽  
pp. 2865-2869
Author(s):  
Praveen Mulki Shenoy ◽  
Amith Ramos ◽  
Narasimha Pai ◽  
Bharath Shetty ◽  
Aravind Pallipady Rao

BACKGROUND The papillary muscle basal connections have significant clinical implications. Variety of studies done on its morphology and function by various specialists in different departments. A close look on these revealed the interconnections of papillary muscles to one another and to the interventricular septum of both ventricles is related to uncoordinated contractions of papillary muscles, leading to hyper or hypokinesia or prolapse or even its rupture. METHODS Our study done in 25 formalin soaked hearts revealed after the deep and meticulous dissection, reflecting the walls of ventricles laterally the numerous interconnections of papillary muscles at its bases and IVS. Ventricles are opened by inverted ‘L’ shaped incision and its reflected more laterally till all the papillary muscles is visible in one frame after incising the moderator band. The connections were noted, measured, photographed, tabulated, compared with similar studies and analysed with experts with respective fields. RESULTS Almost all the specimens did have the interconnections. Further the post mortem findings of the cardiac related deaths with involvement of papillary muscles suggest damage to such ‘bridges’. The moderator band extensions to the base of right APM, and its extension to the posterior groups is noted in all the specimens. The bridge from the IVS to bases of both the groups of papillary muscles is noted in left ventricle. In90% of specimens the one PPM is found to be loosely connected, more so in left ventricle. CONCLUSIONS We are of a conclusion that such basal interconnections and to the interventricular septum are responsible for rhythmic contractions of papillary muscles of both ventricles. Since the AV valves have to open simultaneously, interconnections becomes mandatory as the impulse has to reach it before it reaches the trabeculae carniae. One of the Posterior papillary muscles is loosely connected to other papillary muscles, may be the reason for its rupture, more so in left ventricle. KEYWORDS Papillary Muscle, Interbasal Connection, Moderator Band, Valvular Prolapse, AV Valves


1977 ◽  
Vol 40 (4) ◽  
pp. 366-371 ◽  
Author(s):  
L L Huntsman ◽  
D K Stewart

1956 ◽  
Vol 187 (1) ◽  
pp. 135-138 ◽  
Author(s):  
Martin M. Winbury

Papillary muscles from the right ventricle of the cat were subjected to periods of anoxia ranging from 15–60 minutes with and without glucose in the Krebs-Henseleit (bicarbonate) solution. Under aerobic conditions glucose was not required in the medium for the maintenance of contraction strength. Under anaerobic conditions the contraction strength decreased rapidly and after 30 minutes of oxygen deficiency contractile activity ceased. Reintroduction of oxygen after 15 minutes of anoxia resulted in full recovery of contraction strength for both control and glucose deficient muscles. After longer periods of anoxia, aerobic recovery was greater for muscles with glucose present during the anaerobic period. Little aerobic recovery was noted for muscles in glucose deficient medium during the 60 minutes of anoxia.


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