Graded experimental myocardial contusion: Impact on cardiac rhythm, coronary artery flow, ventricular function, and myocardial oxygen consumption

B. Timothy Baxter, Ernest E. Moore, David P. Synhorst, Michael J. Reiter, Alden H. Harken

Research output: Contribution to journalArticle

28 Citations (Scopus)

Abstract

Current management of myocardial contusion is based on experience with ischemic heart disease, but the mechanism responsible for cardiac dysfunction may be quite different. The purpose of this study was to characterize the pathophysiology of myocardial contusion in a controlled animal model. Sprague-Dawley rat hearts were prepared on a standard Langendorff apparatus, and myocardial function (DP, + dP/dT, – dP/dT) measured via a left ventricular balloon. Bipolar atrial and ventricular leads were placed to define conduction changes. Coronary sinus effluent was sampled for pO2, pH, creatine phosphokinase (CPK), and lactic dehydrogenase (LDH). The hearts were freeze-clamped to measure phosphocreatine (PC) and adenosine triphosphate (ATP). Myocardial contusion was produced by a single blow with a weighted pendulum. Hearts were divided into control (n = 5), moderate impact—Group I (n = 5), and major impact—Group II (n = 5). Group I sustained a 25% decrease in function after an impact of 78 ± 5 mJoules/gm, and Group II a 50% deficit after 87 ± 7 mJoules/gm. Impact resulted in complete electrical arrest, followed by sequential ventricular, atrial, and AV nodal recovery; recovery time correlated directly with degree of injury. Coronary flow at 2 min postinjury was decreased (p < 0.05) in Group I (12.8 ± 0.8 ml/min) and Group II (11.5 ± 1.3) compared to control (17.2 ± 0.5), and returned to baseline levels at 20 min. LDH and CPK levels were twice as high in Group II as in Group I. The PC/ATP ratio in Group II increased from 1.63 at baseline to 2.54 (p < 0.05) at 25 min, confirming ischemic reperfusion. In this study, myocardial dysfunction was due to: A) transient reduction in coronary blood flow resulting in global ischemia and electrical instability; and b) direct irreversible myocyte damage reflected by cardiac enzyme release.

Original languageEnglish (US)
Pages (from-to)1111-1417
Number of pages307
JournalJournal of Trauma - Injury, Infection and Critical Care
Volume28
Issue number10
StatePublished - Oct 1988

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Ventricular Function
Oxygen Consumption
Coronary Vessels
Phosphocreatine
Creatine Kinase
Oxidoreductases
Milk
Adenosine Triphosphate
Coronary Sinus
Muscle Cells
Reperfusion
Myocardial Ischemia
Sprague Dawley Rats
Ischemia
Animal Models
Wounds and Injuries
Enzymes
Myocardial Contusions

ASJC Scopus subject areas

  • Surgery
  • Critical Care and Intensive Care Medicine

Cite this

Graded experimental myocardial contusion : Impact on cardiac rhythm, coronary artery flow, ventricular function, and myocardial oxygen consumption. / Baxter, B. Timothy; Moore, Ernest E.; Synhorst, David P.; Reiter, Michael J.; Harken, Alden H.

In: Journal of Trauma - Injury, Infection and Critical Care, Vol. 28, No. 10, 10.1988, p. 1111-1417.

Research output: Contribution to journalArticle

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abstract = "Current management of myocardial contusion is based on experience with ischemic heart disease, but the mechanism responsible for cardiac dysfunction may be quite different. The purpose of this study was to characterize the pathophysiology of myocardial contusion in a controlled animal model. Sprague-Dawley rat hearts were prepared on a standard Langendorff apparatus, and myocardial function (DP, + dP/dT, – dP/dT) measured via a left ventricular balloon. Bipolar atrial and ventricular leads were placed to define conduction changes. Coronary sinus effluent was sampled for pO2, pH, creatine phosphokinase (CPK), and lactic dehydrogenase (LDH). The hearts were freeze-clamped to measure phosphocreatine (PC) and adenosine triphosphate (ATP). Myocardial contusion was produced by a single blow with a weighted pendulum. Hearts were divided into control (n = 5), moderate impact—Group I (n = 5), and major impact—Group II (n = 5). Group I sustained a 25{\%} decrease in function after an impact of 78 ± 5 mJoules/gm, and Group II a 50{\%} deficit after 87 ± 7 mJoules/gm. Impact resulted in complete electrical arrest, followed by sequential ventricular, atrial, and AV nodal recovery; recovery time correlated directly with degree of injury. Coronary flow at 2 min postinjury was decreased (p < 0.05) in Group I (12.8 ± 0.8 ml/min) and Group II (11.5 ± 1.3) compared to control (17.2 ± 0.5), and returned to baseline levels at 20 min. LDH and CPK levels were twice as high in Group II as in Group I. The PC/ATP ratio in Group II increased from 1.63 at baseline to 2.54 (p < 0.05) at 25 min, confirming ischemic reperfusion. In this study, myocardial dysfunction was due to: A) transient reduction in coronary blood flow resulting in global ischemia and electrical instability; and b) direct irreversible myocyte damage reflected by cardiac enzyme release.",
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