GLORIA

GEOMAR Library Ocean Research Information Access

X

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Online Resource
    Online Resource
    Sensitivity to endotoxin in rabbits is increased after hemorrhagic shock
    American Physiological Society ; 1992
    In:  Journal of Applied Physiology Vol. 73, No. 3 ( 1992-09-01), p. 1146-1149
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 73, No. 3 ( 1992-09-01), p. 1146-1149
    Abstract: The immunoinflammatory response following trauma and hemorrhage may predispose to the development of sepsis and multiple-organ failure syndrome. Cardiac output (CO), arterial pressure, arterial PO2, and pulmonary permeability index were measured. We examined the sensitivity of rabbits to infusions of lipopolysaccharide (LPS) after hemorrhagic shock. Shock was produced by reducing CO to 40% of baseline for 90 min, followed by resuscitation with shed blood and then with lactated Ringer solution to maintain CO near baseline. Animals were assigned to three groups: 1) hemorrhagic shock only, 2) LPS only, and 3) hemorrhagic shock + LPS. Groups 1 and 3 were subjected to hemorrhagic shock on day 1. Escherichia coli LPS was infused (1.0 microgram/kg i.v.) into groups 2 and 3 on day 2. Fluid resuscitation with lactated Ringer solution was continued in an effort to maintain CO at baseline. Five hours after LPS infusion, 125I-albumin was injected intravenously, and rabbits were killed 1 h later for measurement of pulmonary permeability index. LPS infusion after shock (group 3) caused significant decreases in CO, arterial pressure, and PO2 and an increase in pulmonary permeability. These changes were not seen in the groups 1 and 2. We conclude that hemorrhagic shock and resuscitation result in a proinflammatory state, leading to increased sensitivity to subsequent exposure to LPS.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/jappl.1992.73.3.1146
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1992
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 2
    Online Resource
    Online Resource
    The MAFB transcription factor impacts islet α-cell function in rodents and represents a unique signature of primate islet β-cells
    American Physiological Society ; 2016
    In:  American Journal of Physiology-Endocrinology and Metabolism Vol. 310, No. 1 ( 2016-01-01), p. E91-E102
    Details
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 310, No. 1 ( 2016-01-01), p. E91-E102
    Abstract: Analysis of MafB −/− mice has suggested that the MAFB transcription factor was essential to islet α- and β-cell formation during development, although the postnatal physiological impact could not be studied here because these mutants died due to problems in neural development. Pancreas-wide mutant mice were generated to compare the postnatal significance of MafB ( MafB Δpanc ) and MafA/B ( MafAB Δpanc ) with deficiencies associated with the related β-cell-enriched MafA mutant (MafA Δpanc ). Insulin + cell production and β-cell activity were merely delayed in MafB Δpanc islets until MafA was comprehensively expressed in this cell population. We propose that MafA compensates for the absence of MafB in MafB Δpanc mice, which is supported by the death of MafAB Δpanc mice soon after birth from hyperglycemia. However, glucose-induced glucagon secretion was compromised in adult MafB Δpanc islet α-cells. Based upon these results, we conclude that MafB is only essential to islet α-cell activity and not β-cell. Interestingly, a notable difference between mice and humans is that MAFB is coexpressed with MAFA in adult human islet β-cells. Here, we show that nonhuman primate (NHP) islet α- and β-cells also produce MAFB, implying that MAFB represents a unique signature and likely important regulator of the primate islet β-cell.
    Type of Medium: Online Resource
    ISSN: 0193-1849 , 1522-1555
    URL: Article
    DOI: 10.1152/ajpendo.00285.2015
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2016
    detail.hit.zdb_id: 1477331-4
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 3
    Online Resource
    Online Resource
    Role of neutrophils in ischemia-reperfusion-induced microvascular injury
    American Physiological Society ; 1987
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 253, No. 3 ( 1987-09-01), p. H699-H703
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 253, No. 3 ( 1987-09-01), p. H699-H703
    Abstract: Recent studies indicate that polymorphonuclear neutrophils (PMNs) infiltrate the intestinal mucosa during ischemia and after reperfusion. To determine whether PMNs mediate the increased microvascular permeability produced by ischemia-reperfusion (I/R) we treated cats with either saline, antineutrophil serum (ANS), or a monoclonal antibody specific for the beta-chain of the CD18 complex (MoAb 60.3) that prevents neutrophil adherence and extravasation. Intestinal microvascular permeability to plasma proteins was measured in control preparations (0.08 +/- 0.007), in preparations subjected to 1 h of ischemia then reperfusion (I/R, 0.32 +/- 0.02), I/R preparations treated with ANS (0.13 +/- 0.01), and I/R preparations treated with MoAb (0.12 +/- 0.003). Our results indicate that both PMN depletion (to less than 10% control) and prevention of PMN adherence significantly attenuate the increased microvascular permeability induced by I/R. These findings, coupled to previous results obtained from this model, support the hypothesis that neutrophils, which accumulate in the mucosa in response to xanthine oxidase activation, mediate the oxyradical-dependent injury produced by reperfusion of the ischemic bowel.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.1987.253.3.H699
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1987
    detail.hit.zdb_id: 1477308-9
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 4
    Online Resource
    Online Resource
    Metabolic profiling of in vivo right ventricular function and exercise performance in pulmonary arterial hypertension
    American Physiological Society ; 2023
    In:  American Journal of Physiology-Lung Cellular and Molecular Physiology Vol. 324, No. 6 ( 2023-06-01), p. L836-L848
    Details
    In: American Journal of Physiology-Lung Cellular and Molecular Physiology, American Physiological Society, Vol. 324, No. 6 ( 2023-06-01), p. L836-L848
    Abstract: Right ventricular (RV) adaptation is the principal determinant of outcomes in pulmonary arterial hypertension (PAH), however, RV function is challenging to assess. RV responses to hemodynamic stressors are particularly difficult to interrogate without invasive testing. This study sought to identify metabolomic markers of in vivo right ventricular function and exercise performance in PAH. Consecutive subjects with PAH ( n = 23) underwent rest and exercise right heart catheterization with multibeat pressure volume loop analysis. Pulmonary arterial blood was collected at rest and during exercise. Mass spectrometry-based targeted metabolomics were performed, and metabolic associations with hemodynamics and comprehensive measures of RV function were determined using sparse partial least squares regression. Metabolite profiles were compared with N-terminal prohormone of B-type natriuretic peptide (NT-proBNP) measurements for accuracy in modeling ventriculo-arterial parameters. Thirteen metabolites changed in abundance with exercise, including metabolites reflecting increased arginine bioavailability, precursors of catecholamine and nucleotide synthesis, and branched-chain amino acids. Higher resting arginine bioavailability predicted more favorable exercise hemodynamics and pressure-flow relationships. Subjects with more severe PAH augmented arginine bioavailability with exercise to a greater extent than subjects with less severe PAH. We identified relationships between kynurenine pathway metabolism and impaired ventriculo-arterial coupling, worse RV diastolic function, lower RV contractility, diminished RV contractility with exercise, and RV dilation with exercise. Metabolite profiles outperformed NT-proBNP in modeling RV contractility, diastolic function, and exercise performance. Specific metabolite profiles correspond to RV functional measurements only obtainable via invasive pressure-volume loop analysis and predict RV responses to exercise. Metabolic profiling may inform discovery of RV functional biomarkers. NEW & NOTEWORTHY In this cohort of patients with pulmonary arterial hypertension (PAH), we investigate metabolomic associations with comprehensive right ventricular (RV) functional measurements derived from multibeat RV pressure-volume loop analysis. Our results show that tryptophan metabolism, particularly the kynurenine pathway, is linked to intrinsic RV function and PAH pathobiology. Findings also highlight the importance of arginine bioavailability in the cardiopulmonary system’s response to exercise stress. Metabolite profiles selected via unbiased analysis outperformed N-terminal prohormone of B-type natriuretic peptide (NT-proBNP) in predicting load-independent measures of RV function at rest and cardiopulmonary system performance under stress. Overall, this work suggests the potential for select metabolites to function as disease-specific biomarkers, offers insights into PAH pathobiology, and informs discovery of potentially targetable RV-centric pathways.
    Type of Medium: Online Resource
    ISSN: 1040-0605 , 1522-1504
    URL: Article
    DOI: 10.1152/ajplung.00003.2023
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2023
    detail.hit.zdb_id: 1477300-4
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 5
    Online Resource
    Online Resource
    Inhibition of leukocyte adherence and aggregation for treatment of severe cold injury in rabbits
    American Physiological Society ; 1993
    In:  Journal of Applied Physiology Vol. 74, No. 3 ( 1993-03-01), p. 1432-1436
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 74, No. 3 ( 1993-03-01), p. 1432-1436
    Abstract: We tested the hypothesis that blocking neutrophil adherence and/or aggregation reduces tissue injury that results when tissue is frozen and rewarmed. The left hindlimbs of three groups of New Zealand White rabbits were immersed in a -15 degrees C salt water bath for 30 min to freeze the foot. The foot was rewarmed in a 39 degrees C water bath. In two groups, adherence and aggregation were blocked with monoclonal antibody (MAb) 60.3, and the third group was treated with saline. Two of the groups were treated at the time of rewarming with either saline or MAb 60.3, and the third group received MAb 60.3 at the conclusion of rewarming. Tissue edema and tissue loss were significantly less in the two groups receiving MAb 60.3 than in the control group. Rabbits treated at the time of rewarming had less edema and tissue loss than those treated at the completion of rewarming. These studies indicate that a substantial component of severe cold injury is neutrophil mediated and occurs after rewarming.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/jappl.1993.74.3.1432
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1993
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 6
    Online Resource
    Online Resource
    A system for recording neural activity chronically and simultaneously from multiple cortical and subcortical regions in nonhuman primates
    American Physiological Society ; 2012
    In:  Journal of Neurophysiology Vol. 107, No. 7 ( 2012-04-01), p. 1979-1995
    Details
    In: Journal of Neurophysiology, American Physiological Society, Vol. 107, No. 7 ( 2012-04-01), p. 1979-1995
    Abstract: A major goal of neuroscience is to understand the functions of networks of neurons in cognition and behavior. Recent work has focused on implanting arrays of ∼100 immovable electrodes or smaller numbers of individually adjustable electrodes, designed to target a few cortical areas. We have developed a recording system that allows the independent movement of hundreds of electrodes chronically implanted in several cortical and subcortical structures. We have tested this system in macaque monkeys, recording simultaneously from up to 127 electrodes in 14 brain regions for up to one year at a time. A key advantage of the system is that it can be used to sample different combinations of sites over prolonged periods, generating multiple snapshots of network activity from a single implant. Used in conjunction with microstimulation and injection methods, this versatile system represents a powerful tool for studying neural network activity in the primate brain.
    Type of Medium: Online Resource
    ISSN: 0022-3077 , 1522-1598
    URL: Article
    DOI: 10.1152/jn.00625.2011
    RVK:
    XA 10000 ; XA 552555
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2012
    detail.hit.zdb_id: 80161-6
    detail.hit.zdb_id: 1467889-5
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 7
    Online Resource
    Online Resource
    Role of TGF-alpha in the progression of diabetic kidney disease
    American Physiological Society ; 2017
    In:  American Journal of Physiology-Renal Physiology Vol. 312, No. 6 ( 2017-06-01), p. F951-F962
    Details
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 312, No. 6 ( 2017-06-01), p. F951-F962
    Abstract: Transforming growth factor-alpha (TGFA) has been shown to play a role in experimental chronic kidney disease associated with nephron reduction, while its role in diabetic kidney disease (DKD) is unknown. We show here that intrarenal TGFA mRNA expression, as well as urine and serum TGFA, are increased in human DKD. We used a TGFA neutralizing antibody to determine the role of TGFA in two models of renal disease, the remnant surgical reduction model and the uninephrectomized (uniNx) db/db DKD model. In addition, the contribution of TGFA to DKD progression was examined using an adeno-associated virus approach to increase circulating TGFA in experimental DKD. In vivo blockade of TGFA attenuated kidney disease progression in both nondiabetic 129S6 nephron reduction and Type 2 diabetic uniNx db/db models, whereas overexpression of TGFA in uniNx db/db model accelerated renal disease. Therapeutic activity of the TGFA antibody was enhanced with renin angiotensin system inhibition with further improvement in renal parameters. These findings suggest a pathologic contribution of TGFA in DKD and support the possibility that therapeutic administration of neutralizing antibodies could provide a novel treatment for the disease.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    URL: Article
    DOI: 10.1152/ajprenal.00443.2016
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2017
    detail.hit.zdb_id: 1477287-5
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 8
    Online Resource
    Online Resource
    Kynurenine pathway metabolism evolves with development of preclinical and scleroderma-associated pulmonary arterial hypertension
    American Physiological Society ; 2023
    In:  American Journal of Physiology-Lung Cellular and Molecular Physiology
    Details
    In: American Journal of Physiology-Lung Cellular and Molecular Physiology, American Physiological Society
    Abstract: Background: Understanding metabolic evolution underlying pulmonary arterial hypertension (PAH) development may clarify pathobiology and reveal disease-specific biomarkers. Systemic sclerosis (SSc) patients are regularly surveilled for PAH, presenting an opportunity to examine metabolic change as disease develops in an at-risk cohort. Methods: We performed mass spectrometry-based metabolomics on longitudinal serum samples collected prior to and near SSc-PAH diagnosis, compared to time-matched SSc subjects without PAH, in a SSc surveillance cohort. We validated metabolic differences in a second cohort and determined metabolite-phenotype relationships. In parallel, we performed serial metabolomic and hemodynamic assessments as disease developed in a preclinical model. For differentially expressed metabolites, we investigated corresponding gene expression in human and rodent PAH lungs. Results: Kynurenine and its ratio to tryptophan (kyn/trp) increased over the surveillance period in SSc patients who developed PAH. Higher kyn/trp measured two years prior to diagnostic right heart catheterization increased the odds of SSc-PAH diagnosis (OR 1.57, 95% CI 1.05-2.36, p = 0.028). The slope of kyn/trp rise during SSc surveillance predicted PAH development and mortality. In both clinical and experimental PAH, higher kynurenine pathway metabolites correlated with adverse pulmonary vascular and RV measurements. In human and rodent PAH lungs, expression of TDO2, which catalyzes tryptophan conversion to kynurenine, was significantly upregulated and tightly correlated with pulmonary hypertensive features. Conclusions: Upregulated kynurenine pathway metabolism occurs early in PAH, localizes to the lung, and may be modulated by TDO2. Kynurenine pathway metabolites may be candidate PAH biomarkers.
    Type of Medium: Online Resource
    ISSN: 1040-0605 , 1522-1504
    URL: Article
    DOI: 10.1152/ajplung.00177.2023
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2023
    detail.hit.zdb_id: 1477300-4
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 9
    Online Resource
    Online Resource
    Effect of indomethacin on coronary vascular response to increased myocardial oxygen consumption
    American Physiological Society ; 1978
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 235, No. 4 ( 1978-10-01), p. H372-H378
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 235, No. 4 ( 1978-10-01), p. H372-H378
    Abstract: We tested the hypothesis that arachidonic acid metabolites mediate the coronary vascular response to changes in cardiac activity. Isoproterenol was administered intravenously to five chloralose-anesthetized, open-chest dogs. Left anterior descending coronary artery blood flow, systemic arterial blood pressure, and great cardiac vein O2 content were continuously measured, and blood gas determination (including O2 content) were made before and after infusions. From these data, coronary vascular conductance, coronary O2 delivery, and myocardial O2 consumption were calculated. Isoproterenol increased conductance, O2 delivery, and O2 consumption. Indomethacin, a blocker of prostaglandin synthesis, was administered, and the isoproterenol infusions were repeated. The changes in conductance, O2 delivery, and O2 consumption associated with isoproterenol were not different after indomethacin was administered than before indomethacin was administered. Neither were the relations between conductance or O2 delivery and O2 consumption affected by indomethacin. We conclude that, in this preparation and with this stimulus, prostaglandins do not appear to mediate or modulate the coronary vascular response to changes in cardiac activity.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.1978.235.4.H372
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1978
    detail.hit.zdb_id: 1477308-9
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 10
    Online Resource
    Online Resource
    Role of leukocyte CD11/CD18 complex in endotoxic and septic shock in rabbits
    American Physiological Society ; 1992
    In:  Journal of Applied Physiology Vol. 73, No. 4 ( 1992-10-01), p. 1510-1516
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 73, No. 4 ( 1992-10-01), p. 1510-1516
    Abstract: Two models of sepsis were investigated using rabbits. In the first model, rabbits given lipopolysaccharide (LPS) were treated with saline (group II) or CD18 monoclonal antibody (MAb) 60.3 (group III). Group I animals received no LPS. Cardiac output was maintained by infusion of lactated Ringer solution with group II (95 +/- 68 ml/kg) requiring significantly more than group I (0 +/- 0 ml/kg) or group III (39 +/- 27 ml/kg). Lung permeability indexes in groups II (median 0.002, range 0.023) and III (median 0.0035, range 0.053) were not different but were significantly greater than group I (median 0.0007, range 0.001). In the second model, peritonitis was produced by devascularizing the appendix, leaving it in situ for 19 h, and then performing an appendectomy. Saline or MAb 60.3 treatment was at appendectomy and every 12 h for 3 days. Survival was significantly greater in the MAb 60.3-treated group at day 10 (90 vs. 40%). Lung permeability was increased at day 2 and was not different between groups. Day 1 fluid requirements were greater in the saline-treated group. These data are consistent with MAb 60.3 protection of systemic but not pulmonary circulation in two models of sepsis.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/jappl.1992.73.4.1510
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1992
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...