Metabolic syndrome is a clustering of several cardiovascular risk factors including obesity, hypertension, diabetes, high triglyceride etc. Obesity has been shown to decreases key markers of uterine contractility during parturition in the rat and diabetes is associated with impairment of uterine contractility and high caesarean section rate. In this study, the effect of metabolic syndrome on gravid uterine muscle contractility in sprague-dawley rat was determined.
Female sprague-dawley rats were fed control (CON, n=10) and Metabolic Syndrome were fed high salt and high-fat, high-cholesterol (HFHC) diet for 8 weeks and given 60 mg/kg streptozotocin i.P. to induce diabetes (METS, n=10). Animals were mated and, once pregnant, maintained on their diet throughout the experiment. On gestational day 15, rats were killed and a small portion of the uterine muscle was excised and transferred into an organ bath containing physiological salt solution for contractility studies. The organ bath was connected to a force transducer (Grass Model FT03) connected to the ADInstrument Power lab; the tension was adjusted. The transducer was pre-calibrated to give a 2 cm deflection for every 1 gram force. Spontaneous contractions were measured for various graded doses of oxytocin, acetylcholine and potassium chloride and the tension/force and duration of contraction calculated and recorded. Blood was collected for determination of plasma insulin, lipid profile, maternal corticotrophin releasing hormone (CRH), blood glucose, serum calcium and placenta CRH, were also determined. Body and fat depot weights were recorded.
Force and duration of contraction caused by oxytocin was significantly reduced (P<0.05) in MTES rats compared with the control. Acetylcholine and potassium chloride also produced a significantly reduced (P<0.05) force and duration of contraction in METS. Serum calcium, maternal CRH, insulin, blood glucose, triglyceride cholesterol, abdominal and retroperitoneal fats were all significantly increased (P<0.05).
In conclusion, METS impair uterine contractility by reducing the force and duration of uterine contraction.