Effect of temperature during potassium arrest on myocardial metabolism and function

R. L. Kao, Vincent Conti, E. H. Williams

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Past studies have not established the optimal myocardial temperature range for hyperkalemic arrest but have generated controversy regarding the safety of exposing the myocardium to more profound levels of hypothermia. We therefore used the isolated working rat heart model of ischemic arrest to study the metabolic and functional effects of cardioplegia at the full range of temperatures pertinent clinically. Experimental conditions were designed to reliably control and maintain myocardial temperature during the 60 minute arrest period. We found that nearly full recovery of function occurred when hearts were arrested at or below 16°C. High-energy phosphate levels measured immediately after arrest were better maintained at 4° and 8°C, despite evidence of decreased glycolysis. When measured after the recovery period, high-energy phosphate levels returned to somewhat less than control levels in all groups arrested at or below 24°C. Myocardial glucose utilization was best preserved in hearts arrested at or below 12°C. We found no evidence that greater myocardial edema resulted from arrest at colder temperatures. Severe and permanent damage was observed when hearts were arrested at or above 28° C. In this model, therefore, the best overall metabolic and functional protection occurred when hearts were maintained at 12°C or below during potassium-induced cardioplegia. Our results support the idea that cold injury to the heart does not occur and that colder temperatures provide better protection from ischemic myocardial injury.

Original languageEnglish (US)
Pages (from-to)243-249
Number of pages7
JournalJournal of Thoracic and Cardiovascular Surgery
Volume84
Issue number2
StatePublished - 1982

Fingerprint

Potassium
Temperature
Induced Heart Arrest
Phosphates
Recovery of Function
Glycolysis
Hypothermia
Edema
Myocardium
Safety
Glucose
Wounds and Injuries

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Surgery

Cite this

Effect of temperature during potassium arrest on myocardial metabolism and function. / Kao, R. L.; Conti, Vincent; Williams, E. H.

In: Journal of Thoracic and Cardiovascular Surgery, Vol. 84, No. 2, 1982, p. 243-249.

Research output: Contribution to journalArticle

@article{e53a3669bf294ec99c82ae014a431916,
title = "Effect of temperature during potassium arrest on myocardial metabolism and function",
abstract = "Past studies have not established the optimal myocardial temperature range for hyperkalemic arrest but have generated controversy regarding the safety of exposing the myocardium to more profound levels of hypothermia. We therefore used the isolated working rat heart model of ischemic arrest to study the metabolic and functional effects of cardioplegia at the full range of temperatures pertinent clinically. Experimental conditions were designed to reliably control and maintain myocardial temperature during the 60 minute arrest period. We found that nearly full recovery of function occurred when hearts were arrested at or below 16°C. High-energy phosphate levels measured immediately after arrest were better maintained at 4° and 8°C, despite evidence of decreased glycolysis. When measured after the recovery period, high-energy phosphate levels returned to somewhat less than control levels in all groups arrested at or below 24°C. Myocardial glucose utilization was best preserved in hearts arrested at or below 12°C. We found no evidence that greater myocardial edema resulted from arrest at colder temperatures. Severe and permanent damage was observed when hearts were arrested at or above 28° C. In this model, therefore, the best overall metabolic and functional protection occurred when hearts were maintained at 12°C or below during potassium-induced cardioplegia. Our results support the idea that cold injury to the heart does not occur and that colder temperatures provide better protection from ischemic myocardial injury.",
author = "Kao, {R. L.} and Vincent Conti and Williams, {E. H.}",
year = "1982",
language = "English (US)",
volume = "84",
pages = "243--249",
journal = "Journal of Thoracic and Cardiovascular Surgery",
issn = "0022-5223",
publisher = "Mosby Inc.",
number = "2",

}

TY - JOUR

T1 - Effect of temperature during potassium arrest on myocardial metabolism and function

AU - Kao, R. L.

AU - Conti, Vincent

AU - Williams, E. H.

PY - 1982

Y1 - 1982

N2 - Past studies have not established the optimal myocardial temperature range for hyperkalemic arrest but have generated controversy regarding the safety of exposing the myocardium to more profound levels of hypothermia. We therefore used the isolated working rat heart model of ischemic arrest to study the metabolic and functional effects of cardioplegia at the full range of temperatures pertinent clinically. Experimental conditions were designed to reliably control and maintain myocardial temperature during the 60 minute arrest period. We found that nearly full recovery of function occurred when hearts were arrested at or below 16°C. High-energy phosphate levels measured immediately after arrest were better maintained at 4° and 8°C, despite evidence of decreased glycolysis. When measured after the recovery period, high-energy phosphate levels returned to somewhat less than control levels in all groups arrested at or below 24°C. Myocardial glucose utilization was best preserved in hearts arrested at or below 12°C. We found no evidence that greater myocardial edema resulted from arrest at colder temperatures. Severe and permanent damage was observed when hearts were arrested at or above 28° C. In this model, therefore, the best overall metabolic and functional protection occurred when hearts were maintained at 12°C or below during potassium-induced cardioplegia. Our results support the idea that cold injury to the heart does not occur and that colder temperatures provide better protection from ischemic myocardial injury.

AB - Past studies have not established the optimal myocardial temperature range for hyperkalemic arrest but have generated controversy regarding the safety of exposing the myocardium to more profound levels of hypothermia. We therefore used the isolated working rat heart model of ischemic arrest to study the metabolic and functional effects of cardioplegia at the full range of temperatures pertinent clinically. Experimental conditions were designed to reliably control and maintain myocardial temperature during the 60 minute arrest period. We found that nearly full recovery of function occurred when hearts were arrested at or below 16°C. High-energy phosphate levels measured immediately after arrest were better maintained at 4° and 8°C, despite evidence of decreased glycolysis. When measured after the recovery period, high-energy phosphate levels returned to somewhat less than control levels in all groups arrested at or below 24°C. Myocardial glucose utilization was best preserved in hearts arrested at or below 12°C. We found no evidence that greater myocardial edema resulted from arrest at colder temperatures. Severe and permanent damage was observed when hearts were arrested at or above 28° C. In this model, therefore, the best overall metabolic and functional protection occurred when hearts were maintained at 12°C or below during potassium-induced cardioplegia. Our results support the idea that cold injury to the heart does not occur and that colder temperatures provide better protection from ischemic myocardial injury.

UR - http://www.scopus.com/inward/record.url?scp=0020341620&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0020341620&partnerID=8YFLogxK

M3 - Article

VL - 84

SP - 243

EP - 249

JO - Journal of Thoracic and Cardiovascular Surgery

JF - Journal of Thoracic and Cardiovascular Surgery

SN - 0022-5223

IS - 2

ER -