Demir ve uterus kasılması: Demir eksikliği anemisinin miyometriyum kasılması üzerine etkisine yönelik deneysel bir inceleme

Iron-deficiency anemia (IDA) is highly prevalent in pregnancy and linked to adverse outcomes, yet its direct impact on late-gestation myometrial passive tone and spontaneous contractility has not been quantified rigorously. Prior work emphasizes stimulated or amplitude-based responses, with limited, artifact-controlled comparisons of passive uterine tone and rhythmic-phase contractile work (AUC) under IDA versus iron-replete conditions. This thesis tests whether diet-induced IDA (i) lowers baseline passive tension and (ii) markedly reduces spontaneous contractile work during the rhythmic phase in late-pregnant rat myometrium. The priori hypothesis predicted lower resting tone and smaller rhythmic-phase AUC in IDA than in controls. Pregnant Sprague–Dawley dams received control or IDA diets. Longitudinal myometrial strips were recorded isometrically in organ baths across five sequential phases; analyses focused on Baseline and Rhythmic segments. The primary endpoint was the absolute 600-s rhythmic-phase |AUC|; secondary metrics were mean tension, peak force, and frequency. Assumption-appropriate tests were used (paired t/Wilcoxon within strips; Mann–Whitney or Welch t between groups). To minimize technical noise and within-animal duplication, one best strip per dam (highest rhythmic |AUC|) was selected; the focused comparison used n=6 controls vs n=6 IDA. When all channels were pooled, numerous near-zero AUC records (especially in IDA) obscured group differences. Controls showed significant baseline-rhythmic increases in mean tension and |AUC|, consistent with robust spontaneous activity. IDA strips were largely quiescent; in a minority, very high counts of tiny twitches inflated frequency but contributed negligible work, making frequency a poor discriminator. The study demonstrates that maternal IDA profoundly depresses myometrial passive tone and spontaneous contractile work in late pregnancy. This biomechanical deficit offers a mechanistic basis for labor dysfunction associated with IDA and underscores the clinical importance of early detection and correction of iron deficiency to support effective uterine performance at term.