OcrV1, PascalFrancis, Corpus, bibRecord, 000540

Preservation of mitochondrial function during ischemia as a possible mechanism for cardioprotection of diltiazem against ischemia/reperfusion injury

Identifieur interne : 000540 ( PascalFrancis/Corpus ); précédent : 000539; suivant : 000541

Preservation of mitochondrial function during ischemia as a possible mechanism for cardioprotection of diltiazem against ischemia/reperfusion injury

Auteurs : Satoshi Takeo ; Kouichi Tanonaka ; Takeshi Iwai ; Kanataka Motegi ; Yuko Hirota

Source :

Biochemical pharmacology [ 0006-2952 ] ; 2004.

RBID : Pascal:04-0293073

Descripteurs français

Pascal (Inist)
- Mitochondrie, Ischémie, Mécanisme action, Cardioprotecteur, Diltiazem, Reperfusion, Coeur, Pharmacologie, Antiangoreux, Antiarythmique, Vasodilatateur coronarien.

English descriptors

KwdEn :
- Antianginal agent, Antiarrhythmic agent, Cardioprotective agent, Coronary vasodilator agent, Diltiazem, Heart, Ischemia, Mechanism of action, Mitochondria, Pharmacology, Reperfusion.

Abstract

A possible mechanism for D-cis-diltiazem (diltiazem)-mediated improvement of the contractile function of ischemic/reperfused hearts was examined. Thirty-five-min ischemia/60-min reperfusion recovered little the left ventricular developed pressure (LVDP) and decreased myocardial high-energy phosphates (HEPs). Ischemia induced an accumulation of tissue Na⁺ content, an increase in cytochrome c in the cytosolic fraction, and a decrease in the oxygen consumption rate (OCR) in perfused hearts. Treatment of the heart with 1 μM diltiazem for the last 3-min of pre-ischemia did not affect the decrease in HEPs during ischemia, whereas that with 3 μM partially attenuated the decrease in ATP, suggesting that 3 μM diltiazem exerted energy-sparing effect. Treatment with I μM diltiazem enhanced the post-ischemic recovery of LVDP associated with attenuation of the ischemia-induced accumulation of tissue Na⁺, increase in cytochrome c in the cytosolic fraction, and decrease in myocardial OCR, and restoration of the myocardial HEPs during reperfusion. Combined treatment with diltiazem and a Na⁺/H exchange inhibitor, but not a Na⁺ channel blocker, facilitated the attenuation of Na ⁺ accumulation in the ischemic heart and the enhancement of the post-ischemic recovery of LVDP. Sodium lactate, a possible metabolite in ischemic hearts, and sodium chloride increased the Na⁺ concentration in mitochondria, released cytochrome c into incubation medium, and reduced the mitochondrial respiration. Treatment of isolated mitochondria with diltiazem failed to attenuate the sodium lactate- and sodium chloride-induced alterations. These results suggest that the cardioprotection of diltiazem may be exerted via attenuating cytosolic Na⁺ overload through Na⁺ channels in the ischemic heart, leading to preservation of mitochondrial functional ability during ischemia, followed by improvement of post-ischemic energy production and contractile recovery.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A11	`01`	`1`		`@1 TAKEO (Satoshi)`
A11	`02`	`1`		`@1 TANONAKA (Kouichi)`
A11	`03`	`1`		`@1 IWAI (Takeshi)`
A11	`04`	`1`		`@1 MOTEGI (Kanataka)`
A11	`05`	`1`		`@1 HIROTA (Yuko)`
A14	`01`			`@1 Department of Pharmacology, Tokyo University of Pharmacy and Life Science, 1432-1 Horinouchi @2 Hachioji, Tokyo 192-0392 @3 JPN @Z 1 aut. @Z 2 aut. @Z 3 aut. @Z 4 aut. @Z 5 aut.`
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C01	`01`		`ENG`	@0 A possible mechanism for D-cis-diltiazem (diltiazem)-mediated improvement of the contractile function of ischemic/reperfused hearts was examined. Thirty-five-min ischemia/60-min reperfusion recovered little the left ventricular developed pressure (LVDP) and decreased myocardial high-energy phosphates (HEPs). Ischemia induced an accumulation of tissue Na⁺ content, an increase in cytochrome c in the cytosolic fraction, and a decrease in the oxygen consumption rate (OCR) in perfused hearts. Treatment of the heart with 1 μM diltiazem for the last 3-min of pre-ischemia did not affect the decrease in HEPs during ischemia, whereas that with 3 μM partially attenuated the decrease in ATP, suggesting that 3 μM diltiazem exerted energy-sparing effect. Treatment with I μM diltiazem enhanced the post-ischemic recovery of LVDP associated with attenuation of the ischemia-induced accumulation of tissue Na⁺, increase in cytochrome c in the cytosolic fraction, and decrease in myocardial OCR, and restoration of the myocardial HEPs during reperfusion. Combined treatment with diltiazem and a Na⁺/H exchange inhibitor, but not a Na⁺ channel blocker, facilitated the attenuation of Na ⁺ accumulation in the ischemic heart and the enhancement of the post-ischemic recovery of LVDP. Sodium lactate, a possible metabolite in ischemic hearts, and sodium chloride increased the Na⁺ concentration in mitochondria, released cytochrome c into incubation medium, and reduced the mitochondrial respiration. Treatment of isolated mitochondria with diltiazem failed to attenuate the sodium lactate- and sodium chloride-induced alterations. These results suggest that the cardioprotection of diltiazem may be exerted via attenuating cytosolic Na⁺ overload through Na⁺ channels in the ischemic heart, leading to preservation of mitochondrial functional ability during ischemia, followed by improvement of post-ischemic energy production and contractile recovery.
C02	`01`	`X`		`@0 002B02`
C03	`01`	`X`	`FRE`	`@0 Mitochondrie @5 11`
C03	`01`	`X`	`ENG`	`@0 Mitochondria @5 11`
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C03	`02`	`X`	`SPA`	`@0 Isquemia @5 12`
C03	`03`	`X`	`FRE`	`@0 Mécanisme action @5 14`
C03	`03`	`X`	`ENG`	`@0 Mechanism of action @5 14`
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C03	`04`	`X`	`SPA`	`@0 Cardioprotector @5 15`
C03	`05`	`X`	`FRE`	`@0 Diltiazem @2 NK @2 FR @5 16`
C03	`05`	`X`	`ENG`	`@0 Diltiazem @2 NK @2 FR @5 16`
C03	`05`	`X`	`SPA`	`@0 Diltiazem @2 NK @2 FR @5 16`
C03	`06`	`X`	`FRE`	`@0 Reperfusion @5 17`
C03	`06`	`X`	`ENG`	`@0 Reperfusion @5 17`
C03	`06`	`X`	`SPA`	`@0 Reperfusión @5 17`
C03	`07`	`X`	`FRE`	`@0 Coeur @5 18`
C03	`07`	`X`	`ENG`	`@0 Heart @5 18`
C03	`07`	`X`	`SPA`	`@0 Corazón @5 18`
C03	`08`	`X`	`FRE`	`@0 Pharmacologie @5 19`
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C03	`10`	`X`	`SPA`	`@0 Antiarrítmico @5 21`
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C03	`11`	`X`	`ENG`	`@0 Coronary vasodilator agent @5 22`
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C07	`01`	`X`	`FRE`	`@0 Appareil circulatoire pathologie @5 61`
C07	`01`	`X`	`ENG`	`@0 Cardiovascular disease @5 61`
C07	`01`	`X`	`SPA`	`@0 Aparato circulatorio patología @5 61`
C07	`02`	`X`	`FRE`	`@0 Système nerveux pathologie @5 62`
C07	`02`	`X`	`ENG`	`@0 Nervous system diseases @5 62`
C07	`02`	`X`	`SPA`	`@0 Sistema nervioso patología @5 62`
C07	`03`	`X`	`FRE`	`@0 Vaisseau sanguin pathologie @5 63`
C07	`03`	`X`	`ENG`	`@0 Vascular disease @5 63`
C07	`03`	`X`	`SPA`	`@0 Vaso sanguíneo patología @5 63`
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C07	`04`	`X`	`ENG`	`@0 Calcium antagonist @5 64`
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C07	`05`	`X`	`FRE`	`@0 Benzothiazépine dérivé @5 65`
C07	`05`	`X`	`ENG`	`@0 Benzothiazepine derivatives @5 65`
C07	`05`	`X`	`SPA`	`@0 Benzotiazepina derivado @5 65`
C07	`06`	`X`	`FRE`	`@0 Appareil circulatoire @5 66`
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Format Inist (serveur)

NO :	PASCAL 04-0293073 INIST
ET :	Preservation of mitochondrial function during ischemia as a possible mechanism for cardioprotection of diltiazem against ischemia/reperfusion injury
AU :	TAKEO (Satoshi); TANONAKA (Kouichi); IWAI (Takeshi); MOTEGI (Kanataka); HIROTA (Yuko)
AF :	Department of Pharmacology, Tokyo University of Pharmacy and Life Science, 1432-1 Horinouchi/Hachioji, Tokyo 192-0392/Japon (1 aut., 2 aut., 3 aut., 4 aut., 5 aut.)
DT :	Publication en série; Niveau analytique
SO :	Biochemical pharmacology; ISSN 0006-2952; Coden BCPCA6; Etats-Unis; Da. 2004; Vol. 67; No. 3; Pp. 565-574; Bibl. 26 ref.
LA :	Anglais
EA :	A possible mechanism for D-cis-diltiazem (diltiazem)-mediated improvement of the contractile function of ischemic/reperfused hearts was examined. Thirty-five-min ischemia/60-min reperfusion recovered little the left ventricular developed pressure (LVDP) and decreased myocardial high-energy phosphates (HEPs). Ischemia induced an accumulation of tissue Na⁺ content, an increase in cytochrome c in the cytosolic fraction, and a decrease in the oxygen consumption rate (OCR) in perfused hearts. Treatment of the heart with 1 μM diltiazem for the last 3-min of pre-ischemia did not affect the decrease in HEPs during ischemia, whereas that with 3 μM partially attenuated the decrease in ATP, suggesting that 3 μM diltiazem exerted energy-sparing effect. Treatment with I μM diltiazem enhanced the post-ischemic recovery of LVDP associated with attenuation of the ischemia-induced accumulation of tissue Na⁺, increase in cytochrome c in the cytosolic fraction, and decrease in myocardial OCR, and restoration of the myocardial HEPs during reperfusion. Combined treatment with diltiazem and a Na⁺/H exchange inhibitor, but not a Na⁺ channel blocker, facilitated the attenuation of Na ⁺ accumulation in the ischemic heart and the enhancement of the post-ischemic recovery of LVDP. Sodium lactate, a possible metabolite in ischemic hearts, and sodium chloride increased the Na⁺ concentration in mitochondria, released cytochrome c into incubation medium, and reduced the mitochondrial respiration. Treatment of isolated mitochondria with diltiazem failed to attenuate the sodium lactate- and sodium chloride-induced alterations. These results suggest that the cardioprotection of diltiazem may be exerted via attenuating cytosolic Na⁺ overload through Na⁺ channels in the ischemic heart, leading to preservation of mitochondrial functional ability during ischemia, followed by improvement of post-ischemic energy production and contractile recovery.
CC :	002B02
FD :	Mitochondrie; Ischémie; Mécanisme action; Cardioprotecteur; Diltiazem; Reperfusion; Coeur; Pharmacologie; Antiangoreux; Antiarythmique; Vasodilatateur coronarien
FG :	Appareil circulatoire pathologie; Système nerveux pathologie; Vaisseau sanguin pathologie; Antagoniste calcium; Benzothiazépine dérivé; Appareil circulatoire
ED :	Mitochondria; Ischemia; Mechanism of action; Cardioprotective agent; Diltiazem; Reperfusion; Heart; Pharmacology; Antianginal agent; Antiarrhythmic agent; Coronary vasodilator agent
EG :	Cardiovascular disease; Nervous system diseases; Vascular disease; Calcium antagonist; Benzothiazepine derivatives; Circulatory system
SD :	Mitocondria; Isquemia; Mecanismo acción; Cardioprotector; Diltiazem; Reperfusión; Corazón; Farmacología; Antianginoso; Antiarrítmico; Vasodilatator coronario
LO :	INIST-1418.354000119274730180
ID :	04-0293073

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Pascal:04-0293073

Le document en format XML

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<term>Heart</term>
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<front><div type="abstract" xml:lang="en">A possible mechanism for D-cis-diltiazem (diltiazem)-mediated improvement of the contractile function of ischemic/reperfused hearts was examined. Thirty-five-min ischemia/60-min reperfusion recovered little the left ventricular developed pressure (LVDP) and decreased myocardial high-energy phosphates (HEPs). Ischemia induced an accumulation of tissue Na<sup>+</sup>
 content, an increase in cytochrome c in the cytosolic fraction, and a decrease in the oxygen consumption rate (OCR) in perfused hearts. Treatment of the heart with 1 μM diltiazem for the last 3-min of pre-ischemia did not affect the decrease in HEPs during ischemia, whereas that with 3 μM partially attenuated the decrease in ATP, suggesting that 3 μM diltiazem exerted energy-sparing effect. Treatment with I μM diltiazem enhanced the post-ischemic recovery of LVDP associated with attenuation of the ischemia-induced accumulation of tissue Na<sup>+</sup>
, increase in cytochrome c in the cytosolic fraction, and decrease in myocardial OCR, and restoration of the myocardial HEPs during reperfusion. Combined treatment with diltiazem and a Na<sup>+</sup>
/H exchange inhibitor, but not a Na<sup>+</sup>
 channel blocker, facilitated the attenuation of Na <sup>+</sup>
 accumulation in the ischemic heart and the enhancement of the post-ischemic recovery of LVDP. Sodium lactate, a possible metabolite in ischemic hearts, and sodium chloride increased the Na<sup>+</sup>
 concentration in mitochondria, released cytochrome c into incubation medium, and reduced the mitochondrial respiration. Treatment of isolated mitochondria with diltiazem failed to attenuate the sodium lactate- and sodium chloride-induced alterations. These results suggest that the cardioprotection of diltiazem may be exerted via attenuating cytosolic Na<sup>+</sup>
 overload through Na<sup>+</sup>
 channels in the ischemic heart, leading to preservation of mitochondrial functional ability during ischemia, followed by improvement of post-ischemic energy production and contractile recovery.</div>
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<fA21><s1>2004</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>1418</s2>
<s5>354000119274730180</s5>
</fA43>
<fA44><s0>0000</s0>
<s1>© 2004 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>26 ref.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>04-0293073</s0>
</fA47>
<fA60><s1>P</s1>
</fA60>
<fA61><s0>A</s0>
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<fA64 i1="01" i2="1"><s0>Biochemical pharmacology</s0>
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<fA66 i1="01"><s0>USA</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>A possible mechanism for D-cis-diltiazem (diltiazem)-mediated improvement of the contractile function of ischemic/reperfused hearts was examined. Thirty-five-min ischemia/60-min reperfusion recovered little the left ventricular developed pressure (LVDP) and decreased myocardial high-energy phosphates (HEPs). Ischemia induced an accumulation of tissue Na<sup>+</sup>
 content, an increase in cytochrome c in the cytosolic fraction, and a decrease in the oxygen consumption rate (OCR) in perfused hearts. Treatment of the heart with 1 μM diltiazem for the last 3-min of pre-ischemia did not affect the decrease in HEPs during ischemia, whereas that with 3 μM partially attenuated the decrease in ATP, suggesting that 3 μM diltiazem exerted energy-sparing effect. Treatment with I μM diltiazem enhanced the post-ischemic recovery of LVDP associated with attenuation of the ischemia-induced accumulation of tissue Na<sup>+</sup>
, increase in cytochrome c in the cytosolic fraction, and decrease in myocardial OCR, and restoration of the myocardial HEPs during reperfusion. Combined treatment with diltiazem and a Na<sup>+</sup>
/H exchange inhibitor, but not a Na<sup>+</sup>
 channel blocker, facilitated the attenuation of Na <sup>+</sup>
 accumulation in the ischemic heart and the enhancement of the post-ischemic recovery of LVDP. Sodium lactate, a possible metabolite in ischemic hearts, and sodium chloride increased the Na<sup>+</sup>
 concentration in mitochondria, released cytochrome c into incubation medium, and reduced the mitochondrial respiration. Treatment of isolated mitochondria with diltiazem failed to attenuate the sodium lactate- and sodium chloride-induced alterations. These results suggest that the cardioprotection of diltiazem may be exerted via attenuating cytosolic Na<sup>+</sup>
 overload through Na<sup>+</sup>
 channels in the ischemic heart, leading to preservation of mitochondrial functional ability during ischemia, followed by improvement of post-ischemic energy production and contractile recovery.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002B02</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Mitochondrie</s0>
<s5>11</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Mitochondria</s0>
<s5>11</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Mitocondria</s0>
<s5>11</s5>
</fC03>
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<s5>12</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Ischemia</s0>
<s5>12</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Isquemia</s0>
<s5>12</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Mécanisme action</s0>
<s5>14</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Mechanism of action</s0>
<s5>14</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Mecanismo acción</s0>
<s5>14</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Cardioprotecteur</s0>
<s5>15</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Cardioprotective agent</s0>
<s5>15</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Cardioprotector</s0>
<s5>15</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Diltiazem</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>16</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Diltiazem</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>16</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Diltiazem</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>16</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Reperfusion</s0>
<s5>17</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Reperfusion</s0>
<s5>17</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Reperfusión</s0>
<s5>17</s5>
</fC03>
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<s5>18</s5>
</fC03>
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<s5>18</s5>
</fC03>
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<s5>18</s5>
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<fC03 i1="08" i2="X" l="FRE"><s0>Pharmacologie</s0>
<s5>19</s5>
</fC03>
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<s5>19</s5>
</fC03>
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<s5>19</s5>
</fC03>
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<s5>20</s5>
</fC03>
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<s5>20</s5>
</fC03>
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<s5>20</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE"><s0>Antiarythmique</s0>
<s5>21</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG"><s0>Antiarrhythmic agent</s0>
<s5>21</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA"><s0>Antiarrítmico</s0>
<s5>21</s5>
</fC03>
<fC03 i1="11" i2="X" l="FRE"><s0>Vasodilatateur coronarien</s0>
<s5>22</s5>
</fC03>
<fC03 i1="11" i2="X" l="ENG"><s0>Coronary vasodilator agent</s0>
<s5>22</s5>
</fC03>
<fC03 i1="11" i2="X" l="SPA"><s0>Vasodilatator coronario</s0>
<s5>22</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Appareil circulatoire pathologie</s0>
<s5>61</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Cardiovascular disease</s0>
<s5>61</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Aparato circulatorio patología</s0>
<s5>61</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Système nerveux pathologie</s0>
<s5>62</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>62</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>62</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Vaisseau sanguin pathologie</s0>
<s5>63</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Vascular disease</s0>
<s5>63</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Vaso sanguíneo patología</s0>
<s5>63</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Antagoniste calcium</s0>
<s5>64</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Calcium antagonist</s0>
<s5>64</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Antagonista calcio</s0>
<s5>64</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Benzothiazépine dérivé</s0>
<s5>65</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Benzothiazepine derivatives</s0>
<s5>65</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Benzotiazepina derivado</s0>
<s5>65</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Appareil circulatoire</s0>
<s5>66</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Circulatory system</s0>
<s5>66</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Aparato circulatorio</s0>
<s5>66</s5>
</fC07>
<fN21><s1>180</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
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<server><NO>PASCAL 04-0293073 INIST</NO>
<ET>Preservation of mitochondrial function during ischemia as a possible mechanism for cardioprotection of diltiazem against ischemia/reperfusion injury</ET>
<AU>TAKEO (Satoshi); TANONAKA (Kouichi); IWAI (Takeshi); MOTEGI (Kanataka); HIROTA (Yuko)</AU>
<AF>Department of Pharmacology, Tokyo University of Pharmacy and Life Science, 1432-1 Horinouchi/Hachioji, Tokyo 192-0392/Japon (1 aut., 2 aut., 3 aut., 4 aut., 5 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Biochemical pharmacology; ISSN 0006-2952; Coden BCPCA6; Etats-Unis; Da. 2004; Vol. 67; No. 3; Pp. 565-574; Bibl. 26 ref.</SO>
<LA>Anglais</LA>
<EA>A possible mechanism for D-cis-diltiazem (diltiazem)-mediated improvement of the contractile function of ischemic/reperfused hearts was examined. Thirty-five-min ischemia/60-min reperfusion recovered little the left ventricular developed pressure (LVDP) and decreased myocardial high-energy phosphates (HEPs). Ischemia induced an accumulation of tissue Na<sup>+</sup>
 content, an increase in cytochrome c in the cytosolic fraction, and a decrease in the oxygen consumption rate (OCR) in perfused hearts. Treatment of the heart with 1 μM diltiazem for the last 3-min of pre-ischemia did not affect the decrease in HEPs during ischemia, whereas that with 3 μM partially attenuated the decrease in ATP, suggesting that 3 μM diltiazem exerted energy-sparing effect. Treatment with I μM diltiazem enhanced the post-ischemic recovery of LVDP associated with attenuation of the ischemia-induced accumulation of tissue Na<sup>+</sup>
, increase in cytochrome c in the cytosolic fraction, and decrease in myocardial OCR, and restoration of the myocardial HEPs during reperfusion. Combined treatment with diltiazem and a Na<sup>+</sup>
/H exchange inhibitor, but not a Na<sup>+</sup>
 channel blocker, facilitated the attenuation of Na <sup>+</sup>
 accumulation in the ischemic heart and the enhancement of the post-ischemic recovery of LVDP. Sodium lactate, a possible metabolite in ischemic hearts, and sodium chloride increased the Na<sup>+</sup>
 concentration in mitochondria, released cytochrome c into incubation medium, and reduced the mitochondrial respiration. Treatment of isolated mitochondria with diltiazem failed to attenuate the sodium lactate- and sodium chloride-induced alterations. These results suggest that the cardioprotection of diltiazem may be exerted via attenuating cytosolic Na<sup>+</sup>
 overload through Na<sup>+</sup>
 channels in the ischemic heart, leading to preservation of mitochondrial functional ability during ischemia, followed by improvement of post-ischemic energy production and contractile recovery.</EA>
<CC>002B02</CC>
<FD>Mitochondrie; Ischémie; Mécanisme action; Cardioprotecteur; Diltiazem; Reperfusion; Coeur; Pharmacologie; Antiangoreux; Antiarythmique; Vasodilatateur coronarien</FD>
<FG>Appareil circulatoire pathologie; Système nerveux pathologie; Vaisseau sanguin pathologie; Antagoniste calcium; Benzothiazépine dérivé; Appareil circulatoire</FG>
<ED>Mitochondria; Ischemia; Mechanism of action; Cardioprotective agent; Diltiazem; Reperfusion; Heart; Pharmacology; Antianginal agent; Antiarrhythmic agent; Coronary vasodilator agent</ED>
<EG>Cardiovascular disease; Nervous system diseases; Vascular disease; Calcium antagonist; Benzothiazepine derivatives; Circulatory system</EG>
<SD>Mitocondria; Isquemia; Mecanismo acción; Cardioprotector; Diltiazem; Reperfusión; Corazón; Farmacología; Antianginoso; Antiarrítmico; Vasodilatator coronario</SD>
<LO>INIST-1418.354000119274730180</LO>
<ID>04-0293073</ID>
</server>
</inist>
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Preservation of mitochondrial function during ischemia as a possible mechanism for cardioprotection of diltiazem against ischemia/reperfusion injury

Preservation of mitochondrial function during ischemia as a possible mechanism for cardioprotection of diltiazem against ischemia/reperfusion injury

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