Scanning electron microscopy of fetal and neonatal lamb cardiac cells

Sheldon, Curtis A.; Friedman, William F.; Sybers, Harley D.

doi:10.1016/0022-2828(76)90068-7

Cited by 69 publications

(25 citation statements)

References 15 publications

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“…The yield of cardiac SR vesicles from immature myocardium was somewhat decreased as compared to that from more mature myocardium (Table 1). These data were consistent with ultrastructural studies showing a greater ratio of contractile to noncontractile elements in mature myocardium (17,18). Specific activities of Na+, K+-ATPase, a sarcolemmal marker, were statistically higher in Gp I vesicles but this was of doubtful significance (Table I).…”

Section: Resultssupporting

confidence: 88%

Maturation of Calcium Transport in Cardiac Sarcoplasmic Reticulum

Mahony

1988

Pediatr Res

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Section: Resultssupporting

confidence: 88%

Maturation of Calcium Transport in Cardiac Sarcoplasmic Reticulum

Mahony

1988

Pediatr Res

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“…In addition, ryanodine's abolition of phasic tension induced by Ca2+ loading suggests that conditioning clamp protocols augment phasic tension by increasing the Ca2+ content of the SR. Consequently, it may be the case that the mechanism for release of Ca2+ from the SR is present and functional in the newborn period, but participation of the SR in tension development is reduced because of a diminished SR Ca2+ content. This speculation is consistent with the decreased ability to accumulate Ca2+ demonstrated in vesicles of SR isolated from immature lamb, guinea pig, and rabbit (19)(20)(21). However, it should be recognized that the Ca2+ content of the SR may be higher at physiologic heart rates and temperatures than under the experimental conditions used in these studies and those of other investigators.…”

Section: Implications For Generation Of Phasic Component Of Tensionsupporting

confidence: 85%

A Diminished Role for the Sarcoplasmic Reticulum in Newborn Myocardial Contraction: Effects of Ryanodine

Klitzner

Friedman

1989

Pediatr Res

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ABSTRACT. Ryanodine, known to reduce Ca2+ release from the sarcoplasmic reticulum (SR), was used in conjunction with the single sucrose gap voltage clamp technique to study excitation-contraction coupling in papillary muscles isolated from newborn and adult rabbits. Ryanodine altered the components of voltage clamp-induced tension in the adult producing a pattern that closely resembled the normal newborn. The phasic component of tension in mature myocardium was markedly and significantly reduced by ryanodine. In addition, ryanodine significantly altered the voltage dependence of this component of tension, suggesting a change in its mechanism of generation. The appearance of a prominent phasic component of tension, absent normally, but produced in the newborn by CaZ' loading, was also abolished by ryanodine. These results support previous proposals that the phasic component of voltage clamp-induced tension in mammalian myocardium is produced by the release of Ca2+ from the SR. In the newborn, ryanodine caused a significantly smaller decrease in the ratio of phasic to tonic tension than in the adult, suggesting a much less significant role for the SR in excitation-contraction coupling in the younger age group. Although ryanodine had a significant effect on phasic tension, no alteration in the amplitude or voltage dependence of tonic tension, generated by transmembrane Ca2+ influx, could be demonstrated in either newborn or adult heart. This investigation suggests that in newborn myocardium, Ca2+ release from the SR plays a negligible role in excitation-contraction coupling, which depends, rather, on the influx of Ca2+ from the extracellular space. ( characterized by an early peak of tension (phasic tension) which then relaxes to a steady state level (1, 2). It has been postulated that the lack of phasic tension in the immature myocardium reflects structural and functional immaturity of the t-tubules and SR ( 1, 3). To further investigate this hypothesis, experiments were conducted using the alkaloid ryanodine in an attempt to selectively eliminate Ca2+ release from the SR. Ryanodine has been shown to diminish release of Ca2+ from the SR, either by directly inhibiting Ca2+ release mechanisms (4-6), or by enhancing Ca2+ emux, resulting in Ca2+ depletion of the SR (7, 8), with little or no effect on the amplitude of membrane Ca2+ currents (9, 10) or the function of contractile proteins (1 I). It has been demonstrated previously that the negative inotropic effect of ryanodine is less pronounced in immature than mature mammalian myocardium (1 2-14) suggesting that it may be a useful tool in studying the changes which occur in the mechanisms of myocardial excitation-contraction coupling with development. MATERIALS AND METHODSPreparation. Right ventricular papillary muscles, 0.3-0.7 mm in diameter, were dissected from seven newborn (0-10 days) and six adult New Zealand White rabbits. Muscles were isolated and placed in a three compartment single sucrose gap, voltage clamp chamber. The tendinous end of the papillary muscl...

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“…Neonatal ventricular myocardium has fewer contractile elements per unit mass of myocardium than does adult ventricular myocardium (5,16). Furthermore, the sympathetic innervation of the ventricular myocardium is not complete at birth in many species and ventricular stores of norepinephrine are reduced (5-7, 9, 12, 17).…”

Section: Speculationmentioning

confidence: 99%