Role of calcium and free fatty acids in epinephrine-induced myocardial necrosis

Journal Article · Tue Nov 01 00:00:00 EST 1983 · Toxicol. Appl. Pharmacol.; (United States)

DOI:https://doi.org/10.1016/0041-008X(83)90344-7· OSTI ID:5018671

Mallov, S

A possible mechanism by which large doses of catecholamines produce myocardial necrosis was investigated. Male Sprague-Dawley rats, 275 to 325 g in weight, were injected once, sc, with 3 mg/kg epinephrine (E) or infused iv for 1 hr with E at a rate of 1.2 or 1.7 micrograms/min, and also injected iv with either 45Ca or (3H)palmitic acid (3H-PA) at the same time as or at various periods of time after E administration but exactly 0.5 or 1 hr before death. Controls were injected with saline solution. Heart/plasma ratios of radioactivity (H/P) were determined. The ratios increased in the case of both 45Ca and (3H)PA within 0.5 hr after E, reached peak values after 18 to 24 hr with 45Ca and 3 to 6 hr with (3H)PA, and remained above values for the controls for at least 72 hr with 45Ca and 48 hr with (3H)PA. The rate of 45Ca influx into heart 20 hr after E administration paralleled the severity of the myocardial damage that had been produced. When 45Ca and E were injected simultaneously, H/P increased progressively with time to 30 times control values, indicating the accumulation and retention of Ca in the heart. Under the same conditions, H/P values with (3H)PA also rose but remained constant at a level two to three times that in controls. Total cardiac free fatty acids (FFA) rose slightly and remained constant at the elevated level. It was not possible to distinguish a given point in time at which the increase in either Ca or FFA influx, initially due to the normal pharmacological effect of E, began to occur as a consequence of damage produced by the latter. It is concluded that high concentrations of catecholamines promote the deposition of Ca and FFA in myocardial cells in various forms, and that the deposition of these substances as soaps in the plasma membranes may cause permeability changes that lead to cell injury.

• Research Organization: State Univ. of New York, Syracuse
• OSTI ID: 5018671
• Journal Information: Toxicol. Appl. Pharmacol.; (United States), Vol. 71:2
• Country of Publication: United States
• Language: English

Related Subjects

59 BASIC BIOLOGICAL SCIENCES
ADRENALINE
BIOCHEMICAL REACTION KINETICS
BIOLOGICAL EFFECTS
SUBCUTANEOUS INJECTION
CALCIUM COMPOUNDS
RETENTION
HEXADECANOIC ACID
MYOCARDIUM
NECROSIS
CALCIUM 45
INTRAVENOUS INJECTION
LABELLED COMPOUNDS
TRITIUM COMPOUNDS
ADRENAL HORMONES
ALKALINE EARTH ISOTOPES
ALKALINE EARTH METAL COMPOUNDS
AUTONOMIC NERVOUS SYSTEM AGENTS
BETA DECAY RADIOISOTOPES
BETA-MINUS DECAY RADIOISOTOPES
BODY
CALCIUM ISOTOPES
CARBOXYLIC ACIDS
CARDIOTONICS
CARDIOVASCULAR AGENTS
CARDIOVASCULAR SYSTEM
DAYS LIVING RADIOISOTOPES
DRUGS
EVEN-ODD NUCLEI
HEART
HORMONES
INJECTION
INTAKE
INTERMEDIATE MASS NUCLEI
ISOTOPES
KINETICS
MONOCARBOXYLIC ACIDS
MUSCLES
NEUROREGULATORS
NUCLEI
ORGANIC ACIDS
ORGANIC COMPOUNDS
ORGANS
PATHOLOGICAL CHANGES
RADIOISOTOPES
REACTION KINETICS
STEROID HORMONES
SYMPATHOMIMETICS
550901* - Pathology- Tracer Techniques