15 research outputs found

    Apoptotic cell death in the porcine endometrium during the oestrous cycle

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    It has been reported that apoptosis plays an essential role in controlling the physiological cell kinetics in the human and rodent endometrium but this type of death has never been studied in the porcine endometrium. The aim of this study was to investigate the apoptotic cell death in the porcine endometrium during the middle (Days 9–11) and late (Day 13) luteal phase, during the luteolysis (Day 15) and early follicular phase (Days 17–19) of the oestrous cycle. Apoptotic cells were identified by in situ DNA 3â€Č-end labelling method. it was revealed that the greatest number of apoptotic cells in the luminal and glandular epithelium was found on Days 17–19 and on Day 15 of the oestrous cycle, respectively. in the stroma, the greatest number of these cells was found on Days 9–11. Our data have shown that in the porcine endometrium, both epithelial and stromal cells undergo apoptosis and that the number of apoptotic cells varies depending on the phase of the oestrous cycle

    Luteinising hormone attenuates the vascular response to norepinephrine

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    The present study examines the direct effect of luteinising hormone (LH) on the reactivity of the porcine uterine artery to norepinephrine (NE). Three-mm-long arterial segments collected during the luteal phase of the oestrous cycle were mounted in an organ bath for isometric tension recording. After 30 min of equilibration in optimal passive tone, one part of the vessels was treated with 10 ng/ml of LH in PBS (experimental), while a second part of the arterial segments was treated with 10 ng/ml of bovine serum albumin (BSA) in PBS (control). After 30 min of equilibration, NE was given to each organ bath in a cumulative concentration manner, ranging between 1 × 10−8 mol/l to 3 × 10−4mol/l. NE caused a dose-dependent contraction of all experimental and control arteries. The addition of LH caused a rightward shift of the dose-response curve to NE. The corresponding EC50 values were 2.17 (± 0.39) ÎŒmol/l in PBS-pretreated vessels and 3.35 (± 0.41) ÎŒmol/l in LH-pretreated vessels (P < 0.05). The results of the present study demonstrate that LH attenuates the vascular response to NE in third-order branches of the uterine artery. Therefore, it can be suggested that besides the known effect of LH-hCG on the formation of vasoactive eicosanoids, an additional mechanism is involved in the direct action of LH on blood flow in the uterine arteries in pigs
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