Nicorandil Ameliorates Posttransplant Dysfunction in Cardiac Allografts Harvested from Non-Heart-Beating Donors

Makoto Mohri, Kotaro Suehiro, Shu Yamamoto, Hiroki Yamaguchi, Kozo Ishino, Shunji Sano

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Objective: Warm ischemia is a major cause of cardiac allograft dysfunction in non-heart-beating donors (NHBDs). We evaluated the cardioprotective effects of nicorandil, an adenosine triphosphate-sensitive potassium channel opener, on the early posttransplant left ventricular (LV) function of hearts harvested from asphyxiated canine NHBDs. Methods: Hypoxic cardiac arrest was induced in 12 donor dogs. In 6, nicorandil was administered intravenously at 100 μg/kg+25 μg/kg/min after respiratory arrest and hearts were preserved with nicorandil-supplemented cardioplegic solution (nicorandil group). The remaining 6 did not receive nicorandil at any time during the experiment (control group). Hearts were orthotopically transplanted after a mean myocardial ischemic time of 4 hours. Results: All 12 recipients were weaned from cardiopulmonary bypass without inotropic support. In the control group, posttransplant cardiac indices and left ventricular end-systolic pressure (LVESP) decreased significantly, while LV max-dP/dt and Tau increased over pretransplant values. No differences were seen in parameters between pretransplant and posttransplant values in the nicorandil group. Posttransplant cardiac indices, LVESP, and LV max+dP/dt were higher in the nicorandil group than in controls, while posttransplant LV max-dP/dt in the nicorandil group was lower. Conclusions: Our results indicate that pretreatment with nicorandil during hypoxic perfusion before cardiac arrest and subsequent preservation with nicorandil-supplemented cardioplegia ameliorates early posttransplant LV dysfunction of hearts harvested from asphyxiated NHBDs.

Original languageEnglish
Pages (from-to)430-434
Number of pages5
JournalJapanese Journal of Thoracic and Cardiovascular Surgery
Volume50
Issue number10
Publication statusPublished - Oct 2002

Fingerprint

Nicorandil
Allografts
Induced Heart Arrest
Heart Arrest
Control Groups
Cardioplegic Solutions
Blood Pressure
Warm Ischemia
Potassium Channels
Left Ventricular Dysfunction
Cardiopulmonary Bypass
Left Ventricular Function
Canidae
Perfusion
Adenosine Triphosphate
Dogs

Keywords

  • Heart transplantation
  • Nicorandil
  • Non-heart-beating donor

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Nicorandil Ameliorates Posttransplant Dysfunction in Cardiac Allografts Harvested from Non-Heart-Beating Donors. / Mohri, Makoto; Suehiro, Kotaro; Yamamoto, Shu; Yamaguchi, Hiroki; Ishino, Kozo; Sano, Shunji.

In: Japanese Journal of Thoracic and Cardiovascular Surgery, Vol. 50, No. 10, 10.2002, p. 430-434.

Research output: Contribution to journalArticle

Mohri, Makoto ; Suehiro, Kotaro ; Yamamoto, Shu ; Yamaguchi, Hiroki ; Ishino, Kozo ; Sano, Shunji. / Nicorandil Ameliorates Posttransplant Dysfunction in Cardiac Allografts Harvested from Non-Heart-Beating Donors. In: Japanese Journal of Thoracic and Cardiovascular Surgery. 2002 ; Vol. 50, No. 10. pp. 430-434.
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abstract = "Objective: Warm ischemia is a major cause of cardiac allograft dysfunction in non-heart-beating donors (NHBDs). We evaluated the cardioprotective effects of nicorandil, an adenosine triphosphate-sensitive potassium channel opener, on the early posttransplant left ventricular (LV) function of hearts harvested from asphyxiated canine NHBDs. Methods: Hypoxic cardiac arrest was induced in 12 donor dogs. In 6, nicorandil was administered intravenously at 100 μg/kg+25 μg/kg/min after respiratory arrest and hearts were preserved with nicorandil-supplemented cardioplegic solution (nicorandil group). The remaining 6 did not receive nicorandil at any time during the experiment (control group). Hearts were orthotopically transplanted after a mean myocardial ischemic time of 4 hours. Results: All 12 recipients were weaned from cardiopulmonary bypass without inotropic support. In the control group, posttransplant cardiac indices and left ventricular end-systolic pressure (LVESP) decreased significantly, while LV max-dP/dt and Tau increased over pretransplant values. No differences were seen in parameters between pretransplant and posttransplant values in the nicorandil group. Posttransplant cardiac indices, LVESP, and LV max+dP/dt were higher in the nicorandil group than in controls, while posttransplant LV max-dP/dt in the nicorandil group was lower. Conclusions: Our results indicate that pretreatment with nicorandil during hypoxic perfusion before cardiac arrest and subsequent preservation with nicorandil-supplemented cardioplegia ameliorates early posttransplant LV dysfunction of hearts harvested from asphyxiated NHBDs.",
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N2 - Objective: Warm ischemia is a major cause of cardiac allograft dysfunction in non-heart-beating donors (NHBDs). We evaluated the cardioprotective effects of nicorandil, an adenosine triphosphate-sensitive potassium channel opener, on the early posttransplant left ventricular (LV) function of hearts harvested from asphyxiated canine NHBDs. Methods: Hypoxic cardiac arrest was induced in 12 donor dogs. In 6, nicorandil was administered intravenously at 100 μg/kg+25 μg/kg/min after respiratory arrest and hearts were preserved with nicorandil-supplemented cardioplegic solution (nicorandil group). The remaining 6 did not receive nicorandil at any time during the experiment (control group). Hearts were orthotopically transplanted after a mean myocardial ischemic time of 4 hours. Results: All 12 recipients were weaned from cardiopulmonary bypass without inotropic support. In the control group, posttransplant cardiac indices and left ventricular end-systolic pressure (LVESP) decreased significantly, while LV max-dP/dt and Tau increased over pretransplant values. No differences were seen in parameters between pretransplant and posttransplant values in the nicorandil group. Posttransplant cardiac indices, LVESP, and LV max+dP/dt were higher in the nicorandil group than in controls, while posttransplant LV max-dP/dt in the nicorandil group was lower. Conclusions: Our results indicate that pretreatment with nicorandil during hypoxic perfusion before cardiac arrest and subsequent preservation with nicorandil-supplemented cardioplegia ameliorates early posttransplant LV dysfunction of hearts harvested from asphyxiated NHBDs.

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