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The aim of this study was to establish the effect of bacterial endotoxin lipopolysaccharide (LPS) on the release of Type II phospholipase-A2 (PLA2) and prostaglandin E2 (PGE2) from late-pregnant human placental tissue incubated in vitro. Under basal conditions, immunoreactive Type II PLA2 and PGE2 were released from tissue explants in a time-dependent manner (up to 24 h, ANOVA, P<0. 0001, n=6). The release of these mediators was not associated with a loss of cell membrane integrity, as indicated by concentrations of the intracellular enzyme, lactate dehydrogenase (LDH), in the incubation medium. Incubation of explants in the presence of LPS (0. 001-100 microg LPS/ml) significantly decreased PLA2 tissue content (P<0.02, n=6) and increased the accumulation of PLA2 and PGE2 in the incubation medium (P<0.0001, n=6). The data obtained in this study indicated that Type II PLA2 and PGE2 are released from term placenta under basal conditions and that LPS stimulated their release. The associated decrease in PLA2 tissue content is consistent with the hypothesis that LPS induces the release of stored PLA2. This study identifies one pathway by which products of bacterial infection may induce the release of a pro-inflammatory, extracellularly active PLA2 from intrauterine tissues that may promote the formation of phospholipid metabolites involved in the process of labour and delivery (e.g. the prostaglandins).
Department of Internal Medicine, United Arab Emirates University, Al Ain, United Arab Emirates
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Department of Internal Medicine, United Arab Emirates University, Al Ain, United Arab Emirates
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Department of Internal Medicine, United Arab Emirates University, Al Ain, United Arab Emirates
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Department of Internal Medicine, United Arab Emirates University, Al Ain, United Arab Emirates
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The sympathetic nervous system and adrenomedullin (AM) both participate in the regulation of cardiac and circulatory function but their interaction remains uncertain. We have examined the effects of AM on cardiac sympathetic nerve activity (CSNA) and hemodynamics and contrasted these effects with pressure-matched nitro-prusside (NP) administration in normal conscious sheep. Compared with vehicle control, arterial pressure fell similarly with AM (P=0.04) and NP (P<0.001). Heart rate rose in response to both AM (P<0.001) and NP (P=0.002) but the rise with AM was significantly greater than that induced by NP (P<0.001). Cardiac output increased in response to AM compared with both control and NP (both P<0.001). CSNA burst frequency (bursts/min) were increased in response to both AM (P<0.001) and NP (P=0.005) with the rise in burst frequency being greater with AM compared with NP (P<0.001). CSNA burst area/min was also raised by both AM (P=0.03) and NP (P=0.002) with a trend for burst area being greater with AM than NP (P=0.07). CSNA burst incidence (bursts/100 beats) showed no significant differences between any treatment day. In conclusion, we have demonstrated that AM is associated with a greater increase in CSNA and heart rate for a given change in arterial pressure than seen with the classic balanced vasodilator NP.
