The harmful effects of ventricular distention during postischemic reperfusion

S. K. Lucas, Hartzell V Schaff, J. T. Flaherty, V. L. Gott, T. J. Gardner

Research output: Contribution to journalArticle

35 Citations (Scopus)

Abstract

To assess the effects of left ventricular distention during the early reperfusion period following ischemic arrest, 16 canine heart preparations were subjected to 45 minutes of hypothermic (27°C) cardioplegic arrest and normothermic reperfusion. Isovolumic left ventricular developed pressure and rate of rise of left ventricular pressure (dP/dt) were measured with an intraventricular balloon; endocardial/epicardial flow ratios were determined with microspheres; and myocardial gas tensions were monitored with mass spectrometry. During early reperfusion, Group 1 hearts (n=8) were not distended (end-diastolic pressure = 0). Group 2 hearts (n = 8) were subjected to an enddiastolic pressure of 20 mm Hg for the initial 15 minutes of reperfusion. Group 2 hearts demonstrated impaired subendocardial blood flow after 5 minutes of reflow (0.75 ± 0.06 vs 0.96 ± 0.04, endocardial/epicardial flow rates, Group 2 vs Group 1) and persistent elevation of intramycardial carbon dioxide (CO2) tension (68 ± 4 vs 51 ± 4 mm Hg, Group 2 vs Group 1). In addition, postischemic ventricular function was significantly worse in Group 2 hearts (60 ± 7 vs 79 ± 3% of control dP?dt, Group 2 vs Group 1, and 53 ± 6 vs 81 ± 5% of control left ventricular developed pressure, Group 2 vs Group 1). These data demonstrate that even mild distention during early reperfusion can result in recuded subendocardial perfusion and delayed washout of tissue CO2. Although myocardial blood flow and CO2 tension subsequently returned to normal in the distended hearts, left ventricular performance remained significantly depressed. This injury can occur clinically in nonvented hearts prior to the resumption of effective ventricular contraction.

Original languageEnglish (US)
Pages (from-to)486-494
Number of pages9
JournalAnnals of Thoracic Surgery
Volume32
Issue number5
DOIs
StatePublished - 1981
Externally publishedYes

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Reperfusion
Ventricular Pressure
Ventricular Function
Microspheres
Carbon Dioxide
Canidae
Mass Spectrometry
Perfusion
Gases
Blood Pressure
Pressure
Wounds and Injuries

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Surgery

Cite this

The harmful effects of ventricular distention during postischemic reperfusion. / Lucas, S. K.; Schaff, Hartzell V; Flaherty, J. T.; Gott, V. L.; Gardner, T. J.

In: Annals of Thoracic Surgery, Vol. 32, No. 5, 1981, p. 486-494.

Research output: Contribution to journalArticle

Lucas, S. K. ; Schaff, Hartzell V ; Flaherty, J. T. ; Gott, V. L. ; Gardner, T. J. / The harmful effects of ventricular distention during postischemic reperfusion. In: Annals of Thoracic Surgery. 1981 ; Vol. 32, No. 5. pp. 486-494.
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abstract = "To assess the effects of left ventricular distention during the early reperfusion period following ischemic arrest, 16 canine heart preparations were subjected to 45 minutes of hypothermic (27°C) cardioplegic arrest and normothermic reperfusion. Isovolumic left ventricular developed pressure and rate of rise of left ventricular pressure (dP/dt) were measured with an intraventricular balloon; endocardial/epicardial flow ratios were determined with microspheres; and myocardial gas tensions were monitored with mass spectrometry. During early reperfusion, Group 1 hearts (n=8) were not distended (end-diastolic pressure = 0). Group 2 hearts (n = 8) were subjected to an enddiastolic pressure of 20 mm Hg for the initial 15 minutes of reperfusion. Group 2 hearts demonstrated impaired subendocardial blood flow after 5 minutes of reflow (0.75 ± 0.06 vs 0.96 ± 0.04, endocardial/epicardial flow rates, Group 2 vs Group 1) and persistent elevation of intramycardial carbon dioxide (CO2) tension (68 ± 4 vs 51 ± 4 mm Hg, Group 2 vs Group 1). In addition, postischemic ventricular function was significantly worse in Group 2 hearts (60 ± 7 vs 79 ± 3{\%} of control dP?dt, Group 2 vs Group 1, and 53 ± 6 vs 81 ± 5{\%} of control left ventricular developed pressure, Group 2 vs Group 1). These data demonstrate that even mild distention during early reperfusion can result in recuded subendocardial perfusion and delayed washout of tissue CO2. Although myocardial blood flow and CO2 tension subsequently returned to normal in the distended hearts, left ventricular performance remained significantly depressed. This injury can occur clinically in nonvented hearts prior to the resumption of effective ventricular contraction.",
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