Search

Wetlands along upper estuaries are characterized by dynamic transitions between forested and herbaceous communities (marsh) as salinity, hydroperiod, and nutrients change. The importance of belowground net primary productivity (BNPP) associated with fine and coarse root growth also changes but remains the dominant component of overall productivity in these important blue carbon wetlands. Appropriate BNPP assessment techniques to use in various tidal wetlands are not well-defined, and could make a difference in BNPP estimation. We hypothesized that different BNPP techniques applied among tidal wetlands differ in estimation of BNPP and possibly also correlate differently with porewater nutrient concentrations. We compare 6-month and 12-month root ingrowth, serial soil coring techniques utilizing two different calculations, and a mass balance approach (TBCA, Total Belowground Carbon Allocation) among four tidal wetland types along each of two river systems transitioning from freshwater forest to marsh. Median values of BNPP were 266 to 2946 g/m2/year among all techniques used, with lower BNPP estimation from root ingrowth cores and TBCA (266-416 g/m2/year), and higher BNPP estimation from serial coring of standing crop root biomass (using Smalley and Max-Min calculation methods) (2336-2946 g/m2/year). Root turnover (or longevity) to a soil depth of 30 cm was 2.2/year (1.3 years), 2.7/year (1.1 years), 4.5/year (0.9 years), and 1.2/year (2.6 years), respectively, for Upper Forest, Middle Forest, Lower Forest, and Marsh. Marsh had greater root biomass and BNPP, with slower root turnover (greater root longevity) versus forested wetlands. Soil porewater concentrations of NH3 and reactive phosphorus stimulated BNPP in the marsh when assessed with short-deployment BNPP techniques, indicating that pulses of mineralized nutrients may stimulate BNPP to facilitate marsh replacement of forested wetlands. Overall, ingrowth techniques appeared to represent forested wetland BNPP adequately, while serial coring may be necessary to represent herbaceous plant BNPP from rhizomes as marshes replace forested wetlands., Competing Interests: The authors have declared that no competing interests exist.

Chronic kidney disease (CKD) affects over 15 % of the adults in the United States. Pregnant women with CKD present an additional challenge in that they are at increased risk for adverse events such as preterm birth. Exposure to environmental toxicants, such as methylmercury, may exacerbate maternal disease and increase the risk of adverse fetal outcomes. We hypothesized that fetuses of mothers with CKD are more susceptible to accumulation of methylmercury than fetuses of healthy mothers. The current data show that when mothers are in a state of renal insufficiency, uptake of mercury in fetal kidneys is enhanced significantly. Accumulation of Hg in fetal kidneys may be related to the flow of amniotic fluid, maternal handling of Hg, and/or underdeveloped mechanisms for cellular export and urinary excretion. The results of this study indicate that renal insufficiency in mothers leads to significant alterations in the way toxicants such as mercury are handled by maternal and fetal organs., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Global management of wetlands to suppress greenhouse gas (GHG) emissions, facilitate carbon (C) sequestration, and reduce atmospheric CO2 concentrations while simultaneously promoting agricultural gains is paramount. However, studies that relate variability in CO2 and CH4 emissions at large spatial scales are limited. We investigated three-year emissions of soil CO2 and CH4 from the primary wetland types of the Liaohe Delta, China, by focusing on a total wetland area of 3287 km2. One percent is Suaeda salsa, 24% is Phragmites australis, and 75% is rice. While S. salsa wetlands are under somewhat natural tidal influence, P. australis and rice are managed hydrologically for paper and food, respectively. Total C emissions from CO2 and CH4 from these wetland soils were 2.9 Tg C/year, ranging from 2.5 to 3.3 Tg C/year depending on the year assessed. Primary emissions were from CO2 (~98%). Photosynthetic uptake of CO2 would mitigate most of the soil CO2 emissions, but CH4 emissions would persist. Overall, CH4 fluxes were high when soil temperatures were >18°C and pore water salinity <18 PSU. CH4 emissions from rice habitat alone in the Liaohe Delta represent 0.2% of CH4 carbon emissions globally from rice. With such a large area and interannual sensitivity in soil GHG fluxes, management practices in the Delta and similar wetlands around the world have the potential not only to influence local C budgeting, but also to influence global biogeochemical cycling.

We determined the interactive effects of nutrient loading and salinity pulsing on Vallisneria americana Michx., the dominant submerged aquatic vegetation species in the lower St Johns River (LSJR), FL, USA, and its associated algal community. Five hundred and ninety 6-inch diameter intact plant plugs of Vallisneria were collected from the LSJR in March 2003 and transported to US Geological Survey mesocosm facilities in Lafayette, LA, USA. A 3×3 experimental design consisting of three nutrient levels (control, 1/3 control and 3× control) and three salinity pulsing regimes (no pulse, 1-pulse at 18 ppt and 2-pulse at 12 and 18 ppt) was implemented with three replicates per treatment for a total of 27 experimental tanks. Salinity pulsing significantly reduced all measured Vallisneria growth parameters including above- and below-ground biomass, areal productivity and leaf area index. Nutrient levels had little effect on plants subjected to salinity pulses, but in non-salinity pulse treatments we observed higher mean macrophyte biomass in the low-nutrient loading treatments. Macroalgal components (epiphytes and surface algal mats) were not significantly different ( p=0.2998 and p=0.2444, respectively), but water column chlorophyll a (phytoplankton) was significantly higher ( p<0.0001) in all salinity pulse treatments except for the 1-pulse, low-nutrient treatment. A single salinity pulse at 18 ppt resulted in 22% pot mortality and two consecutive pulses of 18 and 12 ppt resulted in an additional 14% mortality. Individual leaves and ramets lost 59.7% and 67.8%, respectively, in the combined salinity pulse treatments. Nutrient loading tends to have a long-term effect on Vallisneria through complex community interactions while salinity pulsing frequency and intensity has an immediate and direct influence on growth and distribution.

To investigate brain water content and ultrastructure in a rat caecal ligation and puncture (CLP) model of sepsis, adult male Wistar rats were assigned to one of the following experimental groups: CLP, Un-operated or Sham. CLP was performed under anaesthesia, Sham rats were exposed to anaesthesia, laparotomy and caecal mobilisation and Un-operated rats did not experience anaesthesia or surgery. CLP and Sham rats were sacrificed 18-20 h following recovery from surgery and Un-operated rats were sacrificed at the same time. Frontal cortex samples (CLP n = 9; Un-operated n = 10; Sham n = 8) were taken immediately post mortem and their water content determined using gravimetry. Similar samples were taken from other rats (CLP n = 8; Un-operated n = 8; Sham n = 8), processed for electron microscopy and subjected to morphometric analysis. There was significantly more brain water in CLP than Un-operated (P < 0.01) and Sham (P < 0.05) rats. Electron microscopy revealed significantly more peri-microvessel oedema in CLP than Un-operated (P < 0.001) and Sham rats (P < 0.05). Microvessel endothelial cell lumen cross-sectional area was significantly smaller in CLP than Un-operated (P < 0.001) and Sham (P < 0.05) rats and microvessel endothelial cell cross-sectional area was significantly smaller in CLP than Un-operated (P < 0.05) rats. Significantly more endothelial cell cytoplasmic area was occupied by mitochondria in CLP than Un-operated (P < 0.05) and Sham (P < 0.05) rats. However, experimental group did not affect the number of mitochondria present in endothelial cell profiles, or their cross-sectional area. Therefore, sepsis-induced cerebral oedema involves an increase in and a redistribution of brain water, together with ultrastructural changes to cerebral microvessels and adjacent tissue.

Vascular interstitial cells (VICs) are non-contractile cells with filopodia previously described in healthy blood vessels of rodents and their function remains unknown. The objective of this study was to identify VICs in human arteries and to ascertain their role. VICs were identified in the wall of human gastro-omental arteries using transmission electron microscopy. Isolated VICs showed ability to form new and elongate existing filopodia and actively change body shape. Most importantly sprouting VICs were also observed in cell dispersal. RT-PCR performed on separately collected contractile vascular smooth muscle cells (VSMCs) and VICs showed that both cell types expressed the gene for smooth muscle myosin heavy chain (SM-MHC). Immunofluorescent labelling showed that both VSMCs and VICs had similar fluorescence for SM-MHC and αSM-actin, VICs, however, had significantly lower fluorescence for smoothelin, myosin light chain kinase, h-calponin and SM22α. It was also found that VICs do not have cytoskeleton as rigid as in contractile VSMCs. VICs express number of VSMC-specific proteins and display features of phenotypically modulated VSMCs with increased migratory abilities. VICs, therefore represent resident phenotypically modulated VSMCs that are present in human arteries under normal physiological conditions., (© 2012 The Authors Journal of Cellular and Molecular Medicine © 2012 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd.)

Background & Aims: Liver failure is associated with progressive cytotoxic brain oedema (astrocyte swelling), which underlies hepatic encephalopathy (HE). Ammonia and superimposed inflammation are key synergistic factors in HE, but the mechanism(s) involved remain unknown. We aimed to determine whether aquaporin-4 (AQP4), an astrocyte endfeet bi-directional water channel, is associated with the brain oedema of HE., Method: Rats (n=60) received sham-operation (sham), 5 days hyperammonaemia-inducing diet (HD), galactosamine (GALN) induced acute liver failure (ALF), 4 weeks bile duct-ligation (BDL) induced cirrhosis, or caecal ligation and puncture (CLP), a 24h model of bacterial peritonitis. Rats from every group (except CLP) were randomised to receive intraperitoneal injections of lipopolysaccharide (LPS; 1mg/kg) or saline, prior to termination 3h later. Brain water, AQP4 protein expression (western blot) and AQP4 localisation by immunogold electron microscopy were investigated., Results: Significant hyperammonaemia was observed in saline-injected BDL (p<0.05), GALN (p<0.01), and HD (p<0.01), compared to sham rats. LPS injection did not affect arterial ammonia or plasma biochemistry in any of the treatment groups. Increased brain water was observed in saline-injected GALN (p<0.05), HD (p<0.01), and CLP (p<0.001) compared to sham rats. Brain water was numerically increased in BDL rats, but this failed to reach significance (p=0.09). LPS treatment further increased oedema significantly in all treatment groups (p<0.05, respectively). AQP4 expression was significantly increased in saline-injected BDL (p<0.05), but not other treatment groups, compared to sham rats. Membrane polarisation was maintained in BDL rats., Conclusion: The results suggest that AQP4 is not directly associated with the development of brain oedema in liver failure, hyperammonaemia, or sepsis. In cirrhosis, there is increased AQP4 protein expression, but membrane polarisation, is maintained, possibly in a compensatory attempt to limit severe brain oedema., (Copyright 2010. Published by Elsevier B.V.)

Accelerated eutrophication is common to many freshwater and marine environments and often co-occurs with the presence of anthropogenic chemicals. However, the toxic effects of common chemical stressors such as herbicides in the presence of elevated nutrients are not well understood for most aquatic flora, particularly vascular species. To provide insight, field-collected Vallisneria americana Michx. (wild celery) were sequentially exposed to three nutrient concentrations for 3 months and then to nominal 11 and 110 microg L(-1) atrazine for 96 h. Nutrient concentrations (combined NH(4)(+), NO(2)(-), NO(3)(-), PO(4)(-)) were based on ambient concentrations in the St. Johns River (FL) and ranged from 0.013 to 0.668 mg L(-1). Nutrient pretreatment potentiated the toxicity of atrazine as determined by chlorophyll fluorescence activity. Electron transport rates (ETR) were significantly less (48-59%) for plants pretreated with low and ambient nutrient levels in the presence of an average of 107.5-128.1 microg L(-1) atrazine. Significant ETR reductions were also observed for plants exposed to an average of 11.4 microg L(-1) atrazine after exposure to nutrients three times the ambient concentration in the St. Johns River. The results indicate the importance of considering the presence of nutrients in chemical hazard assessments, particularly for phytotoxicants and nontarget vascular plants.

It is now established that non-contractile cells with thin filopodia, also called vascular interstitial cells (VICs), are constitutively present in the media of many, if not all, blood vessels. The aim of this study was to determine the type of cell lineage to which arterial VICs belong using immunocytochemical, and real-time and reverse transcription PCR (RT-PCR). Using RT-PCR, we compared gene expression profiles of single VICs and smooth muscle cells (SMCs) freshly dispersed from rat middle cerebral artery. Both VICs and SMCs expressed the SMC marker, smooth muscle myosin heavy chain (SM-MHC), but did not express fibroblast, pericyte, neuronal, mast cell, endothelial or stem cell markers. Freshly isolated VICs also did not express c-kit, which is the marker for interstitial cells of Cajal in the gastrointestinal tract. Immunocytochemical labelling of contractile proteins showed that VICs and SMCs expressed SM-MHC similarly to the same degree, but VICs in contrast to SMCs had decreased expression of alpha-SM-actin and very low or no expression of calponin. Real-time RT-PCR was consistent with immunocytochemical experiments and showed that VICs had four times lower gene expression of calponin comparing to SMCs, which may explain VICs' inability to contract. VICs had greater expression than SMCs of structural proteins such as non-muscular beta-actin and desmin. The results obtained suggest that VICs represent a subtype of SMCs and may originate from the same precursor as SMCs, but later develop filopodia and a non-contractile cell phenotype.

Sepsis is a major clinical challenge that is associated with encephalopathy and multi-organ dysfunction. Current therapeutic interventions are relatively ineffective and the development of novel treatments is hampered by the lack of a well-characterised animal model. Therefore, the behavioural, metabolic, physiological and histological changes resulting from 'through and through' caecal ligation and puncture (CLP) in the rat were investigated to determine its suitability as an animal model of human sepsis. CLP resulted in bacteraemia, characterised by the presence of multiple enteric species within 18-20 h. Locomotor activity was reduced within 4 h of CLP and this reduction increased with time. Pyrexia was evident 4-5 h after CLP and was followed by hypothermia beginning 17 h after intervention. CLP resulted in reduced white blood cell and platelet counts and an increased neutrophil: lymphocyte ratio within 18-20 h. It also resulted in decreased blood glucose, but not lactate levels. CLP caused histopathological changes in the cerebral cortex, liver, lungs and vascular system indicative of multi-organ dysfunction. Therefore, CLP in the rat mimics the cardinal clinical features of human sepsis and the subsequent development of multi-organ dysfunction. It appears to be the best available animal model currently available, in which to investigate the underlying pathophysiology of sepsis and identify therapeutic targets.

This work aimed to establish the lineage of cells similar to the interstitial cells of Cajal (ICC), the arterial ICC-like (AIL) cells, which have recently been described in resistance arteries, and to study their location in the artery wall. Segments of guinea-pig mesenteric arteries and single AIL cells freshly isolated from them were used. Confocal imaging of immunostained cells or segments and electron microscopy of artery segments were used to test for the presence and cellular localization of selected markers, and to localize AIL cells in intact artery segments. AIL cells were negative for PGP9.5, a neural marker, and for von Willebrand factor (vWF), an endothelial cell marker. They were positive for smooth muscle alpha-actin and smooth muscle myosin heavy chain (SM-MHC), but expressed only a small amount of smoothelin, a marker of contractile smooth muscle cells (SMC), and of myosin light chain kinase (MLCK), a critical enzyme in the regulation of smooth muscle contraction. Cell isolation in the presence of latrunculin B, an actin polymerization inhibitor, did not cause the disappearance of AIL cells from cell suspension. The fluorescence of basal lamina protein collagen IV was comparable between the AIL cells and the vascular SMCs and the fluorescence of laminin was higher in AIL cells compared to vascular SMCs. Moreover, cells with thin processes were found in the tunica media of small resistance arteries using transmission electron microscopy. The results suggest that AIL cells are immature or phenotypically modulated vascular SMCs constitutively present in resistance arteries.

Interstitial cells of Cajal (ICCs) were identified in the intact fixed media of the rabbit portal vein (RPV) using c-kit staining. The following experiments were performed using single cell preparations of the enzyme-dispersed vessel. Surviving contacts between the processes of single ICCs and the bodies of smooth muscle cells (SMCs) were observed in electron micrographs and by confocal microscopy. Spontaneous rhythmical [Ca2+]i oscillations were observed in ICCs after loading with the calcium indicator fluo-3 and were associated with depolarizations of the ICCs recorded by tight-seal patch pipette. To investigate signal transmission from ICCs to SMCs in dispersed cell pairs, or within small surviving fragments of the ICC network, an ICC was stimulated under voltage-clamp, while changes in [Ca2+]i in the stimulated cell as well as in a closely adjacent SMC or ICCs were monitored using fast x-y confocal imaging of fluo-3 fluorescence. After stimulation of single voltage-clamped ICC by a depolarizing step similar in duration to depolarizations associated with spontaneous [Ca2+]i oscillations, a depolarization and transient elevation of [Ca2+]i was observed in a closely adjacent SMCs after a delay of up to 4 seconds. In contrast, signal transmission from ICC to ICC was much faster, the delay being less than 200 ms. These results suggest that the an ICC may, in addition to generating an electrical signal (such as a slow wave) and thereby acting as a pacemaker for vascular SMCs of RPV, also release some unknown diffusible substance, which depolarizes the SMCs.

Objective: To investigate the effects of adrenergic agents on the cerebral response to sepsis., Design: Prospective, randomized, controlled, experimental animal study., Setting: Medical school research laboratories., Subjects: Twenty-eight middle white pigs (25-30 kg)., Interventions: Pigs were anesthetized, mechanically ventilated, and randomly assigned to one of the following groups: cecal peritonitis (n = 5), cecal peritonitis with dopexamine (n = 5), cecal peritonitis with dopexamine and the beta2-adrenergic receptor antagonist ICI 118,551 (n = 4), cecal peritonitis with methoxamine (n = 5), cecal peritonitis with dopexamine and methoxamine (n = 4), and sham-operated (n = 5). Sham-operated pigs were killed after laparotomy, and pigs with cecal peritonitis were killed 8 hrs after its induction. Samples of frontal cerebral cortex were taken immediately after death, processed for light and electron microscopy, and then subjected to morphometric analysis., Measurements and Main Results: There was significantly more (p <.0005) cerebral perimicrovessel edema in pigs with cecal peritonitis (80.2 microm2 +/- 5.3 sem) than in sham-operated pigs (26.2 microm2 +/- 2.7 sem) and significantly less (p <.0005) perimicrovessel edema in dopexamine-treated pigs with cecal peritonitis (39.8 microm2 +/- 5.5 sem) than in pigs with cecal peritonitis alone (80.2 microm2 +/- 5.3 sem). There was no significant difference between the amount of perimicrovessel edema in pigs with cecal peritonitis treated with dopexamine plus ICI118,551 and pigs with cecal peritonitis alone. The mean cerebral microvessel endothelial cell cross-sectional area in methoxamine-treated pigs with cecal peritonitis (26.3 microm2 +/- 2.6 sem) was significantly greater than that in pigs with cecal peritonitis alone (16.3 microm2 +/- 2.1 sem, p =.008) or in sham-operated pigs (12.3 microm2 +/- 1.3 sem, p =.0005)., Conclusions: Dopexamine protects against cerebral edema formation in sepsis by stimulation of beta2-adrenergic receptors, whereas the alpha1 adrenoceptor agonist methoxamine induces cerebral microvessel endothelial cell swelling.

Arterial interstitial cells of Cajal (ICC)-like cells (AIL cells) with a multipolar, irregular, elongated shape and with numerous thin (often less than 1 microm), sometimes branching, processes with lengths up to approximately 60 microm were isolated enzymatically from 1st to 7th order branches of guinea-pig mesenteric artery. Some of the processes of AIL cells were growing (average speed approximately 0.15 microm min-1) and their growth was blocked by 10 microM latrunculin B, an inhibitor of actin polymerisation. Staining with BODIPY phalloidin, a fluorescent dye selective for F-actin, showed the presence of F-actin in the processes of AIL cells. Voltage clamp of single AIL cells revealed an inward current that was four times more dense than in myocytes and was abolished by 10 microM nicardipine, and an outward current carried exclusively by potassium ions that was reduced by 1 mM 4-aminopyridine and/or 100 nM iberiotoxin but unaffected by 10 nM dendrotoxin-K. Imaging of intracellular ionised calcium with fluo-4 using a laser scanning confocal microscope showed local or global calcium transients lasting several seconds in approximately 28 % of AIL cells. When membrane current was recorded simultaneously, the calcium transients were found to correspond to long-lasting transient outward currents, which occurred at potentials positive to -40 mV. Unlike myocytes, AIL cells did not contract in response to 1 mM caffeine or 5 microM noradrenaline, although they responded with a [Ca2+]i increase. The segments of intact arteries did not stain for c-kit, a marker of ICCs. Single AIL cells stained positive for vimentin, desmin and smooth muscle myosin. The presence of ICC-like cells is demonstrated for the first time in the media of resistance arteries.

The purpose of this study was to measure the relative contributions of 4 hip and thigh muscles while performing squats at 3 depths. Ten experienced lifters performed randomized trials of squats at partial, parallel, and full depths, using 100-125% of body weight as resistance. Electromyographic (EMG) surface electrodes were placed on the vastus medialis (VMO), the vastus lateralis, (VL), the biceps femoris (BF), and the gluteus maximus (GM). EMG data were quantified by integration and expressed as a percentage of the total electrical activity of the 4 muscles. Analysis of variance (ANOVA) and Tukey post hoc tests indicated a significant difference (p < 0.001*, p = 0.056**) in the relative contribution of the GM during the concentric phases among the partial- (16.9%*), parallel- (28.0%**), and full-depth (35.4%*) squats. There were no significant differences between the relative contributions of the BF, the VMO, and the VL at different squatting depths during this phase. The results suggest that the GM, rather than the BF, the VMO, or the VL, becomes more active in concentric contraction as squat depth increases.

The tight junction protein occludin 'glues' normal, adjacent brain microvessel endothelial cells together. Malignant brain tumours cause cerebral oedema because they have leaky endothelial tight junctions, which allow plasma fluid to enter the brain from the microvessel lumen. In order to identify molecular abnormalities in tumour endothelial tight junctions, we investigated occludin expression in microvessels from adult human non-neoplastic brain tissue using immunohistochemistry and immunoblotting. The proportions of microvessels immunolabelling for occludin were >2/3 in 5/5 non-neoplastic brain tissue samples, >1/3 in 5/5 low grade (Daumas-Duport I or II) astrocytomas and <1/3 in 5/5 high grade (III or IV) astrocytomas and 6/6 metastatic adenocarcinomas. Six non-neoplastic brain tissue immunoblots gave a 55-kDa occludin band, three low-grade astrocytomas gave 55-kDa and 60-kDa bands, 13 high-grade astrocytomas gave 60-kDa or no band and four adenocarcinomas did not give an occludin band. Expression of 55-kDa occludin inversely correlated with the presence of contrast enhancement on computed tomograms (P < 0.001). Electron microscopy showed open endothelial tight junctions in 0/2 non-neoplastic human brain specimens and 2/2 high-grade astrocytomas. We suggest that loss of 55-kDa occludin expression in human brain tumours may contribute to endothelial tight junction opening. Characterizing the molecular pathology of brain endothelial tight junctions may facilitate the design of novel drugs against cerebral oedema.

Objectives: Encephalopathy is a common complication of sepsis. This review describes the different pathologic mechanisms that may be involved in its etiology., Data Sources: The studies described here were derived from the database PubMed (http:¿¿www.nlm.nih.gov) and from references identified in the bibliographies of pertinent articles and books. The citations are largely confined to English language articles between 1966 and 1998. Older publications were used if they were of historical significance., Study Selection: All investigations in which any aspect of septic encephalopathy was reported were included. This selection encompasses clinical, animal, and in vitro cell culture work., Data Extraction: The literature cited was published in peer-reviewed clinical or basic science journals or in books., Data Synthesis: Contradictions between the results of published studies are discussed., Conclusions: The most immediate and serious complication of septic encephalopathy is impaired consciousness, for which the patient may require ventilation. The etiology of septic encephalopathy involves reduced cerebral blood flow and oxygen extraction by the brain, cerebral edema, and disruption of the blood-brain barrier that may arise from the action of inflammatory mediators on the cerebrovascular endothelium, abnormal neurotransmitter composition of the reticular activating system, impaired astrocyte function, and neuronal degeneration. Currently, there is no treatment.

Encephalopathy is a common complication of sepsis. However, little is known about the morphological changes that occur in the brain during sepsis. Faecal peritonitis was induced in pigs that were killed 8 h later and frontal cortex samples were taken immediately after death. The tissue was investigated using light and electron microscopy and compared with frontal cortex samples taken from sham-operated controls. Septic pigs had 49.5% more perimicrovessel oedema than sham pigs. However, the tight junctions between cerebral microvessel endothelial cells appeared morphologically intact in both septic and sham pigs. Sepsis also resulted in neuronal injury, disruption of astrocytic end-feet and swollen, rounded erythrocytes. These morphological changes may be sufficient to underlie the clinical features seen in septic encephalopathy.

We have investigated contamination of extradural catheters during normal handling with starch powdered gloves. In the laboratory, extradural catheters were handled in sterile fields with both powdered and non-powdered gloves, simulating preparation for patient insertion. The catheters together with glove samples were then examined using a Zeiss 940 scanning electron microscope. Microscopy of samples revealed starch contamination of the catheters handled with powdered gloves, especially in the side hole areas. We conclude that extradural catheters may be contaminated easily by starch powder from surgical gloves. This powder may then be deposited into the extradural space. The effect of starch in the extradural space is not known but starch is known to cause inflammatory and granulomatous reactions in other parts of the body as well as being directly allergenic. Powder contamination of catheters may be avoided easily by the use of powder-free gloves and we feel that these should be used whenever possible.

Objective: to compare diafiltered 6% pentastarch (Pentafraction--PDP, MWn 120,000 and MWw 280,000) and native pentastarch (Pentaspan--PSP, MWn 63,000 and MWw 264,000 dalton) in a porcine model of faecal peritonitis., Design: Randomised prospective study in 12 adolescent pigs., Interventions: Prior to infection the study solution was infused to increase Qt by 25%. Thereafter adjustments in infusion rate were made (up to 1 l/h) in an attempt to maintain Qt at 25% above baseline values., Measurements and Results: Animals were sacrificed at 8 h. Tissue was excised from the right lobe of liver and from the right lung and fixed for later electron microscopy and digital morphometric analysis. Patent sinusoidal lumen was significantly greater in group PDP compared to PSP (11.3% +/- 2.3% of liver tissue versus 4.8% +/- 1.1%, p < 0.05) and this was accounted for by a significantly lower proportion of sinusoidal lumen occluded with white cells (2.1% +/- 0.6% versus 6.6% +/- 1.9%, p < 0.05). Similarly, patent capillary represented a significantly higher proportion of lung tissue for group PDP versus PSP (26.2% +/- 1.9% versus 18.5% +/- 2.7%, p < 0.05). The arithmetic mean alveolar capillary barrier thickness was significantly greater in group PSP than in group PDP (4.3 +/- 0.3 microns versus 2.5 +/- 0.3 microns, p < 0.01)., Conclusions: The molecular weight profile of Pentafraction was associated with less structural organ damage including less tissue oedema and less white cell occlusion.

Objective: To compare the effectiveness of two hydroxyethyl starch solutions of different molecular weight ranges for volume maintenance in a porcine model of fecal peritonitis., Design: Randomized prospective trial., Setting: Laboratory investigation., Subjects: Adolescent female pigs weighing approximately 30 kg., Interventions: We compared diafiltered 6% pentastarch with 6% high molecular weight hetastarch for volume maintenance in a porcine model of fecal peritonitis. The number average molecular weight of pentastarch is higher than hetastarch, although the weight average molecular weight is lower, i.e., a narrow range of medium weight molecules. The infusion rate of each agent was adjusted to maintain baseline arterial Hct for less than or equal to 7 hr after instrumentation and induction of fecal peritonitis., Main Outcome Measurements: The volume of fluid required to maintain arterial Hct was compared along with comparisons of hemodynamic and histologic responses associated with the two agents., Results: Significantly less pentastarch was required to prevent hemoconcentration than hetastarch (109 +/- 22.8 vs. 150 +/- 10.3 mL/kg; p less than .05) while hemodynamics, colloid osmotic pressure, and oxygen transport responses were similar. Capillary patency was greater (21.99 +/- 3.68 vs. 10.09 +/- 1.17%; p less than .05) and mean alveolar capillary barrier thickness was less (2.36 +/- 0.13 vs. 3.06 +/- 0.17 microns; p less than .05) with pentastarch than with hetastarch, as judged by electron microscopy., Conclusions: These data suggest that pentastarch is better retained in the circulation in capillary leak syndromes compared with hetastarch.

We studied the effects of two catecholamines with differing receptor profiles on hepatic blood flow and hepatic structure in a porcine model of faecal peritonitis. We treated animals with dopexamine (group Dp) or dobutamine (group Db) and fluid, or fluid alone as a control, to achieve a 25% increase in Qt from baseline values. After the induction of faecal peritonitis the increased Qt was maintained throughout the 8 h study period by adjustment of the fluid infusion rate. The dose of catecholamines remained constant. Hepatic blood flow was correspondingly maintained at above baseline values throughout the study. Post-mortem liver biopsy specimens were analysed from experimental animals and 5 sham animals who had not been instrumented or infected. In experimental animals there was a reduction in sinusoidal patency between sham and group Dp (76% of total sinusoid vs 51%, p less than 0.05) and group Dp and control (51% vs 33%, p less than 0.05) or groups Dp and Db (51% vs 34%, p less than 0.05) animals. This was accounted for by an increase in sinusoidal leukocytes and endothelial swelling. In addition to the changes noted above there was marked hepatocellular destruction in group Db. We conclude that maintenance of organ blood flow does not guarantee structural integrity in the sepsis syndrome and hepatocellular damage was greater in group Db than group Dp or control.

This investigation was the initial step in determining a clinical pulmonary test which could be used to evaluate workers as to their suitability to industrial respirator wear. Sixty subjects, 12 superior, 37 normal, and 11 moderately impaired with respect to lung function tests were evaluated with a battery of clinical pulmonary tests while wearing an industrial respirator. The respirator was a full-face mask (MSA-Ultravue) "demand" breathing type equipped with an inspiratory resistance of 85 mm H2O at 85 L/min air flow and an expiratory resistance of 25 mmH2O at 85 L/min air flow. Comparisons of these tests were made between the three groups of subjects both with and without a respirator. It appears that those lung tests which measure the flow characteristics of the lung especially those that are effort dependent are more susceptible to change as a result of respirator wear. Hence, the respirator affects the person with superior lung function to a greater degree than the moderately impaired person. It was suggested that the clinical test of 15 second maximum voluntary ventilations (MVV.25) may be the test of choice for determining worker capability in wearing an industrial respirator.

The surface features of atrophic rhinitis are shown and it is suggested that these explain the majority of symptoms. It seems clear that any lesion preventing the formation or maturation of large numbers of motile cilia, or the production of mucus capable of forming confluent sheets suitable for continuous propulsion, may cause atrophic rhinitis. In both familial and idiopathic forms of the disease, both abnormalities are present. It would be most interesting to know the ultrastructure of the cilia in transverse section of this condition. Transverse electron microscopic studies in Retinitis Pigmentosa, Usher's syndrome and Kartagener's syndrome now becoming known as the low cilia motility diseases show clearly the primary lesions in the micro-tubules and dynein arms of the cilia. A similar transmission electron microscopic study in atrophic rhinitis may show the fundamental cilial lesions. Surgical closure of the nasal passages has much to offer the patient with severe symptoms as the clinical features of the disease improve with the increasing normal micro-anatomical features demonstrated in this paper as a result of closure. This improvement in structure is not in all cases sufficient to fulfil the above criteria so a complete cure is improbable in the majority of cases.

This investigation determined the cardiorespiratory responses of subjects with normal lung function and exercise tolerance and compared them with subjects with moderate and severe impairment of lung function and exercise tolerance. Comparisons were made during work while wearing an industrial respirator. The respirator was a full-face mask (MSA-ultravue) "demand" breathing type equipped with an inspiratory resistance of 85 mm H2O at 85 L/min air flow and an expiratory resistance of 25 mm H2O at 85 L/min air flow. Physiologically and subjectively the response of the normal and moderately impaired subjects to respirator wear during rest, 35%, 50% and 63% of their maximal workloads were not different. However, when the moderately impaired worked at 63% of their maximum the workload was equivalent to 50% of maximum of the normal subject. Significant differences in the peak flow/pressure ratio of the severely impaired compared to the normals and moderately impaired were found. By relating work performance to the dyspnea index (VI/MBC) it was suggested that the relationship between maximal lung function and maximal work performance needs to be identified both with and without respirators. This relationship may prove suitable in predicting performance during respirator wear.