PubMed · 5208521
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
P Zeskov, S Cicin-Sain, V Nutrizio. 1970. [Milkmann syndrome].. https://pubmed.ncbi.nlm.nih.gov/5208521/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Recent literature reports of myocardial infarction in athletes who self-administer anabolic-androgenic steroid (AAS) and previous animal studies of the effects of AASs on the heart suggest that these drugs may be directly injurious to the myocardium. We have previously demonstrated that 100 microM testosterone cypionate (TC) inhibits all beating activity of primary neonatal rat myocardial cell cultures within 1 hr of exposure and causes significant LDH release by 4 hr of exposure, indicating a direct toxic effect of TC. The purpose of this investigation was to evaluate the effects of commonly abused AASs on primary neonatal rat myocardial cell cultures and to provide insight into early cellular changes that may lead to TC-induced toxicity. Significant LDH release was observed in 5-day-old primary myocardial cell cultures (obtained from 3-to-5-day-old Sprague-Dawley rats) exposed to 100 microM testosterone enanthate (TE), testosterone propionate (TP), and oxymetholone (O) for 4 and 24 hr and in cultures exposed to 100 microM testosterone (T) for 24 hr. Neutral red retention and MTT formazan production were significantly decreased in cell cultures exposed to 100 microM TE, TP, and O after only 4 hr of exposure, indicating a loss of viability and mitochondrial activity. However, there was no effect on viability of cell cultures exposed for 24 hr to 100 microM of a variety of other commonly abused AASs. Phase-contrast microscopy revealed complete disruption of the monolayer in cell cultures treated with 100 microM TE, TP, and O for 4 hr. Treatment of fura-2-loaded myocardial cell cultures with 100 microM TC produced no significant changes in calcium transients or baseline calcium levels for up to 13 min of exposure. These results indicate that O, T, TC, TE, and TP produce a direct toxic effect in heart cell cultures and that early (< 13 min) changes in calcium homeostasis are unlikely to participate in the mechanism of toxicity.
The loss of force and mass in the conditioned latissimus dorsi muscle are principal reasons for the poor improvement in hemodynamic functioning attained by cardiomyoplasty. Using 24 sheep, we investigated the effect of anabolic steroids on the hemodynamic, histologic, and myophysiologic characteristics in the setting of cardiomyoplasty. In 12 of the animals (group A), the latissimus dorsi muscles were electrically conditioned with an Itrel pulse generator; in the remaining 12 animals (group B), the electrical conditioning was combined with the administration of an anabolic hormone (metenolone; 100 mg/week). The hemodynamic measurements were performed during isolated perfusion of the subclavian artery (maintenance of pressure in the muscles), while all other circulation variables were held at the exact and reproducible value of zero by inducing ventricular fibrillation. Maximum force and muscle mass showed a significant increase in group B (maximum force: group A, 4.23 +/- 0.55 kp, and group B, 6.0 +/- 3.14 kp; muscle mass: group A, +11.07% +/- 1.06%, and group B, +79.9% +/- 40.8%). The ratio of type I to type II fibers after 12 weeks was 65.2% to 34.8% in group A and 96.7% to 3.3% in group B, as opposed to 19.9% to 80.1% in the control group. No side effects of the anabolic steroids were observed during the experiment. In the hemodynamic studies, we were able to demonstrate a further significant increase in the left ventricular pressure, fractional fiber shortening value, ejection fraction, stroke volume, cardiac output, and stroke work when using conditioned latissimus dorsi muscles that were additionally treated with metenolone.(ABSTRACT TRUNCATED AT 250 WORDS)
Explore the source record for details and available documents.