Role of calcium in acute hyperthermic myocardial injury.

Introduction: We hypothesized that intracellular calcium overload may play an important role in heat-induced myocardial injury. This postulate was investigated using a model of isolated guinea pig papillary muscle in which resting tension was measured as an indirect indicator of cytosolic free-calci...

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Publicado en:Journal of Cardiovascular Electrophysiology Vol. 12; no. 5; pp. 563 - 570
Autores principales: Everett TH, Nath S, Lynch C III, Beach JM, Whayne JG, Haines DE
Formato: Journal Article
Publicado: Wiley-Blackwell May2001
Acceso en línea:Ver este registro en EBSCOhost
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      dt: May2001
      vid: 12
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      pub: Wiley-Blackwell
      place: Malden, Massachusetts
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        10.1046/j.1540-8167.2001.00563.x
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        atl: Role of calcium in acute hyperthermic myocardial injury.
      aug:
        au:
          Everett TH
          Nath S
          Lynch C III
          Beach JM
          Whayne JG
          Haines DE
      sug:
        subj:
          Calcium Physiology
          Hyperthermia, Induced
          Myocardial Reperfusion Injury Physiopathology
          Acute Disease
          Animals
          Calcium Channel Blockers Pharmacodynamics
          Enzyme Inhibitors Pharmacodynamics
          Female
          Guinea Pigs
          Hydrocarbons Pharmacodynamics
          Male
          Models, Biological
          Myocardial Contraction Drug Effects
          Myocardium Drug Effects
          Myocardium Injuries
          Female
          Male
      ab: Introduction: We hypothesized that intracellular calcium overload may play an important role in heat-induced myocardial injury. This postulate was investigated using a model of isolated guinea pig papillary muscle in which resting tension was measured as an indirect indicator of cytosolic free-calcium concentration and the fluorescence changes of Fluo-3 AM dye was measured as a direct indicator of cytosolic free-calcium concentration. Methods and Results: Excised guinea pig right ventricular papillary muscles were attached to a force transducer in a high-flow tissue hath and superfused with Tyrode's solution at 37° ± 0.5°C. The temperature was rapidly changed to between 38.0° and 56.0°C for 60 seconds and then returned to 37.0°C. Hyperthermia caused a reversible increase in resting tension at temperatures between 45° and 50°C and irreversible contracture at >=50°C. Rapid cooling contracture experiments and experiments measuring fluorescence of myocytes loaded with 5 [mu]M Fluo-3 AM dye demonstrated that the hyperthermia-induced rise in resting tension was likely due to an increase in intracellular calcium content. Inhibition of the sarcoplasmic reticulum calcium pump with 20 [mu]M thapsigargin resulted in irreversible contracture of the papillary muscles at temperatures between 45° and 50°C and significant increases in Fluo-3 fluorescence at 48°C. Blockade of sarcolemmal calcium channels with 0.5 mM cadmium or 40 [mu]M verapamil did not attenuate the heat-induced increase in resting tension and Fluo-3 fluorescence. Conclusion: Hyperthermia causes an increase in resting tension of cardiac muscle that most likely is mediated by a calcium channel-independent increase in calcium permeability of the sarcolemmal membrane and/or release of stored intracellular calcium.
      pubtype: Academic Journal
      doctype: Journal Article
      ougenre: Article
    language: English
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