Effects of diltiazem on anoxic injury in the isolated rat heart

Pacha Meyian Rahamathulla; Muhammad Ashraf; Arnold Schwartz; John Benedict

doi:10.1016/S0735-1097(83)80110-7

Effects of diltiazem on anoxic injury in the isolated rat heart

Pacha Meyian Rahamathulla, Muhammad Ashraf, Arnold Schwartz, John Benedict

Research output: Contribution to journal › Article › peer-review

16 Scopus citations

Abstract

The effect of diltiazem, a calcium channel blocking agent, on anoxic injury was studied in isolated perfused rat hearts. Anoxia for 60 minutes caused a considerable release of creatine kinase and significant cell injury. Reoxygenation of these anoxic hearts for 20 minutes accelerated the creatine kinase release and caused severe cell injury. Reoxygenation of anoxic hearts with diltiazem at a rate of either 2 or 4.5 mg/liter did not reduce creatine kinase release significantly (probability [p] > 0.05). However, the higher dosage of diltiazem (4.5 mg/ liter during both anoxic and reoxygenation phases resulted in significant (p ≤ 0.05) preservation of healthy tissue. The data suggest that diltiazem in the higher concentration prevents cell injury and reduces mitochondrial damage in anoxic injury.

Original language	English (US)
Pages (from-to)	1081-1089
Number of pages	9
Journal	Journal of the American College of Cardiology
Volume	1
Issue number	4
DOIs	https://doi.org/10.1016/S0735-1097(83)80110-7
State	Published - 1983
Externally published	Yes

ASJC Scopus subject areas

Cardiology and Cardiovascular Medicine

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title = "Effects of diltiazem on anoxic injury in the isolated rat heart",

abstract = "The effect of diltiazem, a calcium channel blocking agent, on anoxic injury was studied in isolated perfused rat hearts. Anoxia for 60 minutes caused a considerable release of creatine kinase and significant cell injury. Reoxygenation of these anoxic hearts for 20 minutes accelerated the creatine kinase release and caused severe cell injury. Reoxygenation of anoxic hearts with diltiazem at a rate of either 2 or 4.5 mg/liter did not reduce creatine kinase release significantly (probability [p] > 0.05). However, the higher dosage of diltiazem (4.5 mg/ liter during both anoxic and reoxygenation phases resulted in significant (p ≤ 0.05) preservation of healthy tissue. The data suggest that diltiazem in the higher concentration prevents cell injury and reduces mitochondrial damage in anoxic injury.",

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AU - Rahamathulla, Pacha Meyian

AU - Ashraf, Muhammad

AU - Schwartz, Arnold

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N2 - The effect of diltiazem, a calcium channel blocking agent, on anoxic injury was studied in isolated perfused rat hearts. Anoxia for 60 minutes caused a considerable release of creatine kinase and significant cell injury. Reoxygenation of these anoxic hearts for 20 minutes accelerated the creatine kinase release and caused severe cell injury. Reoxygenation of anoxic hearts with diltiazem at a rate of either 2 or 4.5 mg/liter did not reduce creatine kinase release significantly (probability [p] > 0.05). However, the higher dosage of diltiazem (4.5 mg/ liter during both anoxic and reoxygenation phases resulted in significant (p ≤ 0.05) preservation of healthy tissue. The data suggest that diltiazem in the higher concentration prevents cell injury and reduces mitochondrial damage in anoxic injury.

AB - The effect of diltiazem, a calcium channel blocking agent, on anoxic injury was studied in isolated perfused rat hearts. Anoxia for 60 minutes caused a considerable release of creatine kinase and significant cell injury. Reoxygenation of these anoxic hearts for 20 minutes accelerated the creatine kinase release and caused severe cell injury. Reoxygenation of anoxic hearts with diltiazem at a rate of either 2 or 4.5 mg/liter did not reduce creatine kinase release significantly (probability [p] > 0.05). However, the higher dosage of diltiazem (4.5 mg/ liter during both anoxic and reoxygenation phases resulted in significant (p ≤ 0.05) preservation of healthy tissue. The data suggest that diltiazem in the higher concentration prevents cell injury and reduces mitochondrial damage in anoxic injury.

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