scholarly journals Effects of Non-directional Mechanical Trauma on Gastrointestinal Tract Injury in Rats

2021 ◽  
Vol 12 ◽  
Author(s):  
Lihong Liu ◽  
Lianpu Wen ◽  
Chuanzhou Gao ◽  
Hua Piao ◽  
Hui Zhao ◽  
...  
Keyword(s):  
Gastrointestinal Tract ◽  
Cardiac Dysfunction ◽  
Intercellular Space ◽  
Morphological Changes ◽  
Mucosal Injury ◽  
Cell Junction ◽  
Mechanical Trauma ◽  
Secondary Injury ◽  
Cecal Mucosa ◽  
Time Point

Mechanical trauma can (MT) cause secondary injury, such as cardiomyocyte apoptosis and cardiac dysfunction has been reported. However, the effects of mechanical trauma on gastrointestinal tract is unclear. This study aims to observe the main location and time of gastrointestinal tract injury caused by non-directional trauma and explain the reason of the increase of LPS in blood caused by mechanical injury. Morphological changes in the stomach, ileum and cecum at different time points after MT were observed in this experiment. The results reveal that the injury to the cecal mucosa in the rats was more obvious than that in the ileum and the stomach. The cecal epithelial cell junction was significantly widened at 20 min after MT, and the plasma LPS and D-lactic acid concentrations increased significantly at the same time point. In addition, some bacterial structures in the widened intercellular space and near the capillary wall of the cecal mucosa were detected at 12 h after MT. This finding suggests that the main reason for the increase in LPS in plasma after MT is cecal mucosal injury. This study is important for the early intervention of the gastrointestinal tract to prevent secondary injury after MT.

scholarly journals Echocardiographic Myocardial Strain Analysis Describes Subclinical Cardiac Dysfunction after Craniospinal Irradiation in Pediatric and Young Adult Patients with Central Nervous System Tumors

2020 ◽  
Author(s):  
Thomas D Ryan ◽  
Hugo R. Martinez ◽  
Ralph Salloum ◽  
Erin Wright ◽  
Lauren Bueche ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Cardiac Dysfunction ◽  
Myocardial Strain ◽  
Strain Analysis ◽  
Late Time ◽  
Systolic Strain ◽  
Peak Systolic Strain ◽  
Myocardial Strain Analysis ◽  
Late Time Point ◽  
Time Point

Abstract Background: Craniospinal irradiation (CSI) is part of the treatment of central nervous system (CNS) tumors and is associated with cardiovascular disease in adults. Global myocardial strain analysis including longitudinal peak systolic strain (GLS), circumferential peak systolic strain (GCS) and radial peak systolic strain (GRS) can reveal subclinical cardiac dysfunction.Methods: Retrospective, single-center study in patients managed with CSI vs. age-matched controls. Clinical data and echocardiography, including myocardial strain analysis, were collected at early (<12 months) and late ( 12 months) after completion of CSI.Results: Echocardiograms were available in 20 early and 34 late patients. Patients at the late time point were older (21.7±10.4 vs. 13.3 9.6 years), and further out from CSI (13.1±8.8 vs. 0.2±0.3 years). Standard echocardiographic parameters were normal for all subjects. For the early time, CSI vs. control: GLS was -16.8 3.6% vs. -21.3 4.0% (p=0.0002), GCS was -22.5 5.2% vs. -21.3 3.4% (p=0.28), and GRS was 21.8 11.0% vs. 26.9 7.7% (p=0.07). At the late time point, CSI vs. control: GLS was -16.2 5.4% vs. -21.6 3.7% (p<0.0001), GCS was -20.9 6.8% vs. -21.9 3.5% (p=0.42), and GRS was 22.5 10.0% vs. 27.3 8.3% (p=0.03). Radiation type (proton vs. photon), and radiation dose (<30 Gy vs. 30 Gy) did not impact any parameter.Conclusions: Subclinical cardiac systolic dysfunction by GLS is present both early and late after CSI. These results argue for inclusion of baseline cardiovascular assessment and early initiation of longitudinal follow-up post CSI.

Abstract 22: Transient Receptor Potential M2 is Involved in Secondary Myocardial Injury Induced by Nonlethal Mechanical Trauma in Rats

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Shuzhuang Li ◽  
Tingting Cao ◽  
Shuo Ma ◽  
Xiujie Li ◽  
Yue Bi ◽  
...  
Keyword(s):  
Cardiac Dysfunction ◽  
Myocardial Injury ◽  
Transient Receptor Potential ◽  
Flufenamic Acid ◽  
Mechanical Trauma ◽  
H9c2 Cells ◽  
Sprague Dawley ◽  
Cardiac Damage ◽  
Trpm2 Channel

Background: It is an imperative task to identify the mechanisms responsible for post-traumatic secondary myocardial injury. Our previous experiments showed that mechanical trauma (MT) could induce secondary myocardial injury via oxidative stress. The transient potential receptor M2 (TRPM2) channel has emerged as an important Ca 2+ signaling mechanism in a variety of cells, contributing to cellular functions that include cytokine production, cell motility and cell death. However, the role of TRPM2 channel in nonlethal mechanical traumatic cardiac damage remains unclear. The aim of the present study was to investigate whether TRPM2 channel is involved in myocardial injury in rats subjected to nonlethal MT. Methods and results: Western blot was used to quantify TRPM2 protein levels in Ventricular myocytes of adult male Sprague Dawley rats. Up-regulation of TRPM2 channel protein was observed in the following 12h after MT. It was observed that plasma harvested from MT rats increased cytosolic Ca 2+ concentration dose-dependently in H9c2 cells. To verify the role of TRPM2 further, we administered TRPM2 blockers flufenamic acid (FFA, 100uM) and clotrimazole (CLZ, 30uM) respectively to inhibit Ca 2+ influx, which leads to attenuated intracelluar Ca 2+ overload and apoptosis induced by MT plasma in H9c2 cells. Those two TRPM2 blockers also improved cardiac dysfunction induced MT in rats. When we used TMB-8 (inhibitor of sarcoplasmic reticulum Ca 2+ store) to inhibit calcium store mobilization, intracellular Ca 2+ level, apoptosis and cardiac dysfunction were also ameliorated. However, the administration of KBR-7943 (inhibitor of Na/Ca exchanger) did not reverse the pathological process following MT. Conclusion: These results demonstrate that post-trauma pathological phenomena is associated with TRPM2 closely via a redox-sensitive signal transduction pathway (mainly via MT-initiated Ca 2+ influx, even calcium overload pathway) .We propose that treatments like blockage of TRPM2 channel-associated Ca 2+ influx and mobilization, may shed light on the novel therapeutic strategy in reducing cardiac injury and post-trauma multiple organ failure.

Role of leukocytes in indomethacin-induced small bowel injury in the rat

1994 ◽  
Vol 266 (2) ◽  
pp. G239-G246 ◽  
Author(s):  
H. M. Chmaisse ◽  
J. S. Antoon ◽  
P. R. Kvietys ◽  
M. B. Grisham ◽  
M. A. Perry
Keyword(s):  
Small Bowel ◽  
Morphological Changes ◽  
Mucosal Injury ◽  
Bowel Injury ◽  
Rat Jejunum ◽  
Small Bowel Injury ◽  
Mucosal Permeability ◽  
Quantitative Histology ◽  
51Cr Edta

This study assesses the role of neutrophils in indomethacin-induced small bowel injury and determines the influence of intestinal pH on the magnitude of this injury. Rat jejunum was perfused via the lumen with buffer, and mucosal injury was assessed by blood-to-lumen clearance of 51Cr-EDTA and quantitative histology. Reduction in luminal pH from 7.4 to 6.0 in the presence of indomethacin (1.0 mg/ml) increased 51Cr-EDTA clearance from 2.0 +/- 0.1 to 6.5 +/- 0.3 microliter.min-1.g-1. Indomethacin caused a reduction in villus length, an increase in villus width, and an increase in lesion score. Depletion of neutrophils with antiserum largely prevented the increase in 51Cr-EDTA clearance and morphological changes. Intravenous indomethacin given at a dose to mimic therapeutic plasma levels (1 mg/kg iv) had no significant effect on 51Cr-EDTA clearance but caused similar morphological changes to those observed following intraluminal administration. The data suggest that neutrophils play a role in acute indomethacin injury and that the drug given intravenously can cause morphological changes without necessarily altering mucosal permeability to 51Cr-EDTA.

scholarly journals Nitric oxide as a mediator of gastrointestinal mucosal injury?—Say it ain't so

1995 ◽  
Vol 4 (6) ◽  
pp. 397-405 ◽  
Author(s):  
Paul Kubes ◽  
John L. Wallace
Keyword(s):  
Nitric Oxide ◽  
Gastrointestinal Tract ◽  
Inflammatory Responses ◽  
Tissue Injury ◽  
Mucosal Blood Flow ◽  
Mucosal Injury ◽  
Experimental Models ◽  
Radical Species ◽  
Overwhelming Evidence ◽  
Mucosal Defence

Nitric oxide has been suggested as a contributor to tissue injury in various experimental models of gastrointestinal inflammation. However, there is overwhelming evidence that nitric oxide is one of the most important mediators of mucosal defence, influencing such factors as mucus secretion, mucosal blood flow, ulcer repair and the activity of a variety of mucosal immunocytes. Nitric oxide has the capacity to down-regulate inflammatory responses in the gastrointestinal tract, to scavenge various free radical species and to protect the mucosa from injury induced by topical irritants. Moreover, questions can be raised regarding the evidence purported to support a role for nitric oxide in producing tissue injury. In this review, we provide an overview of the evidence supporting a role for nitric oxide in protecting the gastrointestinal tract from injury.

Monochloramine induces reorganization of nuclear speckles and phosphorylation of SRp30 in human colonic epithelial cells: role of protein kinase C

2003 ◽  
Vol 285 (5) ◽  
pp. C1294-C1303 ◽  
Author(s):  
Ya-Qin Zhu ◽  
Yu Lu ◽  
Xiao-Di Tan
Keyword(s):  
Gastrointestinal Tract ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Morphological Changes ◽  
Sr Proteins ◽  
Mrna Splicing ◽  
Intestinal Epithelial ◽  
Nuclear Speckles ◽  
Colonic Epithelial Cells ◽  
Stimulation Of

Intestinal epithelial cells are constantly stimulated by reactive oxidant metabolites (ROMs) in inflamed mucosa. Monochloramine (NH2Cl), a cell-permeant ROM, is particularly relevant to the pathogenesis of inflammation in the gastrointestinal tract. Nuclear speckles, a unique nuclear subcompartment, accumulate a family of proteins, namely, serine- and arginine-rich (SR) proteins. They play important roles in regulation of pre-mRNA splicing. Currently, little is known about the link between inflammatory stimulation and the pre-mRNA splicing process, although gene expression is changed in inflamed tissues. The present study was designed to investigate whether stimulation of human colonic epithelial cells (HT-29 and Caco-2 cell lines) with NH2Cl affects nuclear speckles and their components. By indirect immunofluorescence, nuclear speckles have been shown to undergo rapid aggregation after NH2Cl stimulation. By utilizing Western blotting, SRp30 (a subset of SR proteins) in intestinal epithelial cells was found to be phosphorylated after NH2Cl treatment, whereas other SR proteins were not responsive to NH2Cl stimulation. The cytotoxic effect of NH2Cl was excluded by both negative lactate dehydrogenase assay and propidium iodide staining. Therefore, NH2Cl-induced morphological changes on nuclear speckles and phosphorylated SRp30 do not result from intestinal epithelial injury. Furthermore, the effect of NH2Cl on nuclear speckles and SRp30 was blocked by bisindolylmaleimide I, a selective PKC inhibitor. Together, the available data suggest that stimulation of intestinal epithelial cells with NH2Cl results in a consequent change on pre-mRNA splicing machinery via a distinctive signal pathway involving activation of PKC. This effect may contribute to oxidant-induced pathophysiological changes in the gastrointestinal tract.

scholarly journals Functional and Morphological Correlations before and after Video-Documented 23-Gauge Pars Plana Vitrectomy with Membrane and ILM Peeling in Patients with Macular Pucker

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Wolfgang J. Mayer ◽  
Clara Fazekas ◽  
Ricarda Schumann ◽  
Armin Wolf ◽  
Denise Compera ◽  
...  
Keyword(s):  
Visual Acuity ◽  
Morphological Changes ◽  
Mechanical Trauma ◽  
Retinal Sensitivity ◽  
Ilm Peeling ◽  
Epiretinal Membranes ◽  
Morphological Alterations ◽  
Inner Limiting Membrane ◽  
Before And After ◽  
23 Gauge

Purpose. To assess functional and morphological alterations following video-documented surgery for epiretinal membranes.Methods. Forty-two patients underwent video-documented 23-gauge vitrectomy with peeling of epiretinal (ERM) and inner limiting membrane (ILM). Patient assessment was performed before and 3 and 6 months including best corrected visual acuity (BCVA), slit lamp biomicroscopy, SD-OCT, and central 2° and 18° microperimetry. In addition, all video-documented areas of peeling on the retinal surface were evaluated postoperatively using an additional focal 2° microperimetry. Retinal sensitivity and BCVA were correlated with morphological changes (EZ and ELM) in the foveal region and in regions of membrane peeling.Results. Overall, BCVA increased from 0.6 (±0.2) to 0.2 (±0.2) logMAR after 6 months with an increase in retinal sensitivity (17.9 ± 2.7 dB to 26.8 ± 3.1 dB,p<0.01). We observed a significant correlation between the integrity of the EZ but not of the ELM and the retinal sensitivity, overall and in peeling areas (p<0.05). However, no significant correlation between alterations in the area of peeling and overall retinal sensitivity regarding visual acuity gain could be observed after 6 months (p>0.05). In contrast, overall postoperative retinal sensitivity was significantly decreased in patients with a visual acuity gain lower than 2 lines (p<0.05) correlating with EZ defects seen in OCT.Conclusions. Mechanical trauma of epiretinal membrane and ILM peeling due to the use of intraocular forceps may affect the outer retinal structure. Nevertheless, these changes seem to have no significant impact on postoperative functional outcome.

Neuroprotection for Spinal Cord Injury

2017 ◽  
Author(s):  
Christopher S. Ahuja ◽  
Michael Fehlings
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Spinal Cord Injuries ◽  
Current Evidence ◽  
Mechanical Trauma ◽  
Secondary Injury ◽  
Loss Of Function ◽  
Cord Injury ◽  
Death And Loss

Traumatic spinal cord injuries (SCI) often have a devastating impact on quality of life for patients and their families. Neuroprotection for spinal cord injury is aimed at improving functional outcomes by limiting secondary injury processes that occur within the first minutes, hours, and days following the primary injury. The primary mechanical trauma initiates a secondary injury cascade where ischemia, inflammatory cell infiltration, and cytotoxic changes in the microenvironment cause further cell death and loss of function. Time-sensitive neuroprotective measures targeting these secondary insults have emerged as key therapeutic strategies. This chapter summarizes current evidence-based neuroprotective treatments, such as blood pressure augmentation, early surgical decompression, and intravenous methylprednisolone, as well as important emerging interventions, including therapeutic hypothermia, sodium channel blockade using riluzole, and the anti-inflammatory actions of minocycline. The chapter concludes by summarizing the current guidelines that all practitioners should be well-versed in prior to providing care for patients with SCI.

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