Cardioprotective mechanism in females during reproductive phase is unclear. New perspective explains cardioprotective function of progesterone. Progesterone, the intermediary metabolic product in synthesis of steroid hormones, with t/2 of 30 min, stimulates respiratory center inducing respiratory alkalosis in turn lowers plasma ionic calcium. This results in decreased blood coagulability and cardiac contractility along with smooth muscle relaxation. Vascular smooth muscle relaxation, leading to generalized vasodilatation causes better tissue perfusion resulting in diminished erythropoietin, and erythrocyte count. This reduces blood viscosity and afterload on the heart. Cardiac contractility remains balanced due to opposing influences of decreased plasma ionic calcium and raised basal body temperature. On sudden withdrawal of progesterone, as during premenstrual, postpartum and postmenopausal periods, cardioprotective changes are reversed. The awareness helps to build better body buffer system, aiming to correct acid-base imbalance, during expected fluctuations of progesterone.

No abstract

Normal parturition concludes with safe delivery of viable conceptus by forceful emptying of uterus in humans. With already well accepted experimental and clinical observations, new perspective tries to explain it by calcium ions [Ca2+] lowering action of Progesterone [PR] and Negative feedback regulation of Oestrogen[OE] on Human chorionic gonadotropin[HCG] as follows. Respiratory centre stimulatory effect of PR causes respiratory alkalosis and consequentially converts biologically active plasma free Ca2+ to its’ inactive protein bound store. Thus PR induced low plasma Ca2 maintains pregnancy by supressing myometrial and neural excitability. At term normal fetal organogenesis coordinated with feto-placental steroidogenesis, cause OE negative feedback on HCG, inhibiting both OE and PR synthesis. Due to shorter biological half-life [t/2 = 30min], PR dip is first observed. So the sudden PR withdrawal at term causing acute respiratory acidosis with spark release of plasma Ca2+, facilitates neuro- myometrial excitability triggering parturition. During each myometrial contraction, sandwiched PR gets squeezed from placental store into maternal circulation again resulting in myometrial relaxation. Thus myometrial alternate cyclical repetition of contraction and relaxation [labour pains] continues till completion of parturition. Awareness of importance of gradual intermittent release of placental PR and spark plasma Ca2+ helps clinicians in prevention of feto-maternal mortality and morbidity including puerperal psychosis associated with clinical conditions of sudden PR withdrawal as in caesarean section, precipitous labour, premature labour, preeclamsia etc. which can be treated by building better body blood buffers.