Wang J, Zhang P J, Zhang L, Qi J H, Wei P J, Jin Z J
Department of Pharmacology, Shanghai Second Medical University, China.
Zhongguo Yao Li Xue Bao. 1997 Mar;18(2):140-2.
To study the mechanisms of captopril (Cap) and enalaprilat (Ena) protective effects on hypoxic and reoxygenated cardiac myocytes.
Using fluorescent probes Fura 2-AM, BCECF/AM, SBFI/AM combined with computer image processing techniques to measure intracellular ion concentrations.
[Ca2+]i (165 +/- 8 nmol.L-1) and [Na+]i (9.2 +/- 0.8 mmol.L-1) were higher but [pH]i (6.7 +/- 0.3) was lower in hypoxic and reoxygenated myocytes (196 +/- 14 nmol.L-1, 9.3 +/- 1.3 mmol.L-1, 6.61 +/- 0.19, respectively) than in normal ones. Cap and Ena reduced [Ca2+]i (149 +/- 11 and 152 +/- 10 nmol.L-1 respectively) and intracellular acidosis (7.11 +/- 0.22 and 7.2 +/- 0.4, respectively) during hypoxia. Cap also decreased [Na+]i in hypoxic myocytes (8.1 +/- 0.9 mmol.L-1). During reoxygenation, Cap decreased [Ca2+]i and [Na+]i but Ena had no significant effect on them. Cap or Ena had no additive effect when combined with verapamil (Ver).
Cap and Ena protected hypoxic and reoxygenated cardiomyocytes, but the mechanisms were not the same.
