Abstract
BackgroundCold, an environmental factor, induces many reproductive diseases. It is known that endothelin (ET) is a potent vasoconstrictor, and cold stress can increase the expression of ET and its receptors. The cold stress rat model was developed to examine two parameters: (1) the effects of cold stress on ovarian and uterine morphology, function, and microvascular circulation and (2) possible mechanisms of ET and its receptors involved in cold stress-induced menstruation disorders.MethodsThe rat cold stress model was prepared with an ice water bath. The estrous cycle was observed by methylene blue and hematoxylin and eosin (H&E) staining. Serum estradiol 2 (E2), testosterone (T), progesterone (P) were detected by radioimmunoassay. Hemorheology indices were measured. The real-time blood flow of auricle and uterine surfaces was measured. Expressions of CD34 and α-SMA in ovarian and uterine tissues were detected by immunohistochemistry. ET-1 contents in serum were tested, and expressions of ET-receptor types A and B (ET-AR and ET-BR) in ovarian tissues were detected via Western blotting.ResultsCold stress extended the estrous cycle, thereby causing reproductive hormone disorder, imbalance of local endothelin/nitric oxide expression, and microcirculation disturbance. Cold-stress led to up-regulation of ET-AR expression and protein and down-regulation of ET-BR expression in rats.ConclusionsThis study suggests that the reason for cold stress-induced dysfunction in reproductive organs may be closely related to the imbalance of ET-1 and its receptor expressions, leading to microvascular circulation disorders in local tissues.
Highlights
Cold, an environmental factor, induces many reproductive diseases
Effects of cold stress on ovarian physiology and function The estrous cycle of rats is 4–5 days (96-120 h), which is split into 4 periods: pre-estrous period (Fig. 1a), primarily nuclear epithelial cells; cell estrous period (Fig. 1b); largely nuclear-free keratinocytes; late estrous period (Fig. 1c), white blood cells, keratinocytes, nuclear epithelial cells show no difference
It was found that the estrous cycle of cold-stressed rats was significantly prolonged, with the longest estrous cycle in 7 days group, shortened slightly after 2–3 weeks of cold stimulation, but still increased significantly compared with the control group (Fig. 1e)
Summary
An environmental factor, induces many reproductive diseases. It is known that endothelin (ET) is a potent vasoconstrictor, and cold stress can increase the expression of ET and its receptors. The cold stress rat model was developed to examine two parameters: (1) the effects of cold stress on ovarian and uterine morphology, function, and microvascular circulation and (2) possible mechanisms of ET and its receptors involved in cold stress-induced menstruation disorders. Cold exposure can cause an increase in germ cell apoptosis and a reduction in the reproductive capacity of. Research by Meidan et al showed that cold stress can cause uterine artery contraction, thereby resulting in the reduction of placental blood flow [14]. The pathological mechanisms of cold stress-induced reproductive organ blood circulation-induced changes remain unclear
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