Early onset of parturition induced by acute alcohol exposure in C57BL/6J mice: role of uterine PGE and PGF2a

These studies were designed to determine the effect of acute alcohol treatment on gestational length and to probe for a mechanism underlying alcohol-induced early onset of parturition (EOP) in mice. Experiment 1: alcohol increases the incidence of EOP. Pregnant C57BL/6J mice were given alcohol (0, 4, 5 or 6 g kg -1 , i.g.) on Gestational Day (GD) 10, 15, 16, 17 or 18. Deliveries were monitored every 6 h from GD 18. Results indicated that 6 g kg -1 alcohol treatment on GD 17 or 18 increased the incidence of EOP. Experiment 2: prostaglandins (PGs) play roles in parturition. The purpose of Experiment 2 was to determine whether PGs mediate alcohol-induced EOP in mice. The results indicated that pretreatment on GD 17 with aspirin, a prostaglandin synthesis inhibitor, prevented alcohol-induced EOP. These data suggest that alcohol-induced EOP in mice may be mediated by PGs. Experiment 3: PGs are influenced by alcohol and are triggers of labour. Experiment3 measured uterine PGs associated with the onset of alcohol-induced EOP in mice. Alcohol increased uterine PGE and PGF2a , with PGE levels higher than control before labour, and elevated PGF2a levels correlating with labour. Changes in gestational length have important implications for pregnancy outcome, as well as for normal fetal growth and development.

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Prevention of Ethanol-induced Gastric Lesions in Rats by Wu-Bei-San

The American Journal of Chinese Medicine ◽

10.1142/s0192415x98000099 ◽

1998 ◽

Vol 26 (01) ◽

pp. 65-72 ◽

Cited By ~ 3

Author(s):

Wen-Chuan Lin

Keyword(s):

Calcium Carbonate ◽

Protective Action ◽

Prostaglandin Synthesis ◽

Simultaneous Administration ◽

Acid Neutralization ◽

Gastric Lesions ◽

Synthesis Inhibitor ◽

Experimental Conditions ◽

Prostaglandin Synthesis Inhibitor

The effects of Wu-Bei-San (WBS) and its components Wu-Tsi-Ku (WTK) and Bei-Mu (BM) on gastric lesions induced by necrotizing agents were investigated in rats. Oral administration of WBS or WTK, but not BM, dose-dependently prevented gastric lesions induced by ethanol. Moreover, the gastric protective action of WTK was potentiated by simultaneous administration of BM under the same experimental conditions. Pretreatment with indomethacin, which is a prostaglandin synthesis inhibitor and idoacetamide, which is a sulfhydryl blocker did not influence the inhibited ethanol lesion of WBS. Gastric lesions induced by acidified aspirin were prevented by both WBS and calcium carbonate, which is a major constituents of WTK. However, pretreatment with calcium carbonate did not affect the gastric lesions induced by ethanol. These results indicate protective action of WBS on the gastric mucosa through both acid neutralization and cytoprotection, although more work is needed to clarify the role of WBS in cytoprotection.

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Prostaglandins mediate skeletal muscle arteriole dilation in hyperdynamic bacteremia

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1990.259.3.h728 ◽

1990 ◽

Vol 259 (3) ◽

pp. H728-H734

Author(s):

H. G. Cryer ◽

R. N. Garrison ◽

P. D. Harris ◽

B. H. Greenwald ◽

N. L. Alsip

Keyword(s):

Skeletal Muscle ◽

Topical Application ◽

Serotonin Receptors ◽

Cremaster Muscle ◽

Synthesis Inhibitor ◽

E Coli ◽

Decerebrate Rat ◽

Prostaglandin Synthesis Inhibitor ◽

Baseline Values

Live Escherichia coli bacteremia during the high cardiac output (hyperdynamic) phase of sepsis causes constriction of large arterioles but dilation of small arterioles in skeletal muscle. This study examines the role of dilator prostaglandins, serotonin, and histamine in these differential microvascular responses in the decerebrate rat that avoids the effects of drug anesthesia. Topical application of meclofenamate, a prostaglandin synthesis inhibitor, to the cremaster muscle 60 min after induction of E. coli bacteremia enhanced the constriction of large arterioles from 20 +/- 8 to 46 +/- 9% less than baseline and blunted the dilation of small arterioles from 39 +/- 9 to 17 +/- 7% above baseline values in the cremaster microcirculation. Induction of E. coli bacteremia after pretreatment of the cremaster with meclofenamate constricted large arterioles to 40 +/- 4% less than baseline and small arterioles to 31 +/- 4% less than baseline. This indicates that prostaglandins initiate small arteriole dilation in response to E. coli, but some other dilator factor is activated by prostaglandins to maintain small arteriole dilation during E. coli bacteremia. Topical application of cyproheptadine, an antagonist of both histamine and serotonin receptors, to the cremaster muscle did not alter the E. coli-induced constriction of large arterioles or the dilation of small arterioles in the cremaster microcirculation.

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