Assessing the impact of nutrient enrichment in estuaries: susceptibility to eutrophication.

The main aim of this study was to develop a generic tool for assessing risks and impacts of nutrient enrichment in estuaries. A simple model was developed to predict the magnitude of primary production by phytoplankton in different estuaries from nutrient input (total available nitrogen and/or phosphorus) and to determine likely trophic status. In the model, primary production is strongly influenced by water residence times and relative light regimes. The model indicates that estuaries with low and moderate light levels are the least likely to show a biological response to nutrient inputs. Estuaries with a good light regime are likely to be sensitive to nutrient enrichment, and to show similar responses, mediated only by site-specific geomorphological features. Nixon's scale was used to describe the relative trophic status of estuaries, and to set nutrient and chlorophyll thresholds for assessing trophic status. Estuaries identified as being eutrophic may not show any signs of eutrophication. Additional attributes need to be considered to assess negative impacts. Here, likely detriment to the oxygen regime was considered, but is most applicable to areas of restricted exchange. Factors which limit phytoplankton growth under high nutrient conditions (water residence times and/or light availability) may favour the growth of other primary producers, such as macrophytes, which may have a negative impact on other biological communities. The assessment tool was developed for estuaries in England and Wales, based on a simple 3-category typology determined by geomorphology and relative light levels. Nixon's scale needs to be validated for estuaries in England and Wales, once more data are available on light levels and primary production.

Modelling potential impacts of bottom trawl fisheries on soft sediment biogeochemistry in the North Sea.

Bottom trawling causes physical disturbance to sediments particularly in shelf areas. The disturbance due to trawling is most significant in deeper areas with softer sediments where levels of natural disturbance due to wave and tidal action are low. In heavily fished areas, trawls may impact the same area of seabed more than four times per year. A single pass of a beam trawl, the heaviest gear routinely used in shelf sea fisheries, can kill 5-65% of the resident fauna and mix the top few cm of sediment. We expect that sediment community function, carbon mineralisation and biogeochemical fluxes will be strongly affected by trawling activity because the physical effects of trawling are equivalent to those of an extreme bioturbator, and yet, unlike bioturbating macrofauna, trawling does not directly contribute to community metabolism. We used an existing box-model of a generalised soft sediment system to examine the effects of trawling disturbance on carbon mineralisation and chemical concentrations. We contrasted the effects of a natural scenario, where bioturbation is a function of macrobenthos biomass, with an anthropogenic impact scenario where physical disturbance results from trawling rather than the action of bioturbating macrofauna. Simulation results suggest that the effects of low levels of trawling disturbance will be similar to those of natural bioturbators but that high levels of trawling disturbance prevent the modelled system from reaching equilibrium due to large carbon fluxes between oxic and anoxic carbon compartments. The presence of macrobenthos in the natural disturbance scenario allowed sediment chemical storage and fluxes to reach equilibrium. This is because the macrobenthos are important carbon consumers in the system whose presence reduces the magnitude of available carbon fluxes. In soft sediment systems, where the level physical disturbance due to waves and tides is low, model results suggest that intensive trawling disturbance could cause large fluctuations in benthic chemical fluxes and storage.

Neurochemistry of the sympathetic innervation to the uterus.

1. The uterus is supplied by numerous noradrenergic sympathetic nerve fibres, which supply the intramural vasculature and also, in some species at least, the myometrium. 2. Pregnancy is associated with progressive loss of catecholamine from these nerves. Although some direct mechanical damage due to stretching of the uterine wall contributes to this effect, it is primarily due to hormonal influences. 3. In animal experiments, the changes in uterine catecholamine occurring during pregnancy are mimicked by intra-uterine administration of progesterone. 4. The action of progesterone appears not to be selective for pelvic sympathetic neurons, or those in which transmitter turnover rate is particularly slow. The mechanism of depletion is probably through inhibition of tyrosine hydroxylase activity. 5. The functional role of this phenomenon during pregnancy, if one exists, seems likely to be related to protection of the fetoplacental blood supply against sympathetically mediated vasospasm. It is also possible that circulating progesterone may have a general inhibitory action on the female sympathetic nervous system.

Observations on the loss of catecholamine fluorescence from intrauterine adrenergic nerves during pregnancy in the guinea-pig.

During unilateral pregnancy in the guinea-pig there is loss of formaldehyde-induced fluorescence from the adrenergic nerves supplying the uterus and its vasculature. This loss occurs initially near the site of implantation at about Day 20 of gestation and spreads progressively. Implantation of wax pellets containing progesterone into the uterine lumen or the gastrocnemius muscle of virgin guinea-pigs for 7 days produced loss of fluorescence from all local adrenergic nerves. No diminution of fluorescence was seen when pellets containing oestradiol were substituted. Chronic denervation studies showed that the adrenergic axons supplying the uterus and its arteries originated from both the ovarian artery and the pelvic region. Our results suggest that loss of adrenergic fluorescence within the uterus during pregnancy is due to an effect of placental progesterone which is localized to the uterus because the high concentration of progesterone necessary to cause fluorescence loss is not attained in the systemic circulation.