Whole body hyperthermia and preconditioning of the heart

Basic concepts, complexity, and potential mechanisms

L. Xi, D. Tekin, Peeyush Bhargava, R. C. Kukreja

Research output: Contribution to journalReview article

35 Citations (Scopus)

Abstract

Whole body hyperthermia (WBH) is a distinctive pathophysiological condition with significant impact on tissue metabolism and organ functions. WBH has been investigated as a promising adjunct therapy to the conventional chemo- or radiotherapy for treating certain types of cancer. Numerous studies have shown that WBH is associated with induction of heat shock proteins (HSPs), which in turn modulate cellular survival or death. A brief period of WBH (40-42°C; 15-20 min) can induce delayed protection against lethal endotoxemia as well as various forms of injury in brain, heart, liver, lungs, small intestine, and skeletal muscle. This review article focuses on discussing the WBH-induced myocardial protection against ischemia/reperfusion injury. Most recently, possible involvement of protein kinase C, mitogen-activated protein kinases, nitric oxide, ATP-sensitive potassium channels, and neural peptides in the signal transduction pathways has been demonstrated. On the other hand, whether HSPs or antioxidant enzymes are the primary end-effector of the cardioprotection continues to be a matter of ongoing debates. It has also been recognized that the complex nature of WBH may be the responsible factor for the discordant results among various studies, especially across different animal species or strains, in terms of the time course and potency of WBH-induced cardioprotection. Nevertheless, a better understanding of the WBH-elicited myocardial ischemic resistance may have a wide spectrum of clinical implications as well as insightful inputs into the hyperthermic biology.

Original languageEnglish (US)
Pages (from-to)439-455
Number of pages17
JournalInternational Journal of Hyperthermia
Volume17
Issue number5
DOIs
StatePublished - Oct 16 2001
Externally publishedYes

Fingerprint

Fever
Induced Hyperthermia
Heat-Shock Proteins
KATP Channels
Endotoxemia
Mitogen-Activated Protein Kinases
Reperfusion Injury
Brain Injuries
Protein Kinase C
Small Intestine
Signal Transduction
Nitric Oxide
Skeletal Muscle
Radiotherapy
Antioxidants
Drug Therapy
Lung
Peptides
Liver
Enzymes

Keywords

  • Antioxidants
  • Delayed preconditioning
  • Heat shock proteins
  • K channel
  • MAP kinases
  • Protein kinase C
  • Signal transduction
  • Whole body heat shock

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)
  • Cancer Research

Cite this

Whole body hyperthermia and preconditioning of the heart : Basic concepts, complexity, and potential mechanisms. / Xi, L.; Tekin, D.; Bhargava, Peeyush; Kukreja, R. C.

In: International Journal of Hyperthermia, Vol. 17, No. 5, 16.10.2001, p. 439-455.

Research output: Contribution to journalReview article

@article{93bb67f2330e485396825093206dd389,
title = "Whole body hyperthermia and preconditioning of the heart: Basic concepts, complexity, and potential mechanisms",
abstract = "Whole body hyperthermia (WBH) is a distinctive pathophysiological condition with significant impact on tissue metabolism and organ functions. WBH has been investigated as a promising adjunct therapy to the conventional chemo- or radiotherapy for treating certain types of cancer. Numerous studies have shown that WBH is associated with induction of heat shock proteins (HSPs), which in turn modulate cellular survival or death. A brief period of WBH (40-42°C; 15-20 min) can induce delayed protection against lethal endotoxemia as well as various forms of injury in brain, heart, liver, lungs, small intestine, and skeletal muscle. This review article focuses on discussing the WBH-induced myocardial protection against ischemia/reperfusion injury. Most recently, possible involvement of protein kinase C, mitogen-activated protein kinases, nitric oxide, ATP-sensitive potassium channels, and neural peptides in the signal transduction pathways has been demonstrated. On the other hand, whether HSPs or antioxidant enzymes are the primary end-effector of the cardioprotection continues to be a matter of ongoing debates. It has also been recognized that the complex nature of WBH may be the responsible factor for the discordant results among various studies, especially across different animal species or strains, in terms of the time course and potency of WBH-induced cardioprotection. Nevertheless, a better understanding of the WBH-elicited myocardial ischemic resistance may have a wide spectrum of clinical implications as well as insightful inputs into the hyperthermic biology.",
keywords = "Antioxidants, Delayed preconditioning, Heat shock proteins, K channel, MAP kinases, Protein kinase C, Signal transduction, Whole body heat shock",
author = "L. Xi and D. Tekin and Peeyush Bhargava and Kukreja, {R. C.}",
year = "2001",
month = "10",
day = "16",
doi = "10.1080/02656730110064342",
language = "English (US)",
volume = "17",
pages = "439--455",
journal = "International Journal of Hyperthermia",
issn = "0265-6736",
publisher = "Informa Healthcare",
number = "5",

}

TY - JOUR

T1 - Whole body hyperthermia and preconditioning of the heart

T2 - Basic concepts, complexity, and potential mechanisms

AU - Xi, L.

AU - Tekin, D.

AU - Bhargava, Peeyush

AU - Kukreja, R. C.

PY - 2001/10/16

Y1 - 2001/10/16

N2 - Whole body hyperthermia (WBH) is a distinctive pathophysiological condition with significant impact on tissue metabolism and organ functions. WBH has been investigated as a promising adjunct therapy to the conventional chemo- or radiotherapy for treating certain types of cancer. Numerous studies have shown that WBH is associated with induction of heat shock proteins (HSPs), which in turn modulate cellular survival or death. A brief period of WBH (40-42°C; 15-20 min) can induce delayed protection against lethal endotoxemia as well as various forms of injury in brain, heart, liver, lungs, small intestine, and skeletal muscle. This review article focuses on discussing the WBH-induced myocardial protection against ischemia/reperfusion injury. Most recently, possible involvement of protein kinase C, mitogen-activated protein kinases, nitric oxide, ATP-sensitive potassium channels, and neural peptides in the signal transduction pathways has been demonstrated. On the other hand, whether HSPs or antioxidant enzymes are the primary end-effector of the cardioprotection continues to be a matter of ongoing debates. It has also been recognized that the complex nature of WBH may be the responsible factor for the discordant results among various studies, especially across different animal species or strains, in terms of the time course and potency of WBH-induced cardioprotection. Nevertheless, a better understanding of the WBH-elicited myocardial ischemic resistance may have a wide spectrum of clinical implications as well as insightful inputs into the hyperthermic biology.

AB - Whole body hyperthermia (WBH) is a distinctive pathophysiological condition with significant impact on tissue metabolism and organ functions. WBH has been investigated as a promising adjunct therapy to the conventional chemo- or radiotherapy for treating certain types of cancer. Numerous studies have shown that WBH is associated with induction of heat shock proteins (HSPs), which in turn modulate cellular survival or death. A brief period of WBH (40-42°C; 15-20 min) can induce delayed protection against lethal endotoxemia as well as various forms of injury in brain, heart, liver, lungs, small intestine, and skeletal muscle. This review article focuses on discussing the WBH-induced myocardial protection against ischemia/reperfusion injury. Most recently, possible involvement of protein kinase C, mitogen-activated protein kinases, nitric oxide, ATP-sensitive potassium channels, and neural peptides in the signal transduction pathways has been demonstrated. On the other hand, whether HSPs or antioxidant enzymes are the primary end-effector of the cardioprotection continues to be a matter of ongoing debates. It has also been recognized that the complex nature of WBH may be the responsible factor for the discordant results among various studies, especially across different animal species or strains, in terms of the time course and potency of WBH-induced cardioprotection. Nevertheless, a better understanding of the WBH-elicited myocardial ischemic resistance may have a wide spectrum of clinical implications as well as insightful inputs into the hyperthermic biology.

KW - Antioxidants

KW - Delayed preconditioning

KW - Heat shock proteins

KW - K channel

KW - MAP kinases

KW - Protein kinase C

KW - Signal transduction

KW - Whole body heat shock

UR - http://www.scopus.com/inward/record.url?scp=0034815319&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0034815319&partnerID=8YFLogxK

U2 - 10.1080/02656730110064342

DO - 10.1080/02656730110064342

M3 - Review article

VL - 17

SP - 439

EP - 455

JO - International Journal of Hyperthermia

JF - International Journal of Hyperthermia

SN - 0265-6736

IS - 5

ER -