Effect of chlormadinone acetate, a synthetic progesterone, on restoring impaired load compensation in chronic obstructive pulmonary disease.

Kimura, Hiroshi; Tatsumi, Kouichiro; Kuriyama, Takayuki; Sugita, Takashi; Watanabe, Shohei; Nishibayashi, Yoshitake; Honda, Yoshiyuki

doi:10.1620/tjem.149.119

Cited by 7 publications

(2 citation statements)

References 31 publications

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“…These variables notwithstanding, postpartum rats produced phrenic responses to hypoxia that were more robust relative to other treatment groups, and they displayed periods of prolonged apnea following each hypoxic challenge. An elevated P/E ratio may be sufficient to explain the exaggerated response to respiratory challenge as progesterone is a potent respiratory stimulant (Dempsey et al, 1986;Tatsumi et al, 1997) that has been used in clinical settings to treat respiratory insufficiency (Dempsey et al, 1986;Kimura et al, 1986Kimura et al, , 1988Tatsumi et al, 1997). However, sufficient circulating E2 may be needed for the respiratory stimulating effects of progesterone (Bayliss and Millhorn, 1992 1999; Balthazart and Ball, 2006;Srivastava et al, 2011;Bean et al, 2014; signaling.…”

Section: Discussionmentioning

confidence: 99%

Nongenomic Actions of 17-β Estradiol Restore Respiratory Neuroplasticity in Young Ovariectomized Female Rats

2017

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Gonadal steroids modulate CNS plasticity, including phrenic long-term facilitation (pLTF), a form of spinal respiratory neuroplasticity resulting in increased phrenic nerve motor output following exposure to acute intermittent hypoxia (aIH; three 5 min episodes, 10.5% O 2 ). Despite the importance of respiratory system neuroplasticity, and its dependence on estrogen in males, little is known about pLTF expression or mechanisms of estrogen signaling in females. Here, we tested the hypotheses that (1) pLTF expression in young, gonadally intact female rats would be expressed during estrous cycle stages in which 17␤-estradiol (E2) is naturally high (e.g., proestrus vs estrus), (2) pLTF would be absent in ovariectomized (OVX) rats and in physiological conditions in which serum progesterone, but not E2, is elevated (e.g., lactating rats, 3-10 d postpartum), and (3) acute E2 administration would be sufficient to restore pLTF in OVX rats. Recordings of phrenic nerve activity in female Sprague Dawley rats (3-4 months) revealed a direct correlation between serum E2 levels and pLTF expression in cycling female rats. pLTF was abolished with OVX, but was re-established by acute E2 replacement (3 h, intraperitoneal). To identify underlying E2 signaling mechanisms, we intrathecally applied BSA-conjugated E2 over the spinal phrenic motor nucleus and found that pLTF expression was restored within 15 min, suggesting nongenomic E2 effects at membrane estrogen receptors. These data are the first to investigate the role of ovarian E2 in young cycling females, and to identify a role for nongenomic estrogen signaling in any form of respiratory system neuroplasticity.

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Section: Discussionmentioning

confidence: 99%

Nongenomic Actions of 17-β Estradiol Restore Respiratory Neuroplasticity in Young Ovariectomized Female Rats

2017

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“…Prior reports suggest that the effects of estrogen on respiratory function likely occur in the CNS vs peripheral sites of action like the carotid chemoreceptors ( Behan et al, 2003 ; Behan and Kinkead, 2011 ). These peripheral sites are more sensitive to progesterone, another abundant female steroid hormone ( Tatsumi et al, 1985 ; Dempsey et al, 1986 ; Kimura et al, 1986 ; Kimura et al, 1988 ). The blood gas data from our neurophysiological studies indicated that rats with E2 supplementation displayed elevated blood CO 2 levels under control conditions, suggesting that E2 supplementation may have impacted CO 2 sensing or sensitivity in this experimental preparation.…”

Section: Discussionmentioning

confidence: 99%

Sex hormone supplementation improves breathing and restores respiratory neuroplasticity following C2 hemisection in rats

Barok,

Grittner,

Miller

et al. 2024

Front. Physiol.

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In addition to loss of sensory and motor function below the level of the lesion, traumatic spinal cord injury (SCI) may reduce circulating steroid hormones that are necessary for maintaining normal physiological function for extended time periods. For men, who comprise nearly 80% of new SCI cases each year, testosterone is the most abundant circulating sex steroid. SCI often results in significantly reduced testosterone production and may result in chronic low testosterone levels. Testosterone plays a role in respiratory function and the expression of respiratory neuroplasticity. When testosterone levels are low, young adult male rats are unable to express phrenic long-term facilitation (pLTF), an inducible form of respiratory neuroplasticity invoked by acute, intermittent hypoxia (AIH). However, testosterone replacement can restore this respiratory neuroplasticity. Complicating the interpretation of this finding is that testosterone may exert its influence in three possible ways: 1) directly through androgen receptor (AR) activation, 2) through conversion to dihydrotestosterone (DHT) by way of the enzyme 5α-reductase, or 3) through conversion to 17β-estradiol (E2) by way of the enzyme aromatase. DHT signals via AR activation similar to testosterone, but with higher affinity, while E2 activates local estrogen receptors. Evidence to date supports the idea that exogenous testosterone supplementation exerts its influence through estrogen receptor signaling under conditions of low circulating testosterone. Here we explored both recovery of breathing function (measured with whole body barometric plethysmography) and the expression of AIH-induced pLTF in male rats following C2-hemisection SCI. One week post injury, rats were supplemented with either E2 or DHT for 7 days. We hypothesized that E2 would enhance ventilation and reveal pLTF following AIH in SCI rats. To our surprise, though E2 did beneficially impact overall breathing recovery following C2-hemisection, both E2 supplementation and DHT restored the expression of AIH-induced pLTF 2 weeks post-SCI.

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Arterial Oxygen Saturation and Hemoglobin Mass in Postmenopausal Untrained and Trained Altitude Residents

Cristancho

Reyes²,

Serrato³

et al. 2007

High Altitude Medicine & Biology

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Because of lacking ventilatory stimulation by sex hormones in postmenopausal women (PW), one might expect a lowered arterial oxygen saturation (S(O(2))) in hypoxia and therefore a stronger erythropoietic reaction than in young women (YW). Nine untrained (UTRPW) and 11 trained (TRPW) postmenopausal altitude residents (2600 m) were compared to 16 untrained (UTRYW) and 16 trained young women (TRYW) to check this hypothesis and to study the combined response to hypoxia and training. S(O(2)) was decreased in PW (89.2% +/- 2.2 vs. 93.6 +/- 0.7% in YW, p < 0.01). Hb mass, however, was similar in UT (UTRYW: 9.2 +/- 0.9 g/kg(1), UTRPW: 8.7 +/- 1.0 g/kg). But if body fat rise with age was excluded by relation to fat-free mass, Hb mass was increased in UTRPW (+1.2 g/kg, p < 0.05) compared to UTRYW. Training caused a similar rise of Hb mass in PW and YW (0.3 g/kg per mL/kg x min(1) rise in V(O(2peak))). There was no difference in erythropoietin among the groups. Ferritin was higher in PW than YW. The results show that female hormones and fitness level have to be considered in studies on erythropoiesis at altitude. The role of erythropoietin during chronic hypoxia still has to be clarified.

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Effect of chlormadinone acetate, a synthetic progesterone, on restoring impaired load compensation in chronic obstructive pulmonary disease.

Cited by 7 publications

References 31 publications

Nongenomic Actions of 17-β Estradiol Restore Respiratory Neuroplasticity in Young Ovariectomized Female Rats

Nongenomic Actions of 17-β Estradiol Restore Respiratory Neuroplasticity in Young Ovariectomized Female Rats

Sex hormone supplementation improves breathing and restores respiratory neuroplasticity following C2 hemisection in rats

Arterial Oxygen Saturation and Hemoglobin Mass in Postmenopausal Untrained and Trained Altitude Residents

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