Altered Ionic Calcium and Cell Motion in Ventricular Myocytes after Cutaneous Thermal Injury

Koshy, Usha S.; Burton, Karen P.; Le, Thuy; Horton, Jureta W.

doi:10.1006/jsre.1997.5032

Cited by 22 publications

(19 citation statements)

References 23 publications

(15 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, assessment of cardiac performance in the intact subject has remained difficult due to burn-mediated changes in preload and afterload, neurohumoral responses, and the release of a host of cytotoxic mediators [4 -9]. The use of isolated heart preparations has confirmed that burn trauma impairs systolic and diastolic cardiac performance [4,8,9] and the use of isolated cardiomyocytes has shown that the postburn mechanical deficits are specific to the cardiac cell [10]. Despite the fact that myocardial depressant substances were described in the serum of burned patients more than 30 years ago [5], the pathogenesis of postburn cardiac dysfunction remains poorly understood.…”

Section: Discussionmentioning

confidence: 98%

“…Decreased cardiac output was initially attributed by numerous investigators to fluid shifts, hypovolemia, and a fall in cardiac preload; however, other investigators have attributed postburn cardiac dysfunction to myocardial depressant factors in the serum and lymph [5][6][7]. The use of ventricular muscle preparations [4,8,9] and isolated cardiomyocytes [10] has confirmed cardiac mechanical dysfunction after a major burn that is intrinsic to the cardiac myocyte. Despite these advances, the cellular mechanisms that contribute to postburn cardiac contractile deficits remain controversial, and recent attention has focused on burn-related changes in intracellular calcium homeostasis.…”

Section: Introductionmentioning

confidence: 97%

See 1 more Smart Citation

Calcium Antagonists Improve Cardiac Mechanical Performance after Thermal Trauma

Horton

White

Maass

et al. 1999

Journal of Surgical Research

Self Cite

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 97%

Calcium Antagonists Improve Cardiac Mechanical Performance after Thermal Trauma

Horton

White

Maass

et al. 1999

Journal of Surgical Research

Self Cite

View full text Add to dashboard Cite

“…A series of studies have suggested that the myocardial contractile defect after thermal injury is associated with altered myocyte Ca 2+ handling (4,5). Ventricular myocytes isolated from hearts 24 h after thermal injury showed an increase in systolic and resting Ca 2+ concentration (4).…”

Section: Introductionmentioning

confidence: 99%

Mesenteric Lymph From Rats With Thermal Injury Prolongs the Action Potential and Increases Ca2+ Transient in Rat Ventricular Myocytes

Yatani¹,

Xu²,

Kim³

et al. 2003

Shock

View full text Add to dashboard Cite

Although gut-derived mesenteric lymph from animals with thermal injury appears to lead to myocardial contractile dysfunction, the cellular mechanisms remain unclear. We examined the direct effects of intestinal lymph on excitation-contraction coupling in rat ventricular myocytes. Lymph from rats receiving burn injury (burn lymph), but not from sham-burned rats, rapidly enhanced myocyte contraction and the amplitude of Ca2+ transient; the average percentage of shortening was increased from 5.5 +/- 0.3% to 10.5 +/- 0.9%. 90% and the Ca2+ transients increased by 80% +/- 20%. Burn lymph had no effect on the amplitude of L-type Ca2+ current (ICa) or the inward rectifier K+ current, but the transient outward K+ currents (Ito) were reduced significantly by burn lymph. Inhibition of Ito was not altered by an alpha1-adrenergic receptor (AR) antagonist, prazosin, indicating that the block was not mediated via alpha1-AR signaling pathway. Action potential (AP) duration, measured at 50% and 90% repolarization, was prolonged by burn lymph. Stimulation of myocytes with AP voltage-clamp waveforms derived from prolonged AP induced by burn lymph revealed a 1.7-fold increase in Ca2+ influx via ICa compared with the Ca2+ influx induced by control AP. Blocking of Ito by 4-aminopyridine prolonged AP duration and increased Ca2+ transients, mimicking the effects of burn lymph. Burn lymph did not affect Na+/Ca2+ exchange currents or caffeine-induced SR Ca2+ release. Thus, acute exposure of normal cardiac myocytes to burn lymph increases Ca2+ transients by a prolongation of AP as a result of a reduction of Ito with no intrinsic change in ICa or exchanger. The electrophysiological changes are similar to those that occur during compensated cardiac hypertrophy, suggesting a common mechanistic link between burn lymph- and hypertrophy-induced cardiac dysfunction.

show abstract

“…However, the source(s) or the signaling pathways involved in thermal injury-induced myocardial dysfunction remain largely unknown. Recent evidence suggests that burn-induced myocardial contractile dysfunction was due to abnormal cardiac myocyte Ca 2ϩ handling (4,16,19,20,25,36). Ventricular myocytes isolated from hearts 24 h after burn injury showed an increase in both systolic and resting Ca 2ϩ concentrations (4,19,20,36).…”

mentioning

confidence: 99%

“…Recent evidence suggests that burn-induced myocardial contractile dysfunction was due to abnormal cardiac myocyte Ca 2ϩ handling (4,16,19,20,25,36). Ventricular myocytes isolated from hearts 24 h after burn injury showed an increase in both systolic and resting Ca 2ϩ concentrations (4,19,20,36). In addition, it has been reported that when animals were treated with inhibitors that regulate cellular Ca 2ϩ cycling, such as diltiazem, a Ca 2ϩ channel blocker; dantrolene, an inhibitor of the sarcoplasmic reticulum (SR) Ca 2ϩ efflux; or ruthenium red, an inhibitor of mitochondrial Ca 2ϩ accumulation, cardiac contractile performance was improved compared with untreated animals (17,20,36).…”

mentioning

confidence: 99%