Insulin improves heart function and metabolism during non-ischemic cardiogenic shock in awake canines

Jeffrey Kline, Richard M. Raymond, Elena D. Leonova, Thomas C. Williams, John A. Watts

Research output: Contribution to journalArticle

64 Citations (Scopus)

Abstract

Objectives: This study was undertaken to examine in-situ heart function and metabolism during insulin treatment of verapamil-induced cardiogenic shock in awake canines. Methods: Twenty mongrel canines were instrumented to monitor myocardial substrate uptakes (glucose, lactate, free fatty acids, oxygen [MVO2]), as well as left ventricular (LV) end-systolic elastance (E(max)), LV efficiency (LV minute work/MVO2), and Tau. Shock was induced by graded intraportal verapamil infusion followed by randomized assignment to one of 4 treatment groups: saline control (3.0 ml/kg/min, n = 5), epinephrine (5 μg/kg/min, n = 5), glucagon (10 μg/kg/min, n = 5) or insulin (1000 mU/min, n = 5) with dextrose to clamp arterial [glucose] ± 10% of basal concentrations. Results: Insulin treatment significantly increased E(max) (34 ± 3 vs. 17 ± 3 mmHg/mm, saline control), and shortened Tau (9 ± 3 ms) compared to saline control (42 ± 5 ms), epinephrine (20 ± 4 ms) and glucagon (35 ± 8 ms). With insulin treatment, mechanical efficiency increased to 20097 ± 2070 vs. 12424 ± 1615 mmHg·mm/ml O2/100 g in controls. Simultaneously, insulin increased myocardial lactate uptake (35 ± 2 vs. 17 ± 4 μmol/min/100 g, saline control), but did not increase glucose uptake. Epinephrine and glucagon decreased mechanical efficiency compared to saline controls, coincident with increased myocardial fatty acid consumption, but without increasing lactate uptake. One dog died early with glucagon treatment before the first death in the saline-treated group. Conclusions: Insulin improves systolic and diastolic heart function during aerobic shock and accelerates in viva myocardial lactate oxidation.

Original languageEnglish (US)
Pages (from-to)289-298
Number of pages10
JournalCardiovascular Research
Volume34
Issue number2
DOIs
StatePublished - May 1997
Externally publishedYes

Fingerprint

Cardiogenic Shock
Canidae
Insulin
Glucagon
Lactic Acid
Epinephrine
Verapamil
Glucose
Shock
Glucose Clamp Technique
Nonesterified Fatty Acids
Fatty Acids
Dogs
Oxygen
Control Groups

Keywords

  • Contractility
  • Dog, anesthetized
  • Epinephrine
  • Glucagon
  • Insulin
  • Metabolism
  • Shock
  • Verapamil

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Insulin improves heart function and metabolism during non-ischemic cardiogenic shock in awake canines. / Kline, Jeffrey; Raymond, Richard M.; Leonova, Elena D.; Williams, Thomas C.; Watts, John A.

In: Cardiovascular Research, Vol. 34, No. 2, 05.1997, p. 289-298.

Research output: Contribution to journalArticle

Kline, Jeffrey ; Raymond, Richard M. ; Leonova, Elena D. ; Williams, Thomas C. ; Watts, John A. / Insulin improves heart function and metabolism during non-ischemic cardiogenic shock in awake canines. In: Cardiovascular Research. 1997 ; Vol. 34, No. 2. pp. 289-298.
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abstract = "Objectives: This study was undertaken to examine in-situ heart function and metabolism during insulin treatment of verapamil-induced cardiogenic shock in awake canines. Methods: Twenty mongrel canines were instrumented to monitor myocardial substrate uptakes (glucose, lactate, free fatty acids, oxygen [MVO2]), as well as left ventricular (LV) end-systolic elastance (E(max)), LV efficiency (LV minute work/MVO2), and Tau. Shock was induced by graded intraportal verapamil infusion followed by randomized assignment to one of 4 treatment groups: saline control (3.0 ml/kg/min, n = 5), epinephrine (5 μg/kg/min, n = 5), glucagon (10 μg/kg/min, n = 5) or insulin (1000 mU/min, n = 5) with dextrose to clamp arterial [glucose] ± 10{\%} of basal concentrations. Results: Insulin treatment significantly increased E(max) (34 ± 3 vs. 17 ± 3 mmHg/mm, saline control), and shortened Tau (9 ± 3 ms) compared to saline control (42 ± 5 ms), epinephrine (20 ± 4 ms) and glucagon (35 ± 8 ms). With insulin treatment, mechanical efficiency increased to 20097 ± 2070 vs. 12424 ± 1615 mmHg·mm/ml O2/100 g in controls. Simultaneously, insulin increased myocardial lactate uptake (35 ± 2 vs. 17 ± 4 μmol/min/100 g, saline control), but did not increase glucose uptake. Epinephrine and glucagon decreased mechanical efficiency compared to saline controls, coincident with increased myocardial fatty acid consumption, but without increasing lactate uptake. One dog died early with glucagon treatment before the first death in the saline-treated group. Conclusions: Insulin improves systolic and diastolic heart function during aerobic shock and accelerates in viva myocardial lactate oxidation.",
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AB - Objectives: This study was undertaken to examine in-situ heart function and metabolism during insulin treatment of verapamil-induced cardiogenic shock in awake canines. Methods: Twenty mongrel canines were instrumented to monitor myocardial substrate uptakes (glucose, lactate, free fatty acids, oxygen [MVO2]), as well as left ventricular (LV) end-systolic elastance (E(max)), LV efficiency (LV minute work/MVO2), and Tau. Shock was induced by graded intraportal verapamil infusion followed by randomized assignment to one of 4 treatment groups: saline control (3.0 ml/kg/min, n = 5), epinephrine (5 μg/kg/min, n = 5), glucagon (10 μg/kg/min, n = 5) or insulin (1000 mU/min, n = 5) with dextrose to clamp arterial [glucose] ± 10% of basal concentrations. Results: Insulin treatment significantly increased E(max) (34 ± 3 vs. 17 ± 3 mmHg/mm, saline control), and shortened Tau (9 ± 3 ms) compared to saline control (42 ± 5 ms), epinephrine (20 ± 4 ms) and glucagon (35 ± 8 ms). With insulin treatment, mechanical efficiency increased to 20097 ± 2070 vs. 12424 ± 1615 mmHg·mm/ml O2/100 g in controls. Simultaneously, insulin increased myocardial lactate uptake (35 ± 2 vs. 17 ± 4 μmol/min/100 g, saline control), but did not increase glucose uptake. Epinephrine and glucagon decreased mechanical efficiency compared to saline controls, coincident with increased myocardial fatty acid consumption, but without increasing lactate uptake. One dog died early with glucagon treatment before the first death in the saline-treated group. Conclusions: Insulin improves systolic and diastolic heart function during aerobic shock and accelerates in viva myocardial lactate oxidation.

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KW - Glucagon

KW - Insulin

KW - Metabolism

KW - Shock

KW - Verapamil

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