ArticleClinical toxicology (Philadelphia, Pa.)2009
Insulin-dependent rescue from cardiogenic shock is not mediated by phospholamban phosphorylation.
Article in Clinical toxicology (Philadelphia, Pa.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 5 citations in OpenAlex.
- Accurate quantitation of phospholamban phosphorylation by immunoblot.Analytical biochemistry · 2012Article
- Phospholamban mutants compete with wild type for SERCA binding in living cells.Biochemical and biophysical research communications · 2012Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
introductionWe used immunoblots to determine whether inotropic and lusitropic effects of high-dose insulin (HDI) in cardiogenic shock, induced by a beta-blocker (BB) or a calcium channel blocker (CCB), are mediated by phosphorylation of phospholamban (PLB). PLB is a membrane protein that regulates calcium uptake into the sarcoplasmic reticulum (SR) by inhibition of the cardiac calcium pump (SERCA2a). Phosphorylation of PLB relieves SERCA inhibition, thus enhancing diastolic relaxation and preload.
methodsOur Institutional Animal Care and Use Committee approved this research. Swine myocardia from six groups were flash frozen immediately upon death or sacrifice. Groups 1-6 received: (1) no medications, (2) HDI and glucose only, (3) toxic propranolol infusions and saline resuscitation, (4) toxic propranolol infusions and HDI resuscitation, (5) toxic verapamil infusions and saline resuscitation, and (6) toxic verapamil infusions and HDI resuscitation. Groups 3-6 were resuscitated for 4 h. Tissue samples from all six groups were analyzed by quantitative immunoblots, using antibodies to both unphosphorylated PLB (uPLB) and phosphorylated PLB (pPLB), to determine the total PLB content and the fraction of PLB phosphorylated.
resultsThere were no differences in either pPLB or total PLB in cardiac tissue among any of the six groups. However, infusion of a pig with the beta-adrenergic agonist, isoproterenol, produced enhanced PLB phosphorylation.
conclusionThe mechanism by which HDI produces its inotropic and lusitropic effects in CCB- and BB-induced cardiovascular toxicity, resulting in resuscitation, is not due to changes in phosphorylation of PLB or a change in the total PLB in the SR.
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