Inhibition of NHE protects reoxygenated cardiomyocytes independently of anoxic Ca2+ overload and acidosis

We investigated the question of whether inhibition of the Na+/H+ exchanger (NHE) during ischemia is protective due to reduction of cytosolic Ca(2+) accumulation or enhanced acidosis in cardiomyocytes. Additionally, the role of the Na+-HCO-/3 symporter (NBS) was investigated.

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Bibliographic Details
Published inAmerican journal of physiology. Heart and circulatory physiology Vol. 48; no. 5; pp. H2143 - H2150
Main Authors SCHÄFER, C, LADILOV, Y. V, SCHAFER, M, PIPER, H. M
Format Journal Article
LanguageEnglish
Published Bethesda, MD American Physiological Society 01.11.2000
Subjects
Acids
Biochemistry
Biological and medical sciences
Calcium
Cardiology. Vascular system
Circulatory system
Coronary heart disease
Heart
Medical sciences
Oxygen
Heart
Rat
Cardiovascular disease
Environmental factor
Heart ventricle
Myocardial disease
Myocyte
Vascular disease
Calcium ion
Ischemia
Sodium ion
Hydrogen ion
Oxygen
Anoxia
Rodentia
Coronary heart disease
Vertebrata
Mammalia
Overload
Animal
Myocardium
Models
Circulatory system
Lesion
Acidosis
Oxygenation
Cation exchanger
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Summary:We investigated the question of whether inhibition of the Na+/H+ exchanger (NHE) during ischemia is protective due to reduction of cytosolic Ca(2+) accumulation or enhanced acidosis in cardiomyocytes. Additionally, the role of the Na+-HCO-/3 symporter (NBS) was investigated.
ISSN:0363-6135
1522-1539