The effect of maternal hypothyroidism on cardiac function and tolerance to ischemia-reperfusion injury in offspring male and female rats.

Abstract

Accumulating evidence indicates that intrauterine evolution disturbance can contribute to myocardial ischemia reperfusion (IR) injury; in addition, thyroid hormones (THs) have a crucial role in the development of different systems during fetal life. The aim of this study was to determine the effect of TH deficiency during fetal life on tolerance of isolated heart to ischemia during adulthood in both genders. Hypothyroidism was induced in pregnant Wistar rats by administrating 0.025 % 6-propyl-2-thiouracil in drinking water throughout pregnancy. Offspring of rats with maternal hypothyroidism (MH) and control groups were tested in adulthood. Isolated hearts were perfused with Langendorff setup and exposed to 30 min of ischemia, followed by 45 min of reperfusion. Baseline values of the left ventricular end-diastolic pressure (LVEDP), left ventricular developed pressure (LVDP), heart rate (HR), and peak rates of positive and negative changes in left ventricular pressure (±dp/dt) were recorded. In the MH groups the baseline levels of LVDP (male: 23 %, female: 33 %), HR (male: 31 %, female: 26 %), and ±dp/dt were significantly (p < 0.01) lower, compared to controls. After ischemia, hearts from male rats with MH had less tolerance to IR injury as assessed in terms of reductions in recovery of hemodynamic parameters compared to controls, while in female rats there were no significant differences between MH and controls. MH decreases hemodynamic parameters in the heart of both male and female offspring in adulthood; in addition, hearts of male rats with MH show less tolerance to ischemia, compared to those of females.