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The relatively complex pattern of temperature selection exhibited by juvenile lemon sharks Negaprion brevirostris in the North Sound differed markedly from many previously described responses of fish preferenda. Thermal data demonstrated that juvenile N. brevirostris did not attempt to behaviourally maintain a constant eccritic temperature. Rather, juveniles selected progressively warmer temperatures throughout the day until reaching the highest temperatures available, and then moved to cooler temperatures during late evening and early morning hours. It is possible that by exploiting habitat thermal heterogeneity juvenile N. brevirostris prolong activities such as feeding or digestion well into the cooler parts of the evening. The complex pattern of temperature occupation by juvenile N. brevirostris within the thermally heterogeneous North Sound nursery is probably linked to key daily activities such as prey capture, predator avoidance and digestive efficiency.

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The effects of post-feeding thermotaxis on ileum evacuation and absorption rates were examined in the laboratory using two elasmobranch species, the Atlantic stingray Dasyatis sabina, which inhabits thermally variable environments, and the whitespotted bamboo shark Chiloscyllium plagiosum, a stenothermic fish living on Indo-Pacific reefs. Experiments at temperatures similar to those experienced in nature revealed temperature change had no significant effect on C. plagiosum absorption or evacuation rates, suggesting stenothermic sharks cannot exploit temperature differences as a means to improve digestion efficiency. On the other hand, D. sabina showed significantly lower evacuation and absorption rates at lower temperatures. The relative decrease was greater for evacuation (Q10 = 3·08) than absorption rates (Q10 = 2·20), resulting in a significant increase in total absorption, suggesting D. sabina can benefit from using shuttling behaviour to exploit thermal variability in their environment to maximize energetic uptake.

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This study quantified physiological responses of skilletfish Gobiesox strumosus exposed to thermal and oxic stress. Fish acclimated at 12, 22 and 32 degrees C had low oxygen tolerance values (mean +/-s.d.) of 0.40 +/- 0.09, 0.40 +/- 0.08 and 0.35 +/- 0.03, and critical thermal maxima (mean +/-s.d.) of 33.2 +/- 0.5, 38.1 +/- 0.0 and 39.5 +/- 0.3 degrees C, respectively. Furthermore, G. strumosus were oxygen conformers at all acclimation temperatures, i.e. the fish allowed oxygen consumption rates to decrease with ambient oxygen concentration. High temperature tolerance, low oxygen tolerance and decreasing metabolic rates during hypoxic events allow the fish to survive harsh environmental conditions encountered in their natural environment.

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Intrauterine infection during pregnancy is associated with early activation of the fetal immune system and poor neurodevelopmental outcomes. Immune activation can lead to alterations in sensorimotor skills, changes in learning and memory and neural plasticity. Both interleukin-10 (IL-10) and Ceftriaxone have been shown to decrease immune system activation and increase memory capacity, respectively. Using a rodent model of intrauterine infection, we examined sensorimotor development in pups, learning and memory, via the Morris water maze, and long-term potentiation in adult rats. Pregnant rats at gestational day 17 were inoculated with 1 x 10(5) colony forming units of Escherichia coli (E. coli) or saline. Animals in the treatment group received IL-10/Ceftriaxone for 3 days following E. coli administration. Intrauterine infection delayed surface righting, negative geotaxis, startle response and eye opening. Treatment with IL-10/Ceftriaxone reduced the delay in these tests. Intrauterine infection impaired performance in the probe trial in the Morris water maze (saline 25.13+/-1.01; E. coli 20.75+/-1.01; E. coli+IL-10/Ceftriaxone 20.2+/-1.62) and reduced the induction of long-term potentiation (saline 141.5+/-4.3; E. coli 128.7+/-3.9; E. coli+IL-10/Ceftriaxone 140.0+/-10). In summary, the results of this study indicate that E. coli induced intrauterine infection delays sensorimotor and learning and memory, while IL-10/Ceftriaxone rescues some of these behaviors. These delays were also accompanied by an increase in interleukin-1beta levels, which indicates immune activation. IL-10/Ceftriaxone prevents these delays as well as decreases E. coli-induced interleukin-1beta activation and may offer a window of time in which suitable treatment could be administered.

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OBJECTIVE: We tested the hypothesis that the inadequately perfused placenta increases production of leptin, which can be detected in maternal serum. STUDY DESIGN: Sprague-Dawley rats (n=13), on day 14 of gestation, had placement of clips on the aorta and the ovarian arteries providing 35 per cent occlusion of the vessels. Eight rats had sham surgery and 14 rats served as non-surgical controls. All animals were sacrificed on day 19 of gestation. Maternal serum was obtained, and pups and placentae were weighed. RESULTS: Both placental weights and pup weights were reduced due to reduced uterine perfusion and were negatively correlated with maternal serum leptin (P=0.018 and 0.028, respectively). Maternal serum leptin was increased in the treatment group (2.21 ng/ml+/-64 ng/ml) compared to controls (1.66 ng/ml+/-38 ng/ml) (P=0.031). CONCLUSIONS: Our findings suggest that reduced placental perfusion results in an increase in maternal serum leptin. Further investigation is needed to determine if maternal serum leptin may be useful in identifying pregnancies with uteroplacental insufficiency.

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Renal plasma flow (RPF) and glomerular filtration rate (GFR) are markedly increased during pregnancy. We recently reported that the renal hemodynamic changes observed during pregnancy in rats are associated with enhanced renal protein expression of neuronal nitric oxide synthase (nNOS). The purpose of this study was to determine the role of nNOS in mediating renal hemodynamic changes observed during pregnancy. To achieve this goal, we examined the effects of the nNOS inhibitor 7-nitroindazole (7-NI) on kidney function in normal conscious, chronically instrumented virgin (n = 6) and pregnant rats (n = 9) at day 16 of gestation. Infusion of 7-NI had no effect on RPF (4.7 +/- 0.7 vs. 4.8 +/- 0.9 ml/min), GFR (2.2 +/- 0.2 vs. 2.5 +/- 0.4 ml/min), or mean arterial pressure (MAP; 127 +/- 7 vs. 129 +/- 10 mmHg) in virgin rats. In contrast, 7-NI infused into pregnant rats decreased RPF (8.9 +/- 1.6 vs. 6.5 +/- 1.4 ml/min) and GFR (4.4 +/- 0.7 vs. 3.3 +/- 0.7 ml/min) while having no effect on MAP (123 +/- 4 vs. 123 +/- 3 mmHg). In summary, inhibition of nNOS in pregnant rats at midgestation results in significant decreases in RPF and GFR. nNOS inhibition in virgin rats had no effect on renal hemodynamics. These data suggest that nNOS may play a role in mediating the renal hemodynamic changes that occur during pregnancy.

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Studies over the past decade have provided a better understanding of the potential mechanisms responsible for the pathogenesis of preeclampsia. The initiating event in preeclampsia has been postulated to be reduced uteroplacental perfusion as a result of abnormal cytotrophoblast invasion of spiral arterioles. Placental ischemia is thought to lead to widespread activation/dysfunction of the maternal vascular endothelium that results in enhanced formation of endothelin and thromboxane, increased vascular sensitivity to angiotensin II, and decreased formation of vasodilators such as NO and prostacyclin. These endothelial abnormalities, in turn, cause hypertension by impairing renal-pressure natriuresis and increasing total peripheral resistance. The quantitative importance of the various endothelial and humoral factors in mediating the reduction in renal hemodynamic and excretory function and elevation in arterial pressure during preeclampsia are still unclear. Results from ongoing basic and clinical studies, however, should provide new and important information regarding the physiological mechanisms responsible for the elevation in arterial pressure in women with preeclampsia.

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OBJECTIVE: To determine whether intra-uterine infusion of interleukin-10 prevents preterm delivery in rats treated with endotoxin. METHODS: Pregnant rats underwent implantation of uterine catheters and were randomly assigned to receive intrauterine infusion of either normal saline, 50 microg lipopolysaccharide endotoxin, or 50 microg lipopolysaccharide with 500 ng interleukin-10 administered either concurrently or 24 hours later. The interval from infusion to delivery for each group was recorded, along with the number of live born pups and their birth weight. We calculated that to obtain a power of 80%, assuming a 24-hour difference in the treatment to delivery times between the test and control subjects, at least six animals would be needed in each group. RESULTS: In females receiving lipopolysaccharide (50 microg) alone, the interval to delivery (P <.05), live birth rate (P <.05), and pup weight (P <.001) were reduced compared with the saline-infused controls. In contrast, females receiving interleukin-10 at the time of the endotoxin challenge or 24 hours after delivered at term with no difference in litter size or live birth weight compared with the controls. CONCLUSION: Animals treated with both lipopolysaccharide and interleukin-10, administered concurrently or 24 hours after the endotoxin challenge, delivered normal weight pups at term with a similar litter size as the saline-infused controls. Interleukin-10 appears to be effective in preventing endotoxin-induced preterm birth and fetal wastage in pregnant rats.

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Pregnancy-induced hypertension (PIH) is estimated to affect 7% to 10% of all pregnancies in the United States. Despite being the leading cause of maternal death and a major contributor of maternal and perinatal morbidity, the mechanisms responsible for the pathogenesis of PIH have not yet been fully elucidated. Studies during the past decade, however, have provided a better understanding of the potential mechanisms responsible for the pathogenesis of PIH. The initiating event in PIH appears to be reduced uteroplacental perfusion as a result of abnormal cytotrophoblast invasion of spiral arterioles. Placental ischemia is thought to lead to widespread activation/dysfunction of the maternal vascular endothelium that results in enhanced formation of endothelin and thromboxane, increased vascular sensitivity to angiotensin II, and decreased formation of vasodilators such as nitric oxide and prostacyclin. The quantitative importance of the various endothelial and humoral factors in mediating the reduction in renal hemodynamic and excretory function and elevation in arterial pressure during PIH is still unclear. Investigators are also attempting to elucidate the placental factors that are responsible for mediating activation/dysfunction of the maternal vascular endothelium. Microarray analysis of genes within the ischemic placenta should provide new insights into the link between placental ischemia and hypertension. More effective strategies for the prevention of preeclampsia should be forthcoming once the underlying pathophysiologic mechanisms that are involved in PIH are completely understood.

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A reduction in nitric oxide (NO) synthesis has been suggested to play a role in pregnancy-induced hypertension. We have recently reported that normal pregnancy in the rat is associated with significant increases in whole-body NO production and renal protein expression of neuronal and inducible NO synthase. The purpose of this study was to determine whether whole-body and renal NO production is reduced in a rat model of pregnancy-induced hypertension produced by chronically reducing uterine perfusion pressure starting at day 14 of gestation. Chronic reductions in uterine perfusion pressure resulted in increases in arterial pressure of 20 to 25 mm Hg, decreases in renal plasma flow (<23%) and glomerular filtration rate (<40%), but no difference in urinary nitrite/nitrate excretion relative to control pregnant rats. In contrast, reductions in uterine perfusion pressure in virgin rats resulted in no significant effects on arterial pressure. Renal endothelial (<4%) and inducible (<11%) NO synthase protein expression did not decrease significantly in the chronically reduced uterine perfusion pressure rats relative to normal pregnant rats; however, significant reductions in neuronal NO synthase were observed (<30%). The results of this study indicate that the reduction in renal hemodynamics and the increase in arterial pressure observed in response to chronic decreases in uterine perfusion pressure in pregnant rats are associated with no change in whole-body NO production and a decrease in renal protein expression of neuronal NO synthase.

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A chronic reduction in uterine perfusion pressure in pregnant rats is associated with a significant elevation in mean arterial pressure (MAP) and reduction in kidney function. The purpose of this study was to examine the role of endothelin in mediating the hypertension in response to chronic reductions in uterine perfusion pressure in conscious, chronically instrumented, pregnant rats. MAP in pregnant rats with chronic reductions in uterine perfusion pressure (123.0+/-1.8 mm Hg) was significantly higher than that in control pregnant rats (101.3+/-4.0 mm Hg). Renal expression of preproendothelin mRNA as determined by ribonuclease protection assay was also significantly elevated in the medulla (>45%, P<0.05) and in the cortex (>22%, P:<0.05) of the pregnant rats with chronic reductions in uterine perfusion pressure compared with control pregnant rats. Chronic administration of the selective endothelin type A receptor antagonist (ABT-627, 5 mg/kg per day for 10 days) markedly attenuated the increase in MAP observed in the pregnant rats with chronic reductions in uterine perfusion pressure (103.3+/-5.6 mm Hg, plus endothelin antagonist; P<0.05). However, endothelin type A receptor blockade had no significant effect on blood pressure in the normal pregnant animals (96.0+/-2.7 mm Hg, plus endothelin antagonist). These findings suggest that endothelin plays a major role in mediating the hypertension produced by chronic reductions in uterine perfusion pressure in pregnant rats.

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OBJECTIVE: This study was designed to examine the effects of intrauterine endotoxin (lipopolysaccharide) on rat pregnancy. STUDY DESIGN: Pregnant Sprague-Dawley rats (N = 26) were implanted with uterine catheters on day 15 or 16 of a 22-day gestation. Animals were randomly assigned to receive either lipopolysaccharide (25 or 50 microg) or sodium chloride solution (1 mL) on day 17 and then were either sacrificed on day 19 or observed until delivery. Placentas were harvested at the time of death, homogenates were prepared, and prostaglandin F(2)(alpha) metabolite levels were determined by means of radioimmunoassay. Data were analyzed by analysis of variance, Student-Newman-Keuls, and Mann-Whitney tests. RESULTS: Lipopolysaccharide-treated groups (25 and 50 microg) displayed a shorter interval to delivery (mean +/- SE, 82 +/- 13 and 63 +/- 8 hours, respectively) than control animals (117 +/- 3 hours). Pups of lipopolysaccharide-treated (25 and 50 microg) female animals had lower live birth weights (4.92 +/- 0.01 and 5.12 +/- 0. 24 g, respectively) compared with control animals (6.04 +/- 0.07 g). Placental homogenates from lipopolysaccharide-treated female animals contained higher levels of prostaglandin F(2)(alpha) metabolite (1567 +/- 64 and 1475 +/- 59 pg/mL) than those from sodium chloride solution-infused control animals (804 +/- 68 pg/mL). CONCLUSION: Bacterial products induce the preterm delivery of low-birth-weight pups in rats, possibly by increasing local prostaglandin biosynthesis.

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OBJECTIVE: We sought to determine whether placental cytokine expression is altered in patients with preeclampsia. STUDY DESIGN: Whole placental tissue was collected at cesarean delivery, and total ribonucleic acid was extracted. Reverse transcriptase-polymerase chain reaction was performed to determine cytokine expression. Product bands were quantitated by scanning densitometry, and results were expressed as a ratio of cytokine/housekeeping gene (cytokine expression index). Statistical analysis was performed by the Student t test and the Mann-Whitney U test. RESULTS: Placentas from 6 patients with preeclampsia and 4 normotensive patients were analyzed. Placental expression of interleukin 1beta and interleukin 10 was greater in preeclamptic women than in normotensive subjects (median interleukin 1beta cytokine expression index, 0.675; range, 0.394-0. 953; vs 0.106; range, 0.084-0.166; P =.011; median interleukin 10 cytokine expression index, 1.042; range, 0.672-1.192; vs 0.126; range, 0.062-0.398; P <.011). Tumor necrosis factor alpha messenger ribonucleic acid was detected in placentas of preeclamptic subjects but not in normotensive control subjects. CONCLUSION: Placentas from preeclamptic patients demonstrated increased expression of interleukin 1beta, interleukin 10, and tumor necrosis factor alpha. This may be in association with placental hypoxia and may contribute to the global endothelial dysfunction observed in preeclampsia.

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PROBLEM: T-helper 2 (TH2)-type cytokines [i.e., interleukin (IL)-6, IL-10, and IL-13] and transforming growth factor (TGF)-beta are expressed by the murine decidua and/or placenta and are likely to suppress inflammatory cytokine [i.e., IL-2, interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha, IL-1 alpha, and IL-1 beta] production at the maternal-fetal interface. In addition, class I IFNs may protect the fetus from immunologic rejection and viral infections. This study examines the expression of inflammatory/immunoregulatory cytokines and IL-10 production by first-trimester chorionic villi. METHOD OF STUDY: Gestational tissues (n = 5) were obtained following elective terminations performed between 7 and 9 weeks of gestation. Chorionic villous tissues were separated from fetal membranes and decidua, and total RNA was extracted. Cytokine expression was assessed by a reverse transcriptase-polymerase chain reaction technique. Chorionic villi (n = 9; 6-12 weeks gestation) were maintained in organ culture, and human chorionic gonadotropin (hCG) and IL-10 levels were determined by immunoradiometric and enzyme-linked immunosorbent assays, respectively. RESULTS: IFN-gamma and IL-2 were generally not expressed by first-trimester chorionic villi. Low to moderate levels of expression were noted for IL-1 alpha, IL-1 beta, and TNF-alpha. High levels of mRNA were noted for IFN-alpha and IFN-beta, but IFN-tau was not expressed. In all tissues, TGF-beta 1 and IL-13 were either weakly expressed or not expressed. In contrast, moderate to high levels of IL-6 and IL-10 mRNA were detected in each chorionic villous sample. In chorionic villous explants obtained at 6-11 weeks gestation production of hCG and IL-10 was greatest during the first 24 hr ([hCG] = 6961 +/- 815 mIU/mL, [IL-10] = 92 +/- 11 pg/mL) and then declined through 72 hr. CONCLUSIONS: TH1-type cytokines (IL-2, IFN-gamma) are not expressed by first-trimester chorionic villous tissues: This is possibly due to local production of IL-10. In contrast, macrophage-associated cytokines (IL-1 beta and TNF-alpha) are expressed and their regulation may be critical for fetal survival. Finally, class 1 IFNs expressed by early chorionic tissues may protect the fetus from maternal rejection and viral transmission.

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OBJECTIVES: Prostaglandins (PGs) are essential mediators of labor during human pregnancy. Phospholipase A2 (PLA2) provides the essential substrate for PG synthesis through the liberation of arachidonic acid from membrane phospholipid stores. Nonlaboring amniotic fluid (NL-AF) contains secretory component (SC)-like protein(s) that suppress in vitro PLA2 activity. This study characterizes the biologic activity, identity, and tissue distribution of these protein(s) in NL-AF and gestational tissues. METHODS: Third-trimester NL-AF was collected by amniocentesis, fractionated by ammonium sulfate precipitation, and submitted to an in vitro PLA2 assay. Identity of the PLA2 inhibitor in NL-AF was confirmed by Western blot and antibody neutralization studies. Secretory component-immunoreactive proteins were purified by immunoaffinity chromatography and visualized by sodium dodecyl sulfate-gel electrophoresis. Tissue distribution of SC in gestational tissues was determined by immunohistochemistry. RESULTS: The 100% pellet and supernatant fractions of NL-AF suppressed PLA2 activity, and this activity was neutralized by a polyclonal antibody to SC. Western blot studies revealed an SC-reactive protein in the 70-80-kD range in the 100% pellet fraction of NL-AF. Two SC-reactive proteins were detected in the 60-80-kD range in the eluate from the SC immunoaffinity column, along with minor proteins of 30 and greater than 100 kD. Immunohistochemical studies revealed SC in placental trophoblast, amniotic membranes, and decidual epithelium. CONCLUSIONS: These results demonstrate that proteins homologous to SC are present in human gestational tissues and possess anti-PLA2 activity. These proteins may contribute to the maintenance of pregnancy by suppressing local PG production.

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PROBLEM: Communication at the human maternal-fetal interface occurs by an intricate cytokine network. This study examines cytokine expression by normal first-trimester human chorionic villi. METHOD OF STUDY: Tissues were obtained at elective pregnancy terminations (7-9 weeks). Total RNA was isolated from chorionic villi by guanidinium isothiocynate-acid phenol extraction. A reverse transcriptase-polymerase chain reaction technique was used to examine cytokine expression. beta-Actin was used as the housekeeping gene, and mitogen-stimulated lymphocytes served as positive controls. RESULTS: beta-Actin was uniformly expressed by all chorionic villous samples. Interferon (IFN)-alpha and -beta also were highly expressed. Moderate expression was noted for interleukin (IL)-10, IL-6, tumor necrosis factor (TNF)-alpha, and IL-1 beta. In contrast, transforming growth factor-beta 1, IFN-gamma, IL-2, and IL-1 alpha were either weakly expressed or absent in first-trimester villi. CONCLUSIONS: Cytokines may contribute to pregnancy immunotolerance (IFN-alpha, IFN-beta, and IL-10), viral resistance (IFNs), hormone secretion (IL-1 and IL-6), and cellular remodeling (IFN-gamma and TNF-alpha) within the chorionic villous.

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Interleukin-10 (IL-10) is a T-helper type-2 (Th2) cytokine noted for its ability to suppress cytokine synthesis by T-helper type-1 (Th1) cells. IL-10 may play a role in pregnancy immunotolerance through the establishment of a Th2 cytokine bias at the maternal-fetal interface. This study examines the expression and production of IL-10 by normal and malignant human trophoblast. Term placental biopsies, cloned choriocarcinoma cell lines and isolated human trophoblast were utilized for the study of IL-10 expression. Choriocarcinoma cells (BeWo, JEG-3, JAR) were maintained in T-flask culture until confluence and then harvested by enzymatic dispersion. Purified term trophoblast were obtained by sequential trypsin/DNAse digests and CD9 immunoaffinity chromatography. Amplified IL-10 mRNA was detected by a reverse transcriptase polymerase chain reaction (RTPCR) technique. BeWo cells were maintained in artificial capillary culture (ACC) and conditioned media assayed for IL-10. Granulocyte macrophage-colony stimulating factor (GM-CSF; 1.0, 10.0 and 100.0 ng/ml) was added to the BeWo cultures to examine its effects on trophoblast IL-10 production. IL-10 determinations were performed using a human ELISA system. IL-10 mRNA was detected in each trophoblast cell type examined with the exception of the JEG-3 choriocarcinoma cell line. IL-10 protein was also detected (range 6-22 pg/ml) in BeWo media on days 8 to 11 of culture. When serum was reduced in the culture media, IL-10 levels fell below the sensitivity of the assay (5 pg/ml). Subsequent addition of GM-CSF stimulated BeWo IL-10 secretion in a dose-related fashion. These results support the concept IL-10 is expressed at the human maternal-fetal interface, and production of this important immunoregulatory molecule may be regulated, in part, by GM-CSF.

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PROBLEM: Cytokines form an important communication network between the mother and fetus. Defining the significance of these factors requires an understanding of their constitutive expression by maternal and fetal tissues. This study examines cytokine expression by human trophoblast. METHODS: A reverse transcription polymerase chain reaction (RT-PCR) technique was used to assess cytokine expression by choriocarcinoma cells (BeWo, JEG-3, and JAR) and term trophoblast. Placental digests were enriched for trophoblast by immunoaffinity (CD-9) columns. RESULTS: Interleukin (IL)-1, tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma were weakly expressed or absent in the choriocarcinoma cells. In contrast, these cytokines were expressed by term trophoblast. IL-6, IL-10, IFN-alpha, IFN-beta, and granulocyte macrophage-colony stimulating factor (GM-CSF) mRNA were detected in all trophoblast cells, except for a paucity of IL-10 expression by JEG-3 cells. CONCLUSIONS: Human choriocarcinoma cells and term trophoblast express cytokines that may regulate critical reproductive events. Expression of inflammatory cytokines such as IL-1, TNF-alpha, and IFN-gamma by term trophoblast could trigger labor or be a consequence of labor-associated events.

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PROBLEMS: The immunologic privilege afforded the fetus relies upon immunoregulation within the maternal-fetal interface. Trophoblast and decidua-derived immunoregulatory factors enforce this privilege by locally suppressing maternal responses to trophoblast antigens. The relative contribution of trophoblast or decidua immunosuppressive factors to pregnancy immunotolerance are not well characterized. The purpose of this study was to compare the suppressive effects of hydatidiform mole trophoblast and decidua extracts on interleukin-2-dependent proliferation. METHOD: Tissue extracts were prepared from hydatidiform mole trophoblast and decidua following uterine evacuation. Samples were submitted to interleukin-2-dependent and -independent cell proliferation assays. RESULTS: Hydatidiform mole trophoblast extract significantly (P < 0.05) suppressed interleukin-2-dependent proliferation but did not affect interleukin-2-dependent cell proliferation. In contrast, molar decidua extract suppressed both cell lines. CONCLUSIONS: Human hydatidiform mole trophoblast contains factor(s) that specifically abrogate interleukin-2-dependent clonal expansion of murine cytotoxic T-cells. In contrast, extracts of molar decidua suppressed both interleukin-2-dependent and -independent responses. This indicates that the trophoblast antagonizes critical interleukin-2-mediated immunologic responses, but that the decidua uses nonspecific antiproliferative mechanisms for immunoregulation.

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