Effects of broad band electromagnetic fields on HSP70 expression and ischemia-reperfusion in rat hearts.

Life sciences · 2004 · Mixed · Low evidence

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MixedLow evidencePaper 5221

Study snapshot

PublicationLife sciences · 2004

Study typeanimal

Reported directionMixed

Evidence ratingLow

Abstract

Although exposure to broad band (0.2-20 MHz) electromagnetic fields (EMF) is part of the treatment of several diseases, little is known as to their effects on myocardial protein expression and resistance to ischemia-reperfusion (I/R). We exposed Sprague-Dawley rats to either high (H, 10 min/day at 200 V/m, 36.1 microT) or low (L, 2 min/day at 30 V/m, 11.4 microT) intensity broad band EMF for 15 days. At the end of the treatment, myocardial HSP70 was 32 +/- 8% (mean +/- SEM) higher in L (P = 0.01) than in control (C), whereas in H it remained the same as in C. Electron microscopy revealed sporadic ruptures of mitochondrial cristae in H hearts, with no differences in other parameters. Malondialdehyde was increased in treated hearts (P < 0.05), but especially in H (P = 0.008). To assess the protective role of HSP70 during I/R, hearts were Langendorff-perfused with Krebs-Henseleit. After I/R, C hearts displayed depressed rate. pressure (-13 +/- 7%) and increased end-diastolic (+9.2 +/- 2.8 mmHg) and perfusion pressures (+30 +/- 10 mmHg). In H and L, rate. pressure recovery was similar to C (-2 +/- 21% and -12 +/- 16%, respectively, P = NS). In contrast, both end-diastolic and perfusion pressures were higher in L than in H (30.8 +/- 5.4 vs 18.2 +/- 3.5, P = 0.01, and 54 +/- 8 vs 21 +/- 8 mmHg, P = 0.01, respectively) indicating diastolic derangement in L. In conclusion, the effects of broad band EMF on HSP70 appear to be biphasic, and HSP70 overexpression might not be directly related to improved protection against I/R.

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AI evidence extraction

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Study typeanimal

Effect directionmixed

PopulationSprague-Dawley rats; isolated rat hearts (Langendorff perfusion)

Sample sizeNot supplied

ExposureRF · 10 min/day (high) or 2 min/day (low) for 15 days

Evidence strengthLowConfidence: 74% · Peer reviewed: yes

Main findings

Low-intensity exposure increased myocardial HSP70 by 32 ± 8% versus control (P=0.01), while high-intensity exposure did not change HSP70 versus control. Malondialdehyde increased in treated hearts (P<0.05), especially in the high-intensity group (P=0.008), and electron microscopy showed sporadic ruptures of mitochondrial cristae in high-intensity hearts. After ischemia-reperfusion, rate-pressure recovery in both exposure groups was similar to control, but end-diastolic and perfusion pressures were higher in the low-intensity group than in the high-intensity group, indicating diastolic derangement in the low-intensity group.

Outcomes measured

Myocardial HSP70 expression
Mitochondrial ultrastructure (electron microscopy)
Malondialdehyde (oxidative stress marker)
Post ischemia-reperfusion functional measures: rate-pressure recovery, end-diastolic pressure, perfusion pressure

Limitations

Sample size not reported in abstract
Exposure source and detailed dosimetry beyond field strength/microtesla not described in abstract
Outcomes assessed in an animal model with ex vivo heart perfusion, limiting direct human generalizability

View raw extracted JSON

{
  "study_type": "animal",
  "exposure": {
    "band": "RF",
    "source": null,
    "frequency_mhz": null,
    "sar_wkg": null,
    "duration": "10 min/day (high) or 2 min/day (low) for 15 days"
  },
  "population": "Sprague-Dawley rats; isolated rat hearts (Langendorff perfusion)",
  "sample_size": null,
  "outcomes": [
    "Myocardial HSP70 expression",
    "Mitochondrial ultrastructure (electron microscopy)",
    "Malondialdehyde (oxidative stress marker)",
    "Post ischemia-reperfusion functional measures: rate-pressure recovery, end-diastolic pressure, perfusion pressure"
  ],
  "main_findings": "Low-intensity exposure increased myocardial HSP70 by 32 ± 8% versus control (P=0.01), while high-intensity exposure did not change HSP70 versus control. Malondialdehyde increased in treated hearts (P<0.05), especially in the high-intensity group (P=0.008), and electron microscopy showed sporadic ruptures of mitochondrial cristae in high-intensity hearts. After ischemia-reperfusion, rate-pressure recovery in both exposure groups was similar to control, but end-diastolic and perfusion pressures were higher in the low-intensity group than in the high-intensity group, indicating diastolic derangement in the low-intensity group.",
  "effect_direction": "mixed",
  "limitations": [
    "Sample size not reported in abstract",
    "Exposure source and detailed dosimetry beyond field strength/microtesla not described in abstract",
    "Outcomes assessed in an animal model with ex vivo heart perfusion, limiting direct human generalizability"
  ],
  "evidence_strength": "low",
  "confidence": 0.74,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "broad band electromagnetic fields",
    "0.2-20 MHz",
    "HSP70",
    "ischemia-reperfusion",
    "rat heart",
    "Langendorff",
    "malondialdehyde",
    "oxidative stress",
    "mitochondria"
  ],
  "suggested_hubs": []
}

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AI-extracted fields are generated from the abstract and metadata and may be incomplete or incorrect. This material is for informational purposes and is not medical advice.

Identifiers and source

DOI: 10.1016/j.lfs.2003.12.033
PubMed: 15306160

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