Ischemia and ischemic preconditioning in the buffer-perfused pigeon heart

Franz Rischard, Tom McKean

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Isolated pigeon hearts were perfused with Krebs-Henseleit bicarbonate buffer with 1.25 mM Ca++ at a pressure of 60 cm H2O and paced at 210 beats per min. After an equilibration perfusion of 30 min, hearts were subjected to 10 min global ischemia and then reperfused for 30 min. Left ventricular +dP/dt(max), systolic, and end diastolic pressures differed significantly from baseline values during reperfusion as did the release of lactate dehydrogenase (LDH). When the hearts were preconditioned by interruption of flow for two 2.5-min intervals, followed by 10 min of ischemia and then reperfusion, the short periods of ischemia, followed by reperfusion, protected the hearts against the longer bout of ischemia as evidenced by significant differences between the left ventricular (LV) pressure, +dP/dt(max) LV end diastolic pressure and LDH values obtained from the hearts of control vs. preconditioned hearts. Substitution of 1 μM adenosine for the preconditioning ischemia also resulted in the preconditioning response. Ischemic preconditioning (IP) was not blocked by addition of 100 μM 8-(-p-sulfophenyl) theophylline, an adenosine receptor antagonist. Therefore, isolated, perfused bird hearts can be preconditioned, and the mechanism may involve adenosine receptors, although their activation is not necessary for IP to occur. Factors in addition to adenosine are likely involved.

Original languageEnglish (US)
Pages (from-to)59-65
Number of pages7
JournalComparative Biochemistry and Physiology - C Pharmacology Toxicology and Endocrinology
Volume119
Issue number1
DOIs
StatePublished - Jan 1998
Externally publishedYes

Fingerprint

Ischemic Preconditioning
Columbidae
Buffers
Ischemia
Reperfusion
L-Lactate Dehydrogenase
Adenosine
Purinergic P1 Receptor Antagonists
Blood Pressure
Purinergic P1 Receptors
Ventricular Pressure
Bicarbonates
Birds
Perfusion
Pressure

Keywords

  • Adenosine
  • Bird
  • Heart
  • Ischemia
  • Ischemic preconditioning
  • Pigeon

ASJC Scopus subject areas

  • Pharmacology
  • Immunology

Cite this

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abstract = "Isolated pigeon hearts were perfused with Krebs-Henseleit bicarbonate buffer with 1.25 mM Ca++ at a pressure of 60 cm H2O and paced at 210 beats per min. After an equilibration perfusion of 30 min, hearts were subjected to 10 min global ischemia and then reperfused for 30 min. Left ventricular +dP/dt(max), systolic, and end diastolic pressures differed significantly from baseline values during reperfusion as did the release of lactate dehydrogenase (LDH). When the hearts were preconditioned by interruption of flow for two 2.5-min intervals, followed by 10 min of ischemia and then reperfusion, the short periods of ischemia, followed by reperfusion, protected the hearts against the longer bout of ischemia as evidenced by significant differences between the left ventricular (LV) pressure, +dP/dt(max) LV end diastolic pressure and LDH values obtained from the hearts of control vs. preconditioned hearts. Substitution of 1 μM adenosine for the preconditioning ischemia also resulted in the preconditioning response. Ischemic preconditioning (IP) was not blocked by addition of 100 μM 8-(-p-sulfophenyl) theophylline, an adenosine receptor antagonist. Therefore, isolated, perfused bird hearts can be preconditioned, and the mechanism may involve adenosine receptors, although their activation is not necessary for IP to occur. Factors in addition to adenosine are likely involved.",
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AB - Isolated pigeon hearts were perfused with Krebs-Henseleit bicarbonate buffer with 1.25 mM Ca++ at a pressure of 60 cm H2O and paced at 210 beats per min. After an equilibration perfusion of 30 min, hearts were subjected to 10 min global ischemia and then reperfused for 30 min. Left ventricular +dP/dt(max), systolic, and end diastolic pressures differed significantly from baseline values during reperfusion as did the release of lactate dehydrogenase (LDH). When the hearts were preconditioned by interruption of flow for two 2.5-min intervals, followed by 10 min of ischemia and then reperfusion, the short periods of ischemia, followed by reperfusion, protected the hearts against the longer bout of ischemia as evidenced by significant differences between the left ventricular (LV) pressure, +dP/dt(max) LV end diastolic pressure and LDH values obtained from the hearts of control vs. preconditioned hearts. Substitution of 1 μM adenosine for the preconditioning ischemia also resulted in the preconditioning response. Ischemic preconditioning (IP) was not blocked by addition of 100 μM 8-(-p-sulfophenyl) theophylline, an adenosine receptor antagonist. Therefore, isolated, perfused bird hearts can be preconditioned, and the mechanism may involve adenosine receptors, although their activation is not necessary for IP to occur. Factors in addition to adenosine are likely involved.

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