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  • 1
    Online Resource
    Online Resource
    Estrogen-induced left ventricular chamber enlargement in ewes
    American Physiological Society ; 1993
    In:  American Journal of Physiology-Endocrinology and Metabolism Vol. 264, No. 4 ( 1993-04-01), p. E490-E496
    Details
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 264, No. 4 ( 1993-04-01), p. E490-E496
    Abstract: We studied the chronic effect of administration of a single large intramuscular dose of 17 beta-estradiol on left ventricular chamber size and output in the ewe. Fourteen oophorectomized ewes were successfully instrumented and studied, with measurements made of left ventricular, aortic, right and left atrial pressures, left ventricular stroke volume, and left ventricular minor axis dimension. Unanesthetized ewes were studied before and 1, 2, and 3 wk after intramuscular administration of 0.6 mg/kg 17 beta-estradiol (7 ewes) or 1.5 ml sesame oil placebo (7 ewes). Left ventricular end-diastolic pressure-end-diastolic dimension (LVEDP-EDD) and left ventricular end-diastolic pressure-stroke volume (LVEDP-SV) relationships were quantified during graded inferior vena caval occlusion and volume infusion. Left ventricular end-diastolic diameter was larger after estrogen but not after placebo administration. The LVEDP-EDD relationship shifted progressively rightward, indicating left ventricular chamber enlargement in the estrogen group but was unchanged in the placebo group. The plateau limb of the LVEDP-SV relationship in the estrogen group shifted up from a mean stroke volume of 77.1-89.5 ml/beat and did not change in the placebo group. We conclude that administration of a single large intramuscular dose of 17 beta-estradiol resulted in left ventricular chamber enlargement and increased stroke volume in the ewe.
    Type of Medium: Online Resource
    ISSN: 0193-1849 , 1522-1555
    URL: Article
    DOI: 10.1152/ajpendo.1993.264.4.E490
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1993
    detail.hit.zdb_id: 1477331-4
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    Gene expression profiles of bovine caruncular and intercaruncular endometrium at implantation
    American Physiological Society ; 2009
    In:  Physiological Genomics Vol. 39, No. 1 ( 2009-09), p. 14-27
    Details
    In: Physiological Genomics, American Physiological Society, Vol. 39, No. 1 ( 2009-09), p. 14-27
    Abstract: At implantation the endometrium undergoes modifications necessary for its physical interactions with the trophoblast as well as the development of the conceptus. We aim to identify endometrial factors and pathways essential for a successful implantation in the caruncular (C) and the intercaruncular (IC) areas in cattle. Using a 13,257-element bovine oligonucleotide array, we established expression profiles at day 20 of the estrous cycle or pregnancy (implantation), revealing 446 and 1,295 differentially expressed genes (DEG) in C and IC areas, respectively (false discovery rate = 0.08). The impact of the conceptus was higher on the immune response function in C but more prominent on the regulation of metabolism function in IC. The C vs. IC direct comparison revealed 1,177 and 453 DEG in cyclic and pregnant animals respectively (false discovery rate = 0.05), with a major impact of the conceptus on metabolism and cell adhesion. We selected 15 genes including C11ORF34, CXCL12, CXCR4, PLAC8, SCARA5, and NPY and confirmed their differential expression by quantitative RT-PCR. The cellular localization was analyzed by in situ hybridization and, upon pregnancy, showed gene-specific patterns of cell distribution, including a high level of expression in the luminal epithelium for C11ORF34 and MX1. Using primary cultures of bovine endometrial cells, we identified PTN, PLAC8, and CXCL12 as interferon-τ (IFNT) target genes and MSX1 and CXCR7 as IFNT-regulated genes, whereas C11ORF34 was not an IFNT-regulated gene. Our transcriptomic data provide novel molecular insights accounting for the biological functions related to the C or IC endometrial areas and may contribute to the identification of potential biomarkers for normal and perturbed early pregnancy.
    Type of Medium: Online Resource
    ISSN: 1094-8341 , 1531-2267
    URL: Article
    DOI: 10.1152/physiolgenomics.90404.2008
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2009
    detail.hit.zdb_id: 2031330-5
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  • 3
    Online Resource
    Online Resource
    Vascular pressure-volume relationships in pregnant and estrogen-treated guinea pigs
    American Physiological Society ; 1989
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 257, No. 5 ( 1989-11-01), p. R1205-R1211
    Details
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 257, No. 5 ( 1989-11-01), p. R1205-R1211
    Abstract: We investigated the relationship between mean circulatory filling pressure (MCFP) and blood volume in nonpregnant (NP), estrogen-treated (E), and pregnant (P) guinea pigs. Reversible circulatory arrest was produced by rapid ventricular pacing or acetylcholine in unanesthetized animals remote from surgery. MCFP (mmHg) was higher for E (7.1 +/- 0.3) than for NP (5.8 +/- 0.5) or P (5.3 +/- 0.4). The gradient for venous return, the difference between MCFP and right atrial pressure (mmHg), did not differ in NP- (6.0 +/- 0.5), P- (5.8 +/- 0.5), or E- (5.8 +/- 0.4) treated animals. Capacitance, the blood volume (ml/kg) at an MCFP of 6 mmHg, was increased in P (84 +/- 6) and E (89 +/- 7), compared with NP (64 +/- 5) animals. Compliance, the ratio of the change in volume to change in pressure in the range of 6-12 mmHg (ml.kg-1.mmHg-1), was greater in P (4.4 +/- 0.3) than NP (3.5 +/- 0.3) animals. Hexamethonium blockade did not affect MCFP, capacitance, or compliance. We conclude that the effect of blood volume expansion on the circulation in pregnancy cannot be predicted from knowledge of MCFP-blood volume relationships in the nonpregnant animal, because capacitance and compliance are altered. Estrogen administration to nonpregnant animals reproduces some of these effects.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    URL: Article
    DOI: 10.1152/ajpregu.1989.257.5.R1205
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1989
    detail.hit.zdb_id: 1477297-8
    SSG: 12
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  • 4
    Online Resource
    Online Resource
    Growth factors associated with gastric mucosal hypertrophy in autoimmune gastritis
    American Physiological Society ; 2004
    In:  American Journal of Physiology-Gastrointestinal and Liver Physiology Vol. 287, No. 4 ( 2004-10), p. G910-G918
    Details
    In: American Journal of Physiology-Gastrointestinal and Liver Physiology, American Physiological Society, Vol. 287, No. 4 ( 2004-10), p. G910-G918
    Abstract: A prominent pathological feature of murine autoimmune gastritis is a pronounced mucosal hypertrophy. Here, we examined factors that may be responsible for inducing this hypertrophy. Because gastrin is known to be both an inducer of gastric mucosal cell proliferation and is elevated in autoimmune gastritis, mice deficient in gastrin were thymectomised at day 3 and assessed for autoimmune gastritis. Gastrin-deficient mice showed all the characteristic features of murine autoimmune gastritis, including gastric unit hypertrophy due to hyperproliferation and accumulation of immature epithelial cells, decreases in the number of zymogenic and parietal cells, and autoantibodies to the gastric H + /K + -ATPase. Hence, gastrin is not required for either the establishment of chronic gastritis or development of the typical pathological features of this disease. We also examined mRNA levels of a number of gastric mucosal growth factors in RNA samples from mice with hypertrophic autoimmune gastritis. Members of the Reg family, RegIIIβ and RegIIIγ, were greatly elevated in mice with hypertrophic gastritis, whereas RegI and amphiregulin (an EGF receptor ligand) were more modestly and/or inconsistently induced. These data demonstrate that induction of gastric mitogenic factors, such as members of the Reg family, can be achieved in inflammatory situations by gastrin-independent pathways. Members of the Reg family, in particular RegIIIβ and RegIIIγ, are good candidates to be involved in inducing the mucosal hyperproliferation in autoimmune gastritis. These findings are likely to be of relevance to other gastric inflammatory conditions.
    Type of Medium: Online Resource
    ISSN: 0193-1857 , 1522-1547
    URL: Article
    DOI: 10.1152/ajpgi.00469.2003
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2004
    detail.hit.zdb_id: 1477329-6
    SSG: 12
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