Prevention of cellular edema directly caused by hypothermic cardioplegia: Studies in isolated human and rabbit atrial myocytes

Shaffer, Robert F.; Baumgarten, Clive M.; Damiano, Ralph J.

doi:10.1016/s0022-5223(98)70420-9

Cited by 21 publications

(30 citation statements)

References 25 publications

(51 reference statements)

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“…Swelling of cardiac myocytes is a common complication in various pathological conditions, including ischaemia (Vandenberg et al 1996) or during application of cardioplegic solutions (Handy et al 1996; Shaffer et al 1998). Given that in most cases osmotic stress is resolved (or at least needs to be resolved), significant t‐tubular remodelling may accompany the recovery from insult, leading to secondary complications.…”

Section: Discussionmentioning

confidence: 99%

Resolution of hyposmotic stress in isolated mouse ventricular myocytes causes sealing of t‐tubules

Moench

Meekhof

Cheng

et al. 2013

Experimental Physiology

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It has been recently shown that various stress-inducing manipulations in isolated ventricular myocytes may lead to significant remodeling of t-tubules. Osmotic stress is one of the most common complications in various experimental and clinical settings. Therefore, this study was designed to determine the effects of a physiologically relevant type of osmotic stress, hypo-osmotic challenge, to the integrity of t-tubular system in mouse ventricular myocytes using two approaches: (1) electrophysiological measurements of membrane capacitance and inward rectifier (IK1) tail currents originating from K+ accumulation in t-tubules, and (2) confocal microscopy of fluorescent dextrans trapped in sealed t-tubules. Importantly, we found that removal of 0.6 Na (60% NaCl) hypo-osmotic solution, but not its application to myocytes, led to ~27% reduction in membrane capacitance, ~2.5-fold reduction in the amplitude of IK1 tail current and ~2-fold reduction in so-called IK1 ‘inactivation’ (due to depletion of t-tubular K+) at negative membrane potentials – all data being consistent with significant detubulation. Confocal imaging experiments also demonstrated that extracellularly applied dextrans become trapped in sealed t-tubules only upon removal of hypo-osmotic solutions, i.e. during shrinking phase, but not during initial swelling period. In light of these data, relevant previous studies, including those on EC coupling phenomena during hypo-osmotic stress, may need to be reinterpreted and the experimental design of future experiments should take into account the novel findings.

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Section: Discussionmentioning

confidence: 99%

Resolution of hyposmotic stress in isolated mouse ventricular myocytes causes sealing of t‐tubules

Moench

Meekhof

Cheng

et al. 2013

Experimental Physiology

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“…Isolated animal myocytes demonstrate significant swelling and reduced contractility during exposure to hypothermic hyperkalemic cardioplegia, MI, or hyposmotic stress . DZX prevents these detrimental consequences secondary to all three stresses in two animal species .…”

Section: Discussionmentioning

confidence: 99%

“…The supernatant was discarded and the pellet resuspended in cell isolation solution and centrifuged again at 100 g at 4°C for 10 minutes, three times. The supernatant was then discarded and the pellet resuspended in cell isolation solution and allowed to settle for 30 minutes …”

Section: Methodsmentioning

confidence: 99%

Diazoxide Maintains Human Myocyte Volume Homeostasis During Stress

Maffit

Sellitto

Al-Dadah

et al. 2012

JAHA

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Background--Exposure to hypothermic hyperkalemic cardioplegia, hyposmotic stress, or metabolic inhibition results in significant animal myocyte swelling (6% to10%) and subsequent reduced contractility (10% to 20%). Both are eliminated by the adenosine triphosphate-sensitive potassium channel opener diazoxide (DZX). The relationship between swelling and reduced contractility suggests that the structural change may represent one mechanism of postoperative myocardial stunning. This study evaluated human myocyte volume during stress to investigate if similar phenomena exist in human myocytes.

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“…Cardiac myocytes swell in response to a variety of stressful conditions [11,46,48,49], including superfusion with hyposmotic solution [13,55]. The swelling is accompanied by alterations in myocyte electrical activity as a consequence of modified ionic concentrations and changes in the activities of membrane ion transporters and ion channels [5,17,23,61].…”

Section: Introductionmentioning

confidence: 99%

Involvement of tyrosine kinase in the hyposmotic stimulation of I Ks in guinea-pig ventricular myocytes

Missan

Linsdell

McDonald

2007

Pflugers Arch - Eur J Physiol

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The objective of this study was to investigate the involvement of tyrosine phosphorylation in the hyposmotic stimulation of cardiac I Ks, a slowly activating delayed-rectifier K+ current that promotes repolarization of the action potential. The current was recorded from whole-cell-configured guinea-pig ventricular myocytes before, during, and after their exposure to solution whose osmolarity was 0.75 times normal. Exposure to hyposmotic solution caused a near-doubling of the amplitude of I Ks, with little change in the voltage dependence of current activation. Stable, hyposmotically stimulated I Ks (I Ks,Hypo) was decreased by broadspectrum tyrosine kinase (TK) inhibitors tyrphostin A23 (IC50 approximately 5 microM) and tyrphostin A25 (IC50 15.8 +/- 1.6 microM) but not by TK-inactive tyrphostin analogs, suggesting that tyrosine phosphorylation is important for maintenance of the current. In agreement with that view, we found that the TK-inhibitor action on I Ks,Hypo was strongly antagonized by vanadate compounds known to inhibit phosphotyrosyl phosphatase. When myocytes were pretreated with TK inhibitors, the stimulation of I Ks was attenuated in a concentration-dependent manner. The attenuation was not due to concomitant attenuation of a stimulation of tyrosine phosphorylation because neither the stimulation of I Ks nor its rate of decay following removal of hyposmotic solution was affected by pretreatment with vanadates. We suggest that the stimulation of I Ks by hyposmotic solution is dependent on a basal tyrosine phosphorylation that modulates a swelling-induced I Ks-stimulatory signal and/or the receptivity of Ks channels to that signal.

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Prevention of cellular edema directly caused by hypothermic cardioplegia: Studies in isolated human and rabbit atrial myocytes

Cited by 21 publications

References 25 publications

Resolution of hyposmotic stress in isolated mouse ventricular myocytes causes sealing of t‐tubules

Resolution of hyposmotic stress in isolated mouse ventricular myocytes causes sealing of t‐tubules

Diazoxide Maintains Human Myocyte Volume Homeostasis During Stress

Involvement of tyrosine kinase in the hyposmotic stimulation of I Ks in guinea-pig ventricular myocytes

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