Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022104 (irritable bowel syndrome)
 8,033 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Estradiol has been considered as an L-type calcium channel blocker in animal studies. The concentration of estradiol decreases after menopause. Therefore, we hypothesized that human myocardial functional changes developed after menopause, and those changes could be evaluated through the use of cyclic variation of integrated backscatter (CVIBS). A total of 16 patients with menopause (native and surgical menopause), follicular stimulating hormone > 40 IU/L and estradiol < 20 pg/mL underwent dobutamine stress IBS examination (study group). Another 12 women with normal menstruation, follicular stimulating hormone < 40 IU/L and estradiol > 20 pg/mL were enrolled as a control group. All patients had a low likelihood of coronary artery disease and negative results of dobutamine stress echocardiography and (201)thallium scintigraphy. To avoid the phenomenon of anisotropy, the amplitude and phase of IBS were acquired only in the midanteroseptal segment from the parasternal short axis view. The baseline amplitudes of CVIBS differed between the control and study groups (5.9 +/- 1.2 dB vs. 8.1 +/- 2.1 dB; p = 0.007). The amplitudes during low-dose (20 microg/kg-min) and peak-dose (40 microg/kg-min) dobutamine infusion were also different between these 2 groups (5.7 +/- 0.9 dB vs. 8.4 +/- 1.7 dB; p < 0.001; 6.0 +/- 1.0 dB vs. 7.7 +/- 2.4 dB; p = 0.026). However, there were no significant differences in amplitudes between these two groups after atropine injection (control group 4.5 +/- 1.2 dB, study group 5.3 +/- 1.0 dB; p = NS). No significant differences of phase were found either at baseline or under dobutamine infusion between the two groups. Multivariate linear regression analysis showed that only menopause status associated significantly with the amplitudes at different doses of dobutamine infusion (p < 0.05). In conclusion, human myocardial functional changes are observed by CVIBS after menopause. Postmenopausal women have higher values of amplitude than premenopausal women. These phenomena persist during low and peak doses of dobutamine infusion, but are abolished by atropine injection.
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PMID:Assessment of menopause-induced myocardial changes by integrated backscatter during inotropic stimulation and atropine injection. 1220 31

Pain symptoms in several chronic pain disorders in women, including irritable bowel syndrome, fluctuate with the menstrual cycle suggesting a gonadal hormone component. In female rats, estrogens modulate visceral sensitivity although the underlying mechanism(s) are unknown. In the present study the effects of 17-beta estradiol on N-methyl-D-aspartate (NMDA) receptor signaling of colorectal nociceptive processing in the spinal cord were examined. Estrogen receptor alpha and the NR1 subunit of the NMDA receptor are co-expressed in dorsal horn neurons, supporting a direct action of estradiol on NMDA receptors. Intrathecal administration of the NMDA receptor antagonist D(-)-2-amino-5-phosphonopentanoic acid (APV) dose-dependently attenuated the visceromotor response with greater potency in ovariectomized (OVx) rats compared to OVx with estradiol replacement (E2) rats. Estradiol significantly increased protein expression of NR1 in the lumbosacral spinal cord compared to OVx rats. Colorectal distention significantly increased phosphorylation of NR1ser-897, a PKA phosphorylation site on the NR1 subunit in E2, but not OVx rats. Intrathecal administration of a PKA inhibitor significantly attenuated the visceromotor response, decreased NR1 phosphorylation and increased the potency of APV to attenuate the visceromotor response compared to vehicle-treated E2 rats. These data suggest that estradiol increases spinal processing of visceral nociception by increasing NMDA receptor NR1 subunit expression and increasing site-specific receptor phosphorylation on the NR1 subunit contributing to an increase in NMDA receptor activity.
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PMID:Estrogen alters spinal NMDA receptor activity via a PKA signaling pathway in a visceral pain model in the rat. 1806 1