Effect of superoxide dismutase and acidified sodium nitrite on infarct size following ischemia and reperfusion in dogs

Yogesh Tripathi, B. M. Hegde, C. V. Raghuveer

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

The effects of superoxide dismutase (SOD) alone or in combination with acidified sodium nitrite (NaNO2), a liberator of nitric oxide were examined in dogs after ischemia and reperfusion. Animals were divided into five groups. Left anterior descending coronary artery was occluded for 90 min followed by 4 hours of reperfusion with or without therapeutic interventions given preceding reperfusion. Left ventricular end diastolic pressure (LVEDP), left ventricular systolic pressure (LVSP) and ECG changes were monitored throughout the study. Area at risk was defined by Evans blue and area of infarction by incubation in triphenyltetrazolium. Myocardial tissue lipid peroxidation was measured in ischemic and non-ischemic zones. There was no evidence of infarction until ninety minutes of ischemia. Percentage area of necrosis vis-a-vis area at risk percentage necrosis in left vertricular mass was significantly low in animals treated with combination of SOD and NaNO2 in comparison with isolated treatment with saline, SOD or NaNO2. LVEDP increased significantly following ischemia and remained unchanged during saline reperfusion. Treatment with SOD, NaNO2 in isolation or its combination significantly lowered LVEDP. Maximum increase in tissue lipid peroxidation was observed in saline and NaNO2 treated animals. SOD alone or in combination with NaNO2 significantly lowered the lipid peroxidation. The results clearly demonstrate that reperfusion can cause necrosis in ischemic myocardium. Combined treatment with SOD and NaNO2 offers significant cardioprotection against oxidative stress.

Original languageEnglish
Pages (from-to)248-256
Number of pages9
JournalIndian Journal of Physiology and Pharmacology
Volume41
Issue number3
Publication statusPublished - 01-07-1997
Externally publishedYes

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Sodium Nitrite
Superoxide Dismutase
Reperfusion
Ischemia
Dogs
Lipid Peroxidation
Blood Pressure
Necrosis
Infarction
Evans Blue
Ventricular Pressure
Coronary Vessels
Myocardium
Nitric Oxide
Electrocardiography
Oxidative Stress

All Science Journal Classification (ASJC) codes

  • Physiology
  • Pharmacology
  • Physiology (medical)

Cite this

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abstract = "The effects of superoxide dismutase (SOD) alone or in combination with acidified sodium nitrite (NaNO2), a liberator of nitric oxide were examined in dogs after ischemia and reperfusion. Animals were divided into five groups. Left anterior descending coronary artery was occluded for 90 min followed by 4 hours of reperfusion with or without therapeutic interventions given preceding reperfusion. Left ventricular end diastolic pressure (LVEDP), left ventricular systolic pressure (LVSP) and ECG changes were monitored throughout the study. Area at risk was defined by Evans blue and area of infarction by incubation in triphenyltetrazolium. Myocardial tissue lipid peroxidation was measured in ischemic and non-ischemic zones. There was no evidence of infarction until ninety minutes of ischemia. Percentage area of necrosis vis-a-vis area at risk percentage necrosis in left vertricular mass was significantly low in animals treated with combination of SOD and NaNO2 in comparison with isolated treatment with saline, SOD or NaNO2. LVEDP increased significantly following ischemia and remained unchanged during saline reperfusion. Treatment with SOD, NaNO2 in isolation or its combination significantly lowered LVEDP. Maximum increase in tissue lipid peroxidation was observed in saline and NaNO2 treated animals. SOD alone or in combination with NaNO2 significantly lowered the lipid peroxidation. The results clearly demonstrate that reperfusion can cause necrosis in ischemic myocardium. Combined treatment with SOD and NaNO2 offers significant cardioprotection against oxidative stress.",
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Effect of superoxide dismutase and acidified sodium nitrite on infarct size following ischemia and reperfusion in dogs. / Tripathi, Yogesh; Hegde, B. M.; Raghuveer, C. V.

In: Indian Journal of Physiology and Pharmacology, Vol. 41, No. 3, 01.07.1997, p. 248-256.

Research output: Contribution to journalArticle

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