The neurohumoral systems of patients with
ischemic heart disease and under emotional-pain stress: the means
for their pharmacological regulation
Fomichev VI, Pchelintsev VP.
Kardiologiia. 1993;33(10):15-8, 3.
The sympathetic-adrenal and kallikrein-kinin systems were studied
in 225 patients with various coronary heart diseases before and
after therapy with lipoic acid (150 mg/day), tocopherol (100 mg/day),
anaprilin (40 mg/day), prodectin (750 mg/day) or their combination.
Myocardial and adrenal catecholamine levels were measured in experiments
on animals exposed to emotional pain stress. Their levels were
found to be affected by lipoic acid, tocopherol, obsidan or their
combinations in the same doses, taking into account species specificity.
Lipoic acid therapy for patients with coronary heart disease decreased
epinephrine excretion, enhanced the elimination of vanillylmandelic
acid and norepinephrine. Tocopherol lowered daily urinary epinephrine
levels and increased the release of vanillylmandelic acid, without
changing epinephrine excretion. Emotional pain stress resulted
in myocardial epinephrine accumulation and adrenal norepinephrine
in the animals. Lipoic acid prevented this accumulation, whereas
tocopherol did not possess this effect.
Protective role of DL-alpha-lipoic acid against
mercury-induced neural lipid peroxidation.
Anuradha B, Varalakshmi P.
Department of Medical Biochemistry, Dr AL Mudaliar Post Graduate
Institute of Basic Medical Sciences, Madras University, Taramani,
Madras, 600 113, India.
Pharmacol Res. 1999 Jan;39(1):67-80.
Experimental neurotoxicity in rat models was
induced by an intramuscular injection of mercuric chloride. dl-alpha-lipoic
acid was administered as an antidote in three protocols of experimental
design. Two protocols of short-term exposure of mercury was designed,
one with prophylactic therapy and the other with curative therapy
of lipoic acid. The third protocol was with prophylactic therapy
of lipoic acid on long-term exposure of mercury. Enhanced lipid
peroxidation, depleted non-enzymic and perturbed enzymic antioxidant
status were observed in cerebral cortex, cerebellum and sciatic
nerves of the toxic groups. The ameliorating effect of lipoic
acid and its therapeutic efficacy during various modes of therapy,
on the antioxidant status was established in the nervous tissues.