Cardioprotection by local heating

Improved myocardial salvage after ischemia and reperfusion

Ashok Gowda, Chun Jie Yang, Gregory K. Asimakis, Johannes Ruef, Sohi Rastegar, Marschall S. Runge, Massoud Motamedi

Research output: Contribution to journalArticle

37 Citations (Scopus)

Abstract

Background. Previous studies have shown that expression of the inducible 70-kD heat-shock protein (HSP72) by whole-body hyperthermia is associated with protection against ischemia-reperfusion injury. To develop techniques for regional elevation of heat-shock proteins that prevent extracardiac sequelae during whole-body hyperthermia, we sought to determine if local heating of the heart in vivo provides protection against ischemia- reperfusion injury in the rat. Methods. A thermal probe was used to locally heat rat hearts at two adjacent sites on the epicardial surface of the left ventricle. Rats were subjected to either 30 minutes of sham surgery (control; n = 10) or two local applications of the probe at 42.5°to 43.5°C for 15 minutes each (n = 9). After 4 hours, rats were subjected to 30 minutes of regional ischemia followed by 120 minutes of reperfusion. Hearts were removed and area at risk and infarct area were determined. Results. Localized heat stress resulted in a significant limitation of infarct size in heat-treated animals versus controls (mean ± standard error of the mean infarct area/area at risk = 4.3% ± 0.85 versus 19.2% ± 3.4%; p < 0.005). Western blot experiments confirmed elevated HSP72 expression in left (heated) and right (nonheated) ventricular samples from treated animals (n = 6; left ventricular = 5.5-fold; right ventricular = 3.7-fold) compared with sham-operated controls. Controls treated with the probe at 37°C (n = 4) showed no increases in HSP72. Conclusions. Local heating of the heart is associated with elevated levels of HSP72 and improved myocardial salvage. The increase in expression of HSP72 is not limited to the heated region, but extends into nonheated regions of the heart as well. This may lead to the development of new techniques that improve methods of myocardial revascularization and heart transplantation procedures.

Original languageEnglish (US)
Pages (from-to)1241-1247
Number of pages7
JournalAnnals of Thoracic Surgery
Volume65
Issue number5
DOIs
StatePublished - 1998

Fingerprint

Heating
Reperfusion
Ischemia
Hot Temperature
Reperfusion Injury
Fever
HSP72 Heat-Shock Proteins
Myocardial Revascularization
HSP70 Heat-Shock Proteins
Heart Transplantation
Heat-Shock Proteins
Heart Ventricles
Western Blotting

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Surgery

Cite this

Cardioprotection by local heating : Improved myocardial salvage after ischemia and reperfusion. / Gowda, Ashok; Yang, Chun Jie; Asimakis, Gregory K.; Ruef, Johannes; Rastegar, Sohi; Runge, Marschall S.; Motamedi, Massoud.

In: Annals of Thoracic Surgery, Vol. 65, No. 5, 1998, p. 1241-1247.

Research output: Contribution to journalArticle

Gowda, Ashok ; Yang, Chun Jie ; Asimakis, Gregory K. ; Ruef, Johannes ; Rastegar, Sohi ; Runge, Marschall S. ; Motamedi, Massoud. / Cardioprotection by local heating : Improved myocardial salvage after ischemia and reperfusion. In: Annals of Thoracic Surgery. 1998 ; Vol. 65, No. 5. pp. 1241-1247.
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abstract = "Background. Previous studies have shown that expression of the inducible 70-kD heat-shock protein (HSP72) by whole-body hyperthermia is associated with protection against ischemia-reperfusion injury. To develop techniques for regional elevation of heat-shock proteins that prevent extracardiac sequelae during whole-body hyperthermia, we sought to determine if local heating of the heart in vivo provides protection against ischemia- reperfusion injury in the rat. Methods. A thermal probe was used to locally heat rat hearts at two adjacent sites on the epicardial surface of the left ventricle. Rats were subjected to either 30 minutes of sham surgery (control; n = 10) or two local applications of the probe at 42.5°to 43.5°C for 15 minutes each (n = 9). After 4 hours, rats were subjected to 30 minutes of regional ischemia followed by 120 minutes of reperfusion. Hearts were removed and area at risk and infarct area were determined. Results. Localized heat stress resulted in a significant limitation of infarct size in heat-treated animals versus controls (mean ± standard error of the mean infarct area/area at risk = 4.3{\%} ± 0.85 versus 19.2{\%} ± 3.4{\%}; p < 0.005). Western blot experiments confirmed elevated HSP72 expression in left (heated) and right (nonheated) ventricular samples from treated animals (n = 6; left ventricular = 5.5-fold; right ventricular = 3.7-fold) compared with sham-operated controls. Controls treated with the probe at 37°C (n = 4) showed no increases in HSP72. Conclusions. Local heating of the heart is associated with elevated levels of HSP72 and improved myocardial salvage. The increase in expression of HSP72 is not limited to the heated region, but extends into nonheated regions of the heart as well. This may lead to the development of new techniques that improve methods of myocardial revascularization and heart transplantation procedures.",
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T2 - Improved myocardial salvage after ischemia and reperfusion

AU - Gowda, Ashok

AU - Yang, Chun Jie

AU - Asimakis, Gregory K.

AU - Ruef, Johannes

AU - Rastegar, Sohi

AU - Runge, Marschall S.

AU - Motamedi, Massoud

PY - 1998

Y1 - 1998

N2 - Background. Previous studies have shown that expression of the inducible 70-kD heat-shock protein (HSP72) by whole-body hyperthermia is associated with protection against ischemia-reperfusion injury. To develop techniques for regional elevation of heat-shock proteins that prevent extracardiac sequelae during whole-body hyperthermia, we sought to determine if local heating of the heart in vivo provides protection against ischemia- reperfusion injury in the rat. Methods. A thermal probe was used to locally heat rat hearts at two adjacent sites on the epicardial surface of the left ventricle. Rats were subjected to either 30 minutes of sham surgery (control; n = 10) or two local applications of the probe at 42.5°to 43.5°C for 15 minutes each (n = 9). After 4 hours, rats were subjected to 30 minutes of regional ischemia followed by 120 minutes of reperfusion. Hearts were removed and area at risk and infarct area were determined. Results. Localized heat stress resulted in a significant limitation of infarct size in heat-treated animals versus controls (mean ± standard error of the mean infarct area/area at risk = 4.3% ± 0.85 versus 19.2% ± 3.4%; p < 0.005). Western blot experiments confirmed elevated HSP72 expression in left (heated) and right (nonheated) ventricular samples from treated animals (n = 6; left ventricular = 5.5-fold; right ventricular = 3.7-fold) compared with sham-operated controls. Controls treated with the probe at 37°C (n = 4) showed no increases in HSP72. Conclusions. Local heating of the heart is associated with elevated levels of HSP72 and improved myocardial salvage. The increase in expression of HSP72 is not limited to the heated region, but extends into nonheated regions of the heart as well. This may lead to the development of new techniques that improve methods of myocardial revascularization and heart transplantation procedures.

AB - Background. Previous studies have shown that expression of the inducible 70-kD heat-shock protein (HSP72) by whole-body hyperthermia is associated with protection against ischemia-reperfusion injury. To develop techniques for regional elevation of heat-shock proteins that prevent extracardiac sequelae during whole-body hyperthermia, we sought to determine if local heating of the heart in vivo provides protection against ischemia- reperfusion injury in the rat. Methods. A thermal probe was used to locally heat rat hearts at two adjacent sites on the epicardial surface of the left ventricle. Rats were subjected to either 30 minutes of sham surgery (control; n = 10) or two local applications of the probe at 42.5°to 43.5°C for 15 minutes each (n = 9). After 4 hours, rats were subjected to 30 minutes of regional ischemia followed by 120 minutes of reperfusion. Hearts were removed and area at risk and infarct area were determined. Results. Localized heat stress resulted in a significant limitation of infarct size in heat-treated animals versus controls (mean ± standard error of the mean infarct area/area at risk = 4.3% ± 0.85 versus 19.2% ± 3.4%; p < 0.005). Western blot experiments confirmed elevated HSP72 expression in left (heated) and right (nonheated) ventricular samples from treated animals (n = 6; left ventricular = 5.5-fold; right ventricular = 3.7-fold) compared with sham-operated controls. Controls treated with the probe at 37°C (n = 4) showed no increases in HSP72. Conclusions. Local heating of the heart is associated with elevated levels of HSP72 and improved myocardial salvage. The increase in expression of HSP72 is not limited to the heated region, but extends into nonheated regions of the heart as well. This may lead to the development of new techniques that improve methods of myocardial revascularization and heart transplantation procedures.

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