A. Piasecka et al., EFFECT OF PERINDOPRIL THERAPY ON FLUIDITY AND POTENTIAL OF ERYTHROCYTE-MEMBRANE FROM INDIVIDUALS WITH CORONARY HEART-DISEASE, Scandinavian journal of clinical & laboratory investigation, 57(1), 1997, pp. 65-71
Erythrocyte membrane fluidity and membrane potential were measured in
patients suffering from coronary heart disease (CHD) and treated with
perindopril. Membrane fluidity was determined using electron paramagne
tic resonance (EPR) spectroscopy, and membrane potential was evaluated
using potential-sensitive fluorescent dyes. CHD does not change membr
ane fluidity at the depth of the 5 carbon in the fatty acid chain of m
embrane phospholipids. However the hydrophobic core of the membrane is
altered in CHD. For 19 CHD patients, the correlation times tau(B) and
tau(C) of a spin label 16DS were higher than for controls: tau(B)=(1.
84+/-0.04)x10(-9) s and tau(C)=(2.54+/-0.04)x10(-9) s vs tau(B)=(1.62/-0.06)x10(-9) s; and tau(C)=(2.24+/-0.07)x10(-9) s (results given as
mean +/- SEM). Such results indicate the increased microviscosity in h
ydrophobic regions of CHD erythrocyte membranes in comparison with con
trols. Perindopril therapy partly abolished these changes. The membran
e potential of CHD red blood cells -17.89+/-1.36 mV was higher than th
e control value -9.83+/-0.59 mV. Perindopril treatment shifted the mem
brane potential value to -13.45+/-0.99 mV when measured after a single
dose of the drug, or even depolarized the membrane after 7 days of th
erapy -4.95+/-0.73 mV. It is concluded that the erythrocyte membrane i
s more rigid and hyperpolarized in CHD, and perindopril therapy partly
abolishes these changes as early as 3 h after administration.