Effects of high potassium cardioplegia and hypothermia on myocardial compliance and distribution of water and potassium. II. The hypertrophied canine heart

Constantine Mavroudis, Paul A. Ebert

Research output: Contribution to journalArticle

Abstract

High potassium solution for elective cardioplegia associated with hypothermia has been shown to be effective for electromechanical arrest and myocardial preservation. The extracellular space (ECS), intracellular potassium, percentage of water change, and ventricular compliance were measured after 1 how of reperfusion following 1 hour of high (35 mEq/liter) and low (5 mEq/liter) potassium (K+) cardioplegia employing normothermia and hypothermia in the isolated perfused hypertrophied heart. The ECS measured with 3H inulin in the hypertrophied control group was 27.80 ± 0.1% with total water content of 81.1 ± 0.4%, both of which were higher than the previously measured normal myocardium (P < 0.05). High potassium hypothermic arrest and reperfusion showed no change in ECS or intracellular K+ in normal hearts but produced an increase in ECS (35.2 ±3.0) (P < 0.001) and intracellular potassium in the hypertrophied group. Low potassium hypothermic arrest and reperfusion showed no change in ECS and increase in intracellular K+ in normal hearts but produced increased ECS (45.0 ± 3.3%) and intercellular K+ in hypertrophied hearts (P < 0.05). High potassium normothermic arrest and reperfusion showed increased ECS and intracellular potassium in both normal hearts, ECS = 27.8 ± 0.1% (four dogs) (P < 0.05) and hypertrophied hearts, ECS = 55.7 ± 1.2% (P < 0.05). Compliance measurements in hypertrophied hearts showed no change with hypothermic high and low potassium arrest but decreased compliance (P < 0.05) when normothermic high K+ arrest was employed. Postperfusion shifts of potassium in the reperfusion period suggest decreased potassium efflux and increased fluid shifts in all groups except the normal myocardium protected with hypothermic high K+ solution. Although different from controls, hypertrophied hearts protected with hypothermic high K+ solution showed less fluid shifts and potassium efflux than did the hypertrophied hypothermic low K+ or hypertrophied normothermic high K+ groups. The hypertrophied heart is more susceptible to fluid and potassium shifts after potassium arrest than is the normal heart with high K+ hypothermic arrest producing the least amount of changes.

Original languageEnglish (US)
Pages (from-to)662-670
Number of pages9
JournalSurgery
Volume85
Issue number6
StatePublished - Jan 1 1979
Externally publishedYes

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Induced Heart Arrest
Hypothermia
Compliance
Canidae
Potassium
Extracellular Space
Water
Reperfusion
Fluid Shifts
Myocardium
Inulin

ASJC Scopus subject areas

  • Surgery

Cite this

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title = "Effects of high potassium cardioplegia and hypothermia on myocardial compliance and distribution of water and potassium. II. The hypertrophied canine heart",
abstract = "High potassium solution for elective cardioplegia associated with hypothermia has been shown to be effective for electromechanical arrest and myocardial preservation. The extracellular space (ECS), intracellular potassium, percentage of water change, and ventricular compliance were measured after 1 how of reperfusion following 1 hour of high (35 mEq/liter) and low (5 mEq/liter) potassium (K+) cardioplegia employing normothermia and hypothermia in the isolated perfused hypertrophied heart. The ECS measured with 3H inulin in the hypertrophied control group was 27.80 ± 0.1{\%} with total water content of 81.1 ± 0.4{\%}, both of which were higher than the previously measured normal myocardium (P < 0.05). High potassium hypothermic arrest and reperfusion showed no change in ECS or intracellular K+ in normal hearts but produced an increase in ECS (35.2 ±3.0) (P < 0.001) and intracellular potassium in the hypertrophied group. Low potassium hypothermic arrest and reperfusion showed no change in ECS and increase in intracellular K+ in normal hearts but produced increased ECS (45.0 ± 3.3{\%}) and intercellular K+ in hypertrophied hearts (P < 0.05). High potassium normothermic arrest and reperfusion showed increased ECS and intracellular potassium in both normal hearts, ECS = 27.8 ± 0.1{\%} (four dogs) (P < 0.05) and hypertrophied hearts, ECS = 55.7 ± 1.2{\%} (P < 0.05). Compliance measurements in hypertrophied hearts showed no change with hypothermic high and low potassium arrest but decreased compliance (P < 0.05) when normothermic high K+ arrest was employed. Postperfusion shifts of potassium in the reperfusion period suggest decreased potassium efflux and increased fluid shifts in all groups except the normal myocardium protected with hypothermic high K+ solution. Although different from controls, hypertrophied hearts protected with hypothermic high K+ solution showed less fluid shifts and potassium efflux than did the hypertrophied hypothermic low K+ or hypertrophied normothermic high K+ groups. The hypertrophied heart is more susceptible to fluid and potassium shifts after potassium arrest than is the normal heart with high K+ hypothermic arrest producing the least amount of changes.",
author = "Constantine Mavroudis and Ebert, {Paul A.}",
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T1 - Effects of high potassium cardioplegia and hypothermia on myocardial compliance and distribution of water and potassium. II. The hypertrophied canine heart

AU - Mavroudis, Constantine

AU - Ebert, Paul A.

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N2 - High potassium solution for elective cardioplegia associated with hypothermia has been shown to be effective for electromechanical arrest and myocardial preservation. The extracellular space (ECS), intracellular potassium, percentage of water change, and ventricular compliance were measured after 1 how of reperfusion following 1 hour of high (35 mEq/liter) and low (5 mEq/liter) potassium (K+) cardioplegia employing normothermia and hypothermia in the isolated perfused hypertrophied heart. The ECS measured with 3H inulin in the hypertrophied control group was 27.80 ± 0.1% with total water content of 81.1 ± 0.4%, both of which were higher than the previously measured normal myocardium (P < 0.05). High potassium hypothermic arrest and reperfusion showed no change in ECS or intracellular K+ in normal hearts but produced an increase in ECS (35.2 ±3.0) (P < 0.001) and intracellular potassium in the hypertrophied group. Low potassium hypothermic arrest and reperfusion showed no change in ECS and increase in intracellular K+ in normal hearts but produced increased ECS (45.0 ± 3.3%) and intercellular K+ in hypertrophied hearts (P < 0.05). High potassium normothermic arrest and reperfusion showed increased ECS and intracellular potassium in both normal hearts, ECS = 27.8 ± 0.1% (four dogs) (P < 0.05) and hypertrophied hearts, ECS = 55.7 ± 1.2% (P < 0.05). Compliance measurements in hypertrophied hearts showed no change with hypothermic high and low potassium arrest but decreased compliance (P < 0.05) when normothermic high K+ arrest was employed. Postperfusion shifts of potassium in the reperfusion period suggest decreased potassium efflux and increased fluid shifts in all groups except the normal myocardium protected with hypothermic high K+ solution. Although different from controls, hypertrophied hearts protected with hypothermic high K+ solution showed less fluid shifts and potassium efflux than did the hypertrophied hypothermic low K+ or hypertrophied normothermic high K+ groups. The hypertrophied heart is more susceptible to fluid and potassium shifts after potassium arrest than is the normal heart with high K+ hypothermic arrest producing the least amount of changes.

AB - High potassium solution for elective cardioplegia associated with hypothermia has been shown to be effective for electromechanical arrest and myocardial preservation. The extracellular space (ECS), intracellular potassium, percentage of water change, and ventricular compliance were measured after 1 how of reperfusion following 1 hour of high (35 mEq/liter) and low (5 mEq/liter) potassium (K+) cardioplegia employing normothermia and hypothermia in the isolated perfused hypertrophied heart. The ECS measured with 3H inulin in the hypertrophied control group was 27.80 ± 0.1% with total water content of 81.1 ± 0.4%, both of which were higher than the previously measured normal myocardium (P < 0.05). High potassium hypothermic arrest and reperfusion showed no change in ECS or intracellular K+ in normal hearts but produced an increase in ECS (35.2 ±3.0) (P < 0.001) and intracellular potassium in the hypertrophied group. Low potassium hypothermic arrest and reperfusion showed no change in ECS and increase in intracellular K+ in normal hearts but produced increased ECS (45.0 ± 3.3%) and intercellular K+ in hypertrophied hearts (P < 0.05). High potassium normothermic arrest and reperfusion showed increased ECS and intracellular potassium in both normal hearts, ECS = 27.8 ± 0.1% (four dogs) (P < 0.05) and hypertrophied hearts, ECS = 55.7 ± 1.2% (P < 0.05). Compliance measurements in hypertrophied hearts showed no change with hypothermic high and low potassium arrest but decreased compliance (P < 0.05) when normothermic high K+ arrest was employed. Postperfusion shifts of potassium in the reperfusion period suggest decreased potassium efflux and increased fluid shifts in all groups except the normal myocardium protected with hypothermic high K+ solution. Although different from controls, hypertrophied hearts protected with hypothermic high K+ solution showed less fluid shifts and potassium efflux than did the hypertrophied hypothermic low K+ or hypertrophied normothermic high K+ groups. The hypertrophied heart is more susceptible to fluid and potassium shifts after potassium arrest than is the normal heart with high K+ hypothermic arrest producing the least amount of changes.

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